The FDA's Controversial Approval of a New Alzheimer's Drug Explained
Link Between High Blood Sugar and Alzheimer's Is Bolstered by New Research in Mice
“Wakefulness” Part of the Brain Attacked First in Alzheimer’s, Study Says
Tech Firms Look to Robotic Pets, Music and VR to Help Treat Alzheimer’s
Late-Life High Blood Pressure May Harm the Brain, Study Says
Early Alzheimer's 'Jalisco' Mutation Is A Curse For Families
You Can Transform Your Genetic Ancestry Data Into Health Info, But Your Results May Vary
When Will Mental Illness Be Diagnosed With a Lab Test?
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It is the first new drug approved by the agency for Alzheimer’s disease since 2003.\u003c/p>\n\u003cp>The drug is the first to show significant progress against the sticky brain plaques that are the hallmark of Alzheimer’s disease.\u003c/p>\n\u003cp>The drug has proved highly effective at reducing the plaques, called beta-amyloid, that build up in the brains of people with Alzheimer’s.\u003c/p>\n\u003cp>But does the drug actually slow the progression of the disease when it reduces the plaques? It’s not yet clear. Two large studies offered conflicting evidence about whether the treatment slows declines in memory and thinking. A panel of expert advisers to the FDA \u003ca href=\"https://www.npr.org/2020/11/06/932215023/fda-advisory-panel-rejects-controversial-alzheimers-drug\">recommended in November\u003c/a> that the agency not approve the drug.\u003c/p>\n\u003cp>As a condition of approval, the FDA is requiring Biogen, the drug’s maker, to conduct another clinical study to confirm that the reduction of amyloid plaques results in clinical improvement for patients. If the subsequent study doesn’t show a clinical improvement, the agency could move to withdraw the approval.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>There are also concerns that the FDA’s approval will make it difficult for Biogen and Eisai, the companies marketing the drug, to find enough patients to participate in its next clinical trials as patients might not want to risk getting the placebo and can get the drug without being in a study.\u003c/p>\n\u003cp>The medicine will be marketed under the trade name Aduhelm.\u003c/p>\n\u003cp>The FDA acknowledged the controversy and attention the drug’s approval has garnered from the Alzheimer’s patient community, elected officials and others.\u003c/p>\n\u003cp>The agency opted to put Aduhelm on the FDA’s accelerated approval pathway, which is meant to speed access to potentially valuable therapies for patients with serious diseases to serve an unmet need, and where a clinical benefit is expected — even if there is still some uncertainty about that benefit.\u003c/p>\n\u003cp>“[T]he Agency concluded that the benefits of Aduhelm for patients with Alzheimer’s disease outweighed the risks of the therapy,” Patrizia Cavazzoni, director of the FDA Center for Drug Evaluation and Research, said in a statement.\u003c/p>\n\u003cp>It could take several years to conclude the clinical trials the FDA is requiring. But in the meantime, Aduhelm will be available to patients.\u003c/p>\n\u003cp>Patients will receive the drug in monthly infusions. They will also need regular brain scans to detect a rare side effect: bleeding or swelling in the brain.\u003c/p>\n\u003cp>Biogen and Eisai said Monday that the annual wholesale cost for those taking maintenance doses \u003ca href=\"https://investors.biogen.com/news-releases/news-release-details/biogen-and-eisai-launch-multiple-initiatives-help-patients\">would be $56,000\u003c/a> a year for a patient of average U.S. weight with mild cognitive impairment or mild dementia. The net price could change based on discounts and rebates.\u003c/p>\n\u003cp>Trading in Biogen shares was halted due to the announcement. After trading resumed midafternoon, shares were up more than $110, or 39%.\u003c/p>\n\u003cp>The Alzheimer’s Association, which has been pushing for approval, applauded the news.\u003c/p>\n\u003cp>“This is the first drug that slows Alzheimer’s disease. And, this is the beginning of a completely new future for Alzheimer’s treatments,” the group said in a statement. “This is a new type of Alzheimer’s treatment; it addresses the disease in a way that has never been done before, compared to currently approved drugs.”\u003c/p>\n\u003cp>But others say the drugmakers have not yet proved that aducanumab’s benefits outweigh its risks.\u003c/p>\n\u003cp>In November, an FDA advisory committee of medical experts voted that the evidence did not show the drug to be effective at slowing Alzheimer’s. One major study found that aducanumab slowed down the progress of Alzheimer’s, while the other showed it didn’t.\u003c/p>\n\u003cp>“Usually, you need two big studies finding the same thing to approve a drug,” NPR \u003ca href=\"https://www.npr.org/2020/11/06/932215023/fda-advisory-panel-rejects-controversial-alzheimers-drug\">reported\u003c/a> after the vote last year. But at that meeting, “the FDA asked its experts to focus only on the positive study, and it also presented analysis of the data that was really very favorable to the drug. All of that did not go over well with these advisers. Some of them seemed to feel like they were being railroaded by the FDA.”\u003c/p>\n\u003cp>An independent think tank also assessed the two phase 3 clinical trials of aducanumab and \u003ca href=\"https://icer.org/wp-content/uploads/2020/10/ICER_ALZ_Draft_Evidence_Report_050521.pdf\">found\u003c/a> the evidence “insufficient to conclude that the clinical benefits of aducanumab outweigh its harms or, indeed, that it reduces progression” of Alzheimer’s disease.\u003c/p>\n\u003cp>Dr. \u003ca href=\"https://www.med.upenn.edu/apps/faculty/index.php/g275/p7909\">Jason Karlawish\u003c/a>, professor of medicine and medical ethics and an Alzheimer’s expert at the University of Pennsylvania’s Perelman School of Medicine, \u003ca href=\"https://www.statnews.com/2021/05/30/if-the-fda-approves-biogens-alzheimers-treatment-i-wont-prescribe-it/\">wrote last week\u003c/a> that he would not prescribe aducanumab to his patients even with FDA approval, due to risks of small bleeds in the brain, financial cost and unclear benefits.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>“[T]he data to make this case are murky and, even if they were clear, the drug’s benefits are ambiguous at best and not worth this cost. Putting it on the market will stress Medicare’s resources,” he wrote.\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2021 NPR. To see more, visit https://www.npr.org.\u003cimg decoding=\"async\" src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=The+FDA+Has+Approved+A+New+Alzheimer%27s+Drug+%E2%80%94+Here%27s+Why+That%27s+Controversial&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n","blocks":[],"excerpt":"This is the first new drug approved for Alzheimer's disease since 2003. It's the first to show significant progress against the sticky brain plaques that are the hallmark of Alzheimer's disease.","status":"publish","parent":0,"modified":1704846568,"stats":{"hasAudio":false,"hasVideo":false,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":24,"wordCount":874},"headData":{"title":"The FDA's Controversial Approval of a New Alzheimer's Drug Explained | KQED","description":"This is the first new drug approved for Alzheimer's disease since 2003. It's the first to show significant progress against the sticky brain plaques that are the hallmark of Alzheimer's disease.","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":"","schema":{"@context":"http://schema.org","@type":"Article","headline":"The FDA's Controversial Approval of a New Alzheimer's Drug Explained","datePublished":"2021-06-08T22:07:45.000Z","dateModified":"2024-01-10T00:29:28.000Z","image":"https://cdn.kqed.org/wp-content/uploads/2020/02/KQED-OG-Image@1x.png"}},"source":"Medical Science","sticky":false,"nprImageCredit":"Matt York","nprByline":"Laurel Wamsley","nprImageAgency":"AP","nprStoryId":"1003964235","nprApiLink":"http://api.npr.org/query?id=1003964235&apiKey=MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004","nprHtmlLink":"https://www.npr.org/2021/06/07/1003964235/fda-approves-controversial-alzheimers-drug-aducanumab?ft=nprml&f=1003964235","nprRetrievedStory":"1","nprPubDate":"Mon, 07 Jun 2021 20:17:00 -0400","nprStoryDate":"Mon, 07 Jun 2021 11:28:00 -0400","nprLastModifiedDate":"Mon, 07 Jun 2021 20:57:08 -0400","nprAudio":"https://ondemand.npr.org/anon.npr-mp3/npr/atc/2021/06/20210607_atc_new_memory_drug.mp3?orgId=1&topicId=1128&d=228&p=2&story=1003964235&ft=nprml&f=1003964235","nprAudioM3u":"http://api.npr.org/m3u/11004141650-da30f1.m3u?orgId=1&topicId=1128&d=228&p=2&story=1003964235&ft=nprml&f=1003964235","path":"/science/1975234/the-fdas-controversial-approval-of-a-new-alzheimers-drug-explained","audioUrl":"https://ondemand.npr.org/anon.npr-mp3/npr/atc/2021/06/20210607_atc_new_memory_drug.mp3?orgId=1&topicId=1128&d=228&p=2&story=1003964235&ft=nprml&f=1003964235","audioTrackLength":null,"parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003cp>The Food and Drug Administration \u003ca href=\"https://www.fda.gov/drugs/news-events-human-drugs/fdas-decision-approve-new-treatment-alzheimers-disease\">approved\u003c/a> the drug \u003ca href=\"https://www.fda.gov/drugs/postmarket-drug-safety-information-patients-and-providers/aducanumab-marketed-aduhelm-information\">aducanumab\u003c/a> to treat patients with Alzheimer’s disease on Monday. It is the first new drug approved by the agency for Alzheimer’s disease since 2003.\u003c/p>\n\u003cp>The drug is the first to show significant progress against the sticky brain plaques that are the hallmark of Alzheimer’s disease.\u003c/p>\n\u003cp>The drug has proved highly effective at reducing the plaques, called beta-amyloid, that build up in the brains of people with Alzheimer’s.\u003c/p>\n\u003cp>But does the drug actually slow the progression of the disease when it reduces the plaques? It’s not yet clear. Two large studies offered conflicting evidence about whether the treatment slows declines in memory and thinking. A panel of expert advisers to the FDA \u003ca href=\"https://www.npr.org/2020/11/06/932215023/fda-advisory-panel-rejects-controversial-alzheimers-drug\">recommended in November\u003c/a> that the agency not approve the drug.\u003c/p>\n\u003cp>As a condition of approval, the FDA is requiring Biogen, the drug’s maker, to conduct another clinical study to confirm that the reduction of amyloid plaques results in clinical improvement for patients. If the subsequent study doesn’t show a clinical improvement, the agency could move to withdraw the approval.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>","attributes":{"named":{},"numeric":[]}},{"type":"component","content":"","name":"ad","attributes":{"named":{"label":"fullwidth"},"numeric":["fullwidth"]}},{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>There are also concerns that the FDA’s approval will make it difficult for Biogen and Eisai, the companies marketing the drug, to find enough patients to participate in its next clinical trials as patients might not want to risk getting the placebo and can get the drug without being in a study.\u003c/p>\n\u003cp>The medicine will be marketed under the trade name Aduhelm.\u003c/p>\n\u003cp>The FDA acknowledged the controversy and attention the drug’s approval has garnered from the Alzheimer’s patient community, elected officials and others.\u003c/p>\n\u003cp>The agency opted to put Aduhelm on the FDA’s accelerated approval pathway, which is meant to speed access to potentially valuable therapies for patients with serious diseases to serve an unmet need, and where a clinical benefit is expected — even if there is still some uncertainty about that benefit.\u003c/p>\n\u003cp>“[T]he Agency concluded that the benefits of Aduhelm for patients with Alzheimer’s disease outweighed the risks of the therapy,” Patrizia Cavazzoni, director of the FDA Center for Drug Evaluation and Research, said in a statement.\u003c/p>\n\u003cp>It could take several years to conclude the clinical trials the FDA is requiring. But in the meantime, Aduhelm will be available to patients.\u003c/p>\n\u003cp>Patients will receive the drug in monthly infusions. They will also need regular brain scans to detect a rare side effect: bleeding or swelling in the brain.\u003c/p>\n\u003cp>Biogen and Eisai said Monday that the annual wholesale cost for those taking maintenance doses \u003ca href=\"https://investors.biogen.com/news-releases/news-release-details/biogen-and-eisai-launch-multiple-initiatives-help-patients\">would be $56,000\u003c/a> a year for a patient of average U.S. weight with mild cognitive impairment or mild dementia. The net price could change based on discounts and rebates.\u003c/p>\n\u003cp>Trading in Biogen shares was halted due to the announcement. After trading resumed midafternoon, shares were up more than $110, or 39%.\u003c/p>\n\u003cp>The Alzheimer’s Association, which has been pushing for approval, applauded the news.\u003c/p>\n\u003cp>“This is the first drug that slows Alzheimer’s disease. And, this is the beginning of a completely new future for Alzheimer’s treatments,” the group said in a statement. “This is a new type of Alzheimer’s treatment; it addresses the disease in a way that has never been done before, compared to currently approved drugs.”\u003c/p>\n\u003cp>But others say the drugmakers have not yet proved that aducanumab’s benefits outweigh its risks.\u003c/p>\n\u003cp>In November, an FDA advisory committee of medical experts voted that the evidence did not show the drug to be effective at slowing Alzheimer’s. One major study found that aducanumab slowed down the progress of Alzheimer’s, while the other showed it didn’t.\u003c/p>\n\u003cp>“Usually, you need two big studies finding the same thing to approve a drug,” NPR \u003ca href=\"https://www.npr.org/2020/11/06/932215023/fda-advisory-panel-rejects-controversial-alzheimers-drug\">reported\u003c/a> after the vote last year. But at that meeting, “the FDA asked its experts to focus only on the positive study, and it also presented analysis of the data that was really very favorable to the drug. All of that did not go over well with these advisers. Some of them seemed to feel like they were being railroaded by the FDA.”\u003c/p>\n\u003cp>An independent think tank also assessed the two phase 3 clinical trials of aducanumab and \u003ca href=\"https://icer.org/wp-content/uploads/2020/10/ICER_ALZ_Draft_Evidence_Report_050521.pdf\">found\u003c/a> the evidence “insufficient to conclude that the clinical benefits of aducanumab outweigh its harms or, indeed, that it reduces progression” of Alzheimer’s disease.\u003c/p>\n\u003cp>Dr. \u003ca href=\"https://www.med.upenn.edu/apps/faculty/index.php/g275/p7909\">Jason Karlawish\u003c/a>, professor of medicine and medical ethics and an Alzheimer’s expert at the University of Pennsylvania’s Perelman School of Medicine, \u003ca href=\"https://www.statnews.com/2021/05/30/if-the-fda-approves-biogens-alzheimers-treatment-i-wont-prescribe-it/\">wrote last week\u003c/a> that he would not prescribe aducanumab to his patients even with FDA approval, due to risks of small bleeds in the brain, financial cost and unclear benefits.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>“[T]he data to make this case are murky and, even if they were clear, the drug’s benefits are ambiguous at best and not worth this cost. Putting it on the market will stress Medicare’s resources,” he wrote.\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2021 NPR. To see more, visit https://www.npr.org.\u003cimg decoding=\"async\" src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=The+FDA+Has+Approved+A+New+Alzheimer%27s+Drug+%E2%80%94+Here%27s+Why+That%27s+Controversial&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/science/1975234/the-fdas-controversial-approval-of-a-new-alzheimers-drug-explained","authors":["byline_science_1975234"],"categories":["science_39","science_3890","science_40","science_4450"],"tags":["science_235","science_309"],"featImg":"science_1975235","label":"source_science_1975234"},"science_1949607":{"type":"posts","id":"science_1949607","meta":{"index":"posts_1591205157","site":"science","id":"1949607","score":null,"sort":[1571680539000]},"guestAuthors":[],"slug":"link-between-high-blood-sugar-and-alzheimers-is-bolstered-by-new-research-in-mice","title":"Link Between High Blood Sugar and Alzheimer's Is Bolstered by New Research in Mice","publishDate":1571680539,"format":"standard","headTitle":"Link Between High Blood Sugar and Alzheimer’s Is Bolstered by New Research in Mice | KQED","labelTerm":{},"content":"\u003cp>Brain scientists are offering a new reason to control blood sugar levels: It might help lower your risk of developing Alzheimer’s disease.\u003c/p>\n\u003cp>“There’s many reasons to get [blood sugar] under control,” says \u003ca href=\"https://neuro.wustl.edu/labs/holtzman_d/Lab-Home/Dr-Holtzman-Bio\" target=\"_blank\" rel=\"noopener\">David Holtzman\u003c/a>, chairman of neurology at Washington University in St. Louis. “But this is certainly one.”\u003c/p>\n\u003cp>Holtzman moderated a panel Sunday at the Society for Neuroscience \u003ca href=\"https://www.sfn.org/meetings/neuroscience-2019\" target=\"_blank\" rel=\"noopener\">meeting\u003c/a> in Chicago that featured new research exploring the links between Alzheimer’s and diabetes.\u003c/p>\n\u003cp>“The risk for dementia is elevated about twofold in people who have diabetes or \u003ca href=\"https://medlineplus.gov/metabolicsyndrome.html\" target=\"_blank\" rel=\"noopener\">metabolic syndrome\u003c/a> (a group of risk factors that often precedes diabetes),” Holtzman says. “But what’s not been clear is what’s the connection?”\u003c/p>\n\u003cp>One possibility involves the way the brain metabolizes sugar, says \u003ca href=\"https://pharmtox.ku.edu/people/liqin-zhao\" target=\"_blank\" rel=\"noopener\">Liqin Zhao\u003c/a>, an associate professor in the school of pharmacy at the University of Kansas.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>Zhao wanted to know why people whose bodies produce\u003ca href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4829000/\" target=\"_blank\" rel=\"noopener\"> a protein called ApoE2\u003c/a> are less likely to get Alzheimer’s.\u003c/p>\n\u003cp>Previous research has shown that these people are less likely to develop the sticky plaques in the brain associated with the disease. But Zhao looked at how ApoE2 affects glycolysis, a part of the process that allows brain cells to turn sugar into energy.\u003c/p>\n\u003cp>Her research found that glycolysis helps brain cells communicate and get rid of toxins associated with Alzheimer’s.\u003c/p>\n\u003cp>So she gave ApoE2 to mice that develop a form of Alzheimer’s. And sure enough, Zhao says, the substance not only improved energy production in brain cells, it made the cells healthier overall.\u003c/p>\n\u003cp>“All of this together increased the brain’s resilience against Alzheimer’s disease,” she says.\u003c/p>\n\u003cp>Another scientist described how mice fed a diet that includes lots of fat and sugar were more likely to develop both diabetes and memory impairment.\u003c/p>\n\u003cp>The diet caused an increase in dysfunctional brain cells in the mice, says \u003ca href=\"http://uef.academia.edu/SamiGabbouj/CurriculumVitae\" target=\"_blank\" rel=\"noopener\">Sami Gabbouj\u003c/a> of the Institute of Biomedicine at the University of Eastern Finland. In people, he says, that could “exacerbate” the development of Alzheimer’s.\u003c/p>\n\u003cp>Sleep problems are another common feature of both Alzheimer’s and diabetes, says \u003ca href=\"https://school.wakehealth.edu/Faculty/M/Shannon-Lynn-Macauley-Rambach\" target=\"_blank\" rel=\"noopener\">Shannon Macauley\u003c/a>, an assistant professor of gerontology and geriatric medicine at Wake Forest School of Medicine.\u003c/p>\n\u003cp>She presented research showing that in mice, the brain changes associated with Alzheimer’s do interfere with sleep. But abnormal levels of blood sugar, both high and low, also “lead to disrupted sleep,” she says\u003c/p>\n\u003cp>That’s concerning, she says, because poor sleep is a known risk factor for Alzheimer’s. So maintaining normal blood sugar levels in Alzheimer’s patients could improve their sleep, and might even slow down the disease, she says.\u003c/p>\n\u003cp>All of this research on animals could eventually help people, Washington University’s Holtzman says.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>“If we can figure out what diabetes is doing to increase risk, maybe that would lead us to new targets, drug targets or treatment targets,” he says\u003c/p>\n\u003cdiv class=\"fullattribution\">\u003cem>Copyright 2019 \u003ca href=\"https://www.npr.org\" target=\"_blank\" rel=\"noopener\">NPR\u003c/a>.\u003c/em>\u003c/div>\n\n","blocks":[],"excerpt":"Diabetes can double a person's chances of developing Alzheimer's. Now researchers are beginning to understand the role of brain metabolism in the development of the dementia.","status":"publish","parent":0,"modified":1704848220,"stats":{"hasAudio":false,"hasVideo":false,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":19,"wordCount":515},"headData":{"title":"Link Between High Blood Sugar and Alzheimer's Is Bolstered by New Research in Mice | KQED","description":"Diabetes can double a person's chances of developing Alzheimer's. Now researchers are beginning to understand the role of brain metabolism in the development of the dementia.","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":"","schema":{"@context":"http://schema.org","@type":"Article","headline":"Link Between High Blood Sugar and Alzheimer's Is Bolstered by New Research in Mice","datePublished":"2019-10-21T17:55:39.000Z","dateModified":"2024-01-10T00:57:00.000Z","image":"https://cdn.kqed.org/wp-content/uploads/2020/02/KQED-OG-Image@1x.png"}},"source":"NPR","sticky":false,"nprByline":"Jon Hamilton\u003c/br>NPR","nprImageAgency":"Science Source","nprStoryId":"771894448","nprApiLink":"http://api.npr.org/query?id=771894448&apiKey=MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004","nprHtmlLink":"https://www.npr.org/sections/health-shots/2019/10/21/771894448/keeping-your-blood-sugar-in-check-could-lower-your-alzheimers-risk?ft=nprml&f=771894448","nprRetrievedStory":"1","nprPubDate":"Mon, 21 Oct 2019 12:07:00 -0400","nprStoryDate":"Mon, 21 Oct 2019 12:07:49 -0400","nprLastModifiedDate":"Mon, 21 Oct 2019 12:08:41 -0400","nprAudio":"https://ondemand.npr.org/anon.npr-mp3/npr/me/2019/10/20191021_me_low_blood_sugar_levels_may_keep_alzheimers_at_bay.mp3?orgId=1&topicId=1128&d=139&story=771894448&ft=nprml&f=771894448","nprAudioM3u":"http://api.npr.org/m3u/1771916466-abead5.m3u?orgId=1&topicId=1128&d=139&story=771894448&ft=nprml&f=771894448","audioTrackLength":139,"path":"/science/1949607/link-between-high-blood-sugar-and-alzheimers-is-bolstered-by-new-research-in-mice","audioUrl":"https://ondemand.npr.org/anon.npr-mp3/npr/me/2019/10/20191021_me_low_blood_sugar_levels_may_keep_alzheimers_at_bay.mp3?orgId=1&topicId=1128&d=139&story=771894448&ft=nprml&f=771894448","parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003cp>Brain scientists are offering a new reason to control blood sugar levels: It might help lower your risk of developing Alzheimer’s disease.\u003c/p>\n\u003cp>“There’s many reasons to get [blood sugar] under control,” says \u003ca href=\"https://neuro.wustl.edu/labs/holtzman_d/Lab-Home/Dr-Holtzman-Bio\" target=\"_blank\" rel=\"noopener\">David Holtzman\u003c/a>, chairman of neurology at Washington University in St. Louis. “But this is certainly one.”\u003c/p>\n\u003cp>Holtzman moderated a panel Sunday at the Society for Neuroscience \u003ca href=\"https://www.sfn.org/meetings/neuroscience-2019\" target=\"_blank\" rel=\"noopener\">meeting\u003c/a> in Chicago that featured new research exploring the links between Alzheimer’s and diabetes.\u003c/p>\n\u003cp>“The risk for dementia is elevated about twofold in people who have diabetes or \u003ca href=\"https://medlineplus.gov/metabolicsyndrome.html\" target=\"_blank\" rel=\"noopener\">metabolic syndrome\u003c/a> (a group of risk factors that often precedes diabetes),” Holtzman says. “But what’s not been clear is what’s the connection?”\u003c/p>\n\u003cp>One possibility involves the way the brain metabolizes sugar, says \u003ca href=\"https://pharmtox.ku.edu/people/liqin-zhao\" target=\"_blank\" rel=\"noopener\">Liqin Zhao\u003c/a>, an associate professor in the school of pharmacy at the University of Kansas.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>","attributes":{"named":{},"numeric":[]}},{"type":"component","content":"","name":"ad","attributes":{"named":{"label":"fullwidth"},"numeric":["fullwidth"]}},{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>Zhao wanted to know why people whose bodies produce\u003ca href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4829000/\" target=\"_blank\" rel=\"noopener\"> a protein called ApoE2\u003c/a> are less likely to get Alzheimer’s.\u003c/p>\n\u003cp>Previous research has shown that these people are less likely to develop the sticky plaques in the brain associated with the disease. But Zhao looked at how ApoE2 affects glycolysis, a part of the process that allows brain cells to turn sugar into energy.\u003c/p>\n\u003cp>Her research found that glycolysis helps brain cells communicate and get rid of toxins associated with Alzheimer’s.\u003c/p>\n\u003cp>So she gave ApoE2 to mice that develop a form of Alzheimer’s. And sure enough, Zhao says, the substance not only improved energy production in brain cells, it made the cells healthier overall.\u003c/p>\n\u003cp>“All of this together increased the brain’s resilience against Alzheimer’s disease,” she says.\u003c/p>\n\u003cp>Another scientist described how mice fed a diet that includes lots of fat and sugar were more likely to develop both diabetes and memory impairment.\u003c/p>\n\u003cp>The diet caused an increase in dysfunctional brain cells in the mice, says \u003ca href=\"http://uef.academia.edu/SamiGabbouj/CurriculumVitae\" target=\"_blank\" rel=\"noopener\">Sami Gabbouj\u003c/a> of the Institute of Biomedicine at the University of Eastern Finland. In people, he says, that could “exacerbate” the development of Alzheimer’s.\u003c/p>\n\u003cp>Sleep problems are another common feature of both Alzheimer’s and diabetes, says \u003ca href=\"https://school.wakehealth.edu/Faculty/M/Shannon-Lynn-Macauley-Rambach\" target=\"_blank\" rel=\"noopener\">Shannon Macauley\u003c/a>, an assistant professor of gerontology and geriatric medicine at Wake Forest School of Medicine.\u003c/p>\n\u003cp>She presented research showing that in mice, the brain changes associated with Alzheimer’s do interfere with sleep. But abnormal levels of blood sugar, both high and low, also “lead to disrupted sleep,” she says\u003c/p>\n\u003cp>That’s concerning, she says, because poor sleep is a known risk factor for Alzheimer’s. So maintaining normal blood sugar levels in Alzheimer’s patients could improve their sleep, and might even slow down the disease, she says.\u003c/p>\n\u003cp>All of this research on animals could eventually help people, Washington University’s Holtzman says.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>“If we can figure out what diabetes is doing to increase risk, maybe that would lead us to new targets, drug targets or treatment targets,” he says\u003c/p>\n\u003cdiv class=\"fullattribution\">\u003cem>Copyright 2019 \u003ca href=\"https://www.npr.org\" target=\"_blank\" rel=\"noopener\">NPR\u003c/a>.\u003c/em>\u003c/div>\n\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/science/1949607/link-between-high-blood-sugar-and-alzheimers-is-bolstered-by-new-research-in-mice","authors":["byline_science_1949607"],"categories":["science_30","science_39","science_16","science_40"],"tags":["science_235","science_233","science_5181","science_3838"],"featImg":"science_1949608","label":"source_science_1949607"},"science_1946573":{"type":"posts","id":"science_1946573","meta":{"index":"posts_1591205157","site":"science","id":"1946573","score":null,"sort":[1566324458000]},"guestAuthors":[],"slug":"wakefulness-part-of-the-brain-attacked-first-in-alzheimers-study-says","title":"“Wakefulness” Part of the Brain Attacked First in Alzheimer’s, Study Says","publishDate":1566324458,"format":"standard","headTitle":"“Wakefulness” Part of the Brain Attacked First in Alzheimer’s, Study Says | KQED","labelTerm":{"site":"science"},"content":"\u003cp>People who donate their bodies to science might never have dreamed what information lies deep within their brains.\u003c/p>\n\u003cp>Even when that information has to do with sleep.\u003c/p>\n\u003cp>Scientists used to believe that people who napped a lot were at risk for developing Alzheimer’s disease. But Lea Grinberg with the UCSF Memory and Aging Center started to wonder if “risk” was too light a term — what if, instead, napping indicated an early stage of Alzheimer’s?\u003c/p>\n\u003cp>About a decade ago, Grinberg — a neuropathologist and associate professor — was working with her team to map a protein called tau in donated brains. Some of their data, published \u003ca href=\"https://www.alzheimersanddementia.com/article/S1552-5260(19)34081-6/abstract\" target=\"_blank\" rel=\"noopener\">last week\u003c/a>, revealed drastic differences between healthy brains and those from Alzheimer’s patients in the parts of the brain responsible for wakefulness.\u003c/p>\n\u003cfigure id=\"attachment_1946582\" class=\"wp-caption alignright\" style=\"max-width: 500px\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"wp-image-1946582\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/08/Brains_006-800x560.jpg\" alt=\"\" width=\"500\" height=\"350\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2019/08/Brains_006-800x560.jpg 800w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/08/Brains_006-160x112.jpg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/08/Brains_006-768x538.jpg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/08/Brains_006-1020x715.jpg 1020w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/08/Brains_006-1200x841.jpg 1200w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/08/Brains_006.jpg 1920w\" sizes=\"(max-width: 500px) 100vw, 500px\">\u003cfigcaption class=\"wp-caption-text\">Lea Grinberg uses a program that takes a microscope’s magnification of brain tissue on a slide and projects it on a computer screen on August 15, 2019. The different colors represent different biological features in the brain tissue sample, including neurons and tau protein. \u003ccite>(Lindsey Moore/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>Wakefulness centers in the brain showed the buildup of tau — a protein that clogs neurons, Grinberg says, and lets debris accumulate. Gradually, these clogged neurons die. Some areas of the diseased brains had lost as much as 75% of their neurons. That may have led to the excessive napping scientists had observed before. Although the team only studied brains from 13 Alzheimer’s patients and 7 healthy individuals, Grinberg says that the degeneration caused by Alzheimer’s was so profound they were sure of its significance.\u003c/p>\n\u003cp>“We are kind of changing our understanding of what Alzheimer’s disease is,” she says. “It’s not only a memory problem, but it’s a problem in the brain that causes many other symptoms.”\u003c/p>\n\u003cp>Although these symptoms aren’t as severe as complete loss of memory or motor functions, Grinberg says they can still hold real consequences for a person’s quality of life. “Because if you don’t sleep well every day and if you… are not in the mood to do things like you were before, it’s very disappointing, right? My grandparents were like this.”\u003c/p>\n\u003cp>Grinberg says it’s important to know whether napping could be an early sign of Alzheimer’s, for treating symptoms and developing drugs that could slow the progression of the disease. Although there are no prescription drugs available to treat tau buildup, she says, a few are in clinical trials.\u003c/p>\n\u003cfigure id=\"attachment_1946586\" class=\"wp-caption alignleft\" style=\"max-width: 500px\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"wp-image-1946586\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/08/Brains_002-800x574.jpg\" alt=\"\" width=\"500\" height=\"359\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2019/08/Brains_002-800x574.jpg 800w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/08/Brains_002-160x115.jpg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/08/Brains_002-768x551.jpg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/08/Brains_002-1020x732.jpg 1020w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/08/Brains_002-1200x861.jpg 1200w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/08/Brains_002.jpg 1920w\" sizes=\"(max-width: 500px) 100vw, 500px\">\u003cfigcaption class=\"wp-caption-text\">Lea Grinberg holds boxes filled with samples of brain tissue for study on August 15, 2019. \u003ccite>(Lindsey Moore/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>A public health professor and neuroscientist at UC Berkeley says the new information offers hope to researchers. William Jagust, who has studied Alzheimer’s for over 30 years, says the results could help select patients for clinical trials of new drugs that require early treatment. “It’s also just very important for understanding the evolution of Alzheimer’s disease with the hope that we eventually \u003cem>will\u003c/em> have a drug,” he adds.\u003c/p>\n\u003cp>It’ll be awhile before doctors can diagnose anyone with Alzheimer’s based on how often they doze off. “There’s no practical application of this to clinical medicine as of today,” Jagust says, “but I think it’s on the cutting edge of the very, very important questions.”\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>\u003c/p>\n","blocks":[],"excerpt":"Changes in the biology of our brains may lead to excessive napping -- and help doctors better understand a life-altering disease.","status":"publish","parent":0,"modified":1704848391,"stats":{"hasAudio":false,"hasVideo":false,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":12,"wordCount":594},"headData":{"title":"“Wakefulness” Part of the Brain Attacked First in Alzheimer’s, Study Says | KQED","description":"Changes in the biology of our brains may lead to excessive napping -- and help doctors better understand a life-altering disease.","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":"","schema":{"@context":"http://schema.org","@type":"Article","headline":"“Wakefulness” Part of the Brain Attacked First in Alzheimer’s, Study Says","datePublished":"2019-08-20T18:07:38.000Z","dateModified":"2024-01-10T00:59:51.000Z","image":"https://cdn.kqed.org/wp-content/uploads/2020/02/KQED-OG-Image@1x.png"}},"sticky":false,"path":"/science/1946573/wakefulness-part-of-the-brain-attacked-first-in-alzheimers-study-says","audioTrackLength":null,"parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003cp>People who donate their bodies to science might never have dreamed what information lies deep within their brains.\u003c/p>\n\u003cp>Even when that information has to do with sleep.\u003c/p>\n\u003cp>Scientists used to believe that people who napped a lot were at risk for developing Alzheimer’s disease. But Lea Grinberg with the UCSF Memory and Aging Center started to wonder if “risk” was too light a term — what if, instead, napping indicated an early stage of Alzheimer’s?\u003c/p>\n\u003cp>About a decade ago, Grinberg — a neuropathologist and associate professor — was working with her team to map a protein called tau in donated brains. Some of their data, published \u003ca href=\"https://www.alzheimersanddementia.com/article/S1552-5260(19)34081-6/abstract\" target=\"_blank\" rel=\"noopener\">last week\u003c/a>, revealed drastic differences between healthy brains and those from Alzheimer’s patients in the parts of the brain responsible for wakefulness.\u003c/p>\n\u003cfigure id=\"attachment_1946582\" class=\"wp-caption alignright\" style=\"max-width: 500px\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"wp-image-1946582\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/08/Brains_006-800x560.jpg\" alt=\"\" width=\"500\" height=\"350\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2019/08/Brains_006-800x560.jpg 800w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/08/Brains_006-160x112.jpg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/08/Brains_006-768x538.jpg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/08/Brains_006-1020x715.jpg 1020w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/08/Brains_006-1200x841.jpg 1200w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/08/Brains_006.jpg 1920w\" sizes=\"(max-width: 500px) 100vw, 500px\">\u003cfigcaption class=\"wp-caption-text\">Lea Grinberg uses a program that takes a microscope’s magnification of brain tissue on a slide and projects it on a computer screen on August 15, 2019. The different colors represent different biological features in the brain tissue sample, including neurons and tau protein. \u003ccite>(Lindsey Moore/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>Wakefulness centers in the brain showed the buildup of tau — a protein that clogs neurons, Grinberg says, and lets debris accumulate. Gradually, these clogged neurons die. Some areas of the diseased brains had lost as much as 75% of their neurons. That may have led to the excessive napping scientists had observed before. Although the team only studied brains from 13 Alzheimer’s patients and 7 healthy individuals, Grinberg says that the degeneration caused by Alzheimer’s was so profound they were sure of its significance.\u003c/p>\n\u003cp>“We are kind of changing our understanding of what Alzheimer’s disease is,” she says. “It’s not only a memory problem, but it’s a problem in the brain that causes many other symptoms.”\u003c/p>\n\u003cp>Although these symptoms aren’t as severe as complete loss of memory or motor functions, Grinberg says they can still hold real consequences for a person’s quality of life. “Because if you don’t sleep well every day and if you… are not in the mood to do things like you were before, it’s very disappointing, right? My grandparents were like this.”\u003c/p>\n\u003cp>Grinberg says it’s important to know whether napping could be an early sign of Alzheimer’s, for treating symptoms and developing drugs that could slow the progression of the disease. Although there are no prescription drugs available to treat tau buildup, she says, a few are in clinical trials.\u003c/p>\n\u003cfigure id=\"attachment_1946586\" class=\"wp-caption alignleft\" style=\"max-width: 500px\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"wp-image-1946586\" src=\"https://ww2.kqed.org/science/wp-content/uploads/sites/35/2019/08/Brains_002-800x574.jpg\" alt=\"\" width=\"500\" height=\"359\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2019/08/Brains_002-800x574.jpg 800w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/08/Brains_002-160x115.jpg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/08/Brains_002-768x551.jpg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/08/Brains_002-1020x732.jpg 1020w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/08/Brains_002-1200x861.jpg 1200w, https://cdn.kqed.org/wp-content/uploads/sites/35/2019/08/Brains_002.jpg 1920w\" sizes=\"(max-width: 500px) 100vw, 500px\">\u003cfigcaption class=\"wp-caption-text\">Lea Grinberg holds boxes filled with samples of brain tissue for study on August 15, 2019. \u003ccite>(Lindsey Moore/KQED)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>A public health professor and neuroscientist at UC Berkeley says the new information offers hope to researchers. William Jagust, who has studied Alzheimer’s for over 30 years, says the results could help select patients for clinical trials of new drugs that require early treatment. “It’s also just very important for understanding the evolution of Alzheimer’s disease with the hope that we eventually \u003cem>will\u003c/em> have a drug,” he adds.\u003c/p>\n\u003cp>It’ll be awhile before doctors can diagnose anyone with Alzheimer’s based on how often they doze off. “There’s no practical application of this to clinical medicine as of today,” Jagust says, “but I think it’s on the cutting edge of the very, very important questions.”\u003c/p>\n\u003cp>\u003c/p>\u003c/div>","attributes":{"named":{},"numeric":[]}},{"type":"component","content":"","name":"ad","attributes":{"named":{"label":"fullwidth"},"numeric":["fullwidth"]}},{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>\u003c/p>\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/science/1946573/wakefulness-part-of-the-brain-attacked-first-in-alzheimers-study-says","authors":["11615"],"categories":["science_30","science_39","science_3890"],"tags":["science_235","science_1785","science_3370","science_5155"],"featImg":"science_1946577","label":"science"},"science_1936659":{"type":"posts","id":"science_1936659","meta":{"index":"posts_1591205157","site":"science","id":"1936659","score":null,"sort":[1547494714000]},"guestAuthors":[],"slug":"tech-firms-look-to-robotic-pets-music-and-vr-to-help-treat-alzheimers","title":"Tech Firms Look to Robotic Pets, Music and VR to Help Treat Alzheimer’s","publishDate":1547494714,"format":"standard","headTitle":"Tech Firms Look to Robotic Pets, Music and VR to Help Treat Alzheimer’s | KQED","labelTerm":{},"content":"\u003cp>[dropcap]L[/dropcap]AS VEGAS — The drug industry’s\u003ca href=\"https://www.statnews.com/2018/08/10/alzheimers-pipeline-clinical-trials/\" target=\"_blank\" rel=\"noopener\"> foundering search for an Alzheimer’s cure\u003c/a> is fueling a parallel quest by technology companies to help patients and family caregivers cope with the disease by using virtual reality software, robotics and novel communication tools.\u003c/p>\n\u003cp>Several companies engaged in the effort \u003ca href=\"https://digitalhealthsummit.com/Sessions/who-will-rescue-alzheimers-if-pharma-cant/\" target=\"_blank\" rel=\"noopener\">gathered here on Wednesday\u003c/a> to deliver a unified message: Waiting for pharma to deliver a miracle is a recipe for financial Armageddon, as the cost of treating Alzheimer’s is expected to quadruple, to more than $1 trillion in the U.S. by 2030, if no breakthrough treatments reach the market.\u003c/p>\n\u003cp>The solution is not simply developing tools to manage patient symptoms, but to deliver better support to family caregivers who are collectively spending more than $500 billion annually to care for elderly relatives.\u003c/p>\n\u003cp>“If we do not support the role of family caregivers and value them in this process, there is nothing we can do to bend the cost curve beyond what we’re doing,” said Thomas Riley, chief executive of Seniorlink, which developed a digital communication platform to help coordinate care for Alzheimer’s patients.\u003c/p>\n\u003cp>Technology firms are also selling digital products to help patients: A company called Dthera Sciences has built a therapy that uses music and images to help patients recover memories. The product analyzes facial expressions to monitor the emotional impact on patients and discover the sounds and visuals that provide the greatest relief. Earlier this year, Dthera received breakthrough device designation from the Food and Drug Administration, which provides an expedited pathway for the product’s approval.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>Another firm, Ageless Innovation, has developed robotic cats and dogs that help to treat the depression and social isolation that so often afflicts people with Alzheimer’s. Ted Fischer, the company’s CEO, said Wednesday that research conducted by Pace University showed the products resulted in better patient outcomes across several measures, including a reduction in hospitalizations. “And it produces joy and meaningful connections for these patients,” Fischer said.\u003c/p>\n\u003cp>The pharmaceutical industry has racked up a long list of failures in recent years, with many drug candidates following a similar narrative. A promising treatment in early-stage research turns out to be a flop in late-stage trials, putting investors, patients, and caregivers on a roller coaster that always ends in disappointment and a return to the drawing board.\u003c/p>\n\u003cp>Fischer and other technology executives gathered here said their products are neither panaceas nor substitutes for a hoped-for pharmaceutical breakthrough that could reverse or prevent the symptoms of the disease. But they also urged public and private funders to step up investments in technology solutions that, in the short term, represent the best option for patients and families.\u003c/p>\n\u003cp>Carrie Shaw, chief executive of Embodied Labs, said the fear and stigma of Alzheimer’s has undermined the development of tools to help families, clinicians, and payers confront the disease in a meaningful way. “We’re afraid of it, so we’re not addressing it,” she said, adding that more investment is needed to diagnose the onset of the disease at an earlier stage, to ensure more effective treatment.\u003c/p>\n\u003cp>Her company developed a virtual reality program to educate caregivers about the disease and help them understand its impact on their relatives. The product immerses users in various scenarios Alzheimer’s patients and caregivers commonly face — from the loss of cognitive function, to changes in family relationships, to caregiver burnout.\u003c/p>\n\u003cp>“We not only go inside their lives, but inside their bodies, so they actually know what it’s like to have this disease,” Shaw said.\u003c/p>\n\u003cp>Effective training and education for caregivers is especially important as the population ages, dramatically increasing the need for Alzheimer’s treatment as government investment in nursing home beds continues to decline.\u003c/p>\n\u003cp>Riley, the CEO of Seniorlink, said that means care will be increasingly delivered in home settings, where technology can help facilitate access to timely information and care. Seniorlink’s communication platform, called Vela, is a digital messaging service that can be used by all the family members, clinicians, and service providers involved in a patient’s care. Similar to workplace platforms like Slack, it lets the parties communicate in real time to address emergent problems and share information about changes in a patient’s condition and level of need.\u003c/p>\n\u003cp>Riley said the company is using analytics to help recognize patterns in patients’ symptoms, in an effort to flag optimal interventions for caregivers. He cautioned, however, that such technology should be used only to augment human care — not replace it.\u003c/p>\n\u003cp>“Money always rushes to technology,” he said. “But what technology gives you is data that humans still have to act on. And to act on it, they have to be able to trust it.”\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\u003cem>This \u003ca href=\"https://www.statnews.com/2019/01/10/alzheimers-tech-firms-solutions/\">story\u003c/a> was originally published by STAT, an online publication of Boston Globe Media that covers health, medicine, and scientific discovery.\u003c/em>\u003c/p>\n\n","blocks":[],"excerpt":"The drug industry’s faltering search for an Alzheimer’s cure is fueling a parallel quest by technology companies to help patients and family caregivers cope with the disease by using virtual reality software, robotics and novel communication tools.","status":"publish","parent":0,"modified":1704927203,"stats":{"hasAudio":false,"hasVideo":false,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":18,"wordCount":845},"headData":{"title":"Tech Firms Look to Robotic Pets, Music and VR to Help Treat Alzheimer’s | KQED","description":"The drug industry’s faltering search for an Alzheimer’s cure is fueling a parallel quest by technology companies to help patients and family caregivers cope with the disease by using virtual reality software, robotics and novel communication tools.","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":"","schema":{"@context":"http://schema.org","@type":"Article","headline":"Tech Firms Look to Robotic Pets, Music and VR to Help Treat Alzheimer’s","datePublished":"2019-01-14T19:38:34.000Z","dateModified":"2024-01-10T22:53:23.000Z","image":"https://cdn.kqed.org/wp-content/uploads/2020/02/KQED-OG-Image@1x.png"}},"source":"Health","sticky":false,"nprByline":"Casey Ross\u003c/br>STAT","path":"/science/1936659/tech-firms-look-to-robotic-pets-music-and-vr-to-help-treat-alzheimers","audioTrackLength":null,"parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003cp>\u003c/p>\u003cp>\u003cspan class=\"utils-parseShortcode-shortcodes-__dropcapShortcode__dropcap\">L\u003c/span>\u003c/p>\u003cp>AS VEGAS — The drug industry’s\u003ca href=\"https://www.statnews.com/2018/08/10/alzheimers-pipeline-clinical-trials/\" target=\"_blank\" rel=\"noopener\"> foundering search for an Alzheimer’s cure\u003c/a> is fueling a parallel quest by technology companies to help patients and family caregivers cope with the disease by using virtual reality software, robotics and novel communication tools.\u003c/p>\n\u003cp>Several companies engaged in the effort \u003ca href=\"https://digitalhealthsummit.com/Sessions/who-will-rescue-alzheimers-if-pharma-cant/\" target=\"_blank\" rel=\"noopener\">gathered here on Wednesday\u003c/a> to deliver a unified message: Waiting for pharma to deliver a miracle is a recipe for financial Armageddon, as the cost of treating Alzheimer’s is expected to quadruple, to more than $1 trillion in the U.S. by 2030, if no breakthrough treatments reach the market.\u003c/p>\n\u003cp>The solution is not simply developing tools to manage patient symptoms, but to deliver better support to family caregivers who are collectively spending more than $500 billion annually to care for elderly relatives.\u003c/p>\n\u003cp>“If we do not support the role of family caregivers and value them in this process, there is nothing we can do to bend the cost curve beyond what we’re doing,” said Thomas Riley, chief executive of Seniorlink, which developed a digital communication platform to help coordinate care for Alzheimer’s patients.\u003c/p>\n\u003cp>Technology firms are also selling digital products to help patients: A company called Dthera Sciences has built a therapy that uses music and images to help patients recover memories. The product analyzes facial expressions to monitor the emotional impact on patients and discover the sounds and visuals that provide the greatest relief. Earlier this year, Dthera received breakthrough device designation from the Food and Drug Administration, which provides an expedited pathway for the product’s approval.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>","attributes":{"named":{},"numeric":[]}},{"type":"component","content":"","name":"ad","attributes":{"named":{"label":"fullwidth"},"numeric":["fullwidth"]}},{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>Another firm, Ageless Innovation, has developed robotic cats and dogs that help to treat the depression and social isolation that so often afflicts people with Alzheimer’s. Ted Fischer, the company’s CEO, said Wednesday that research conducted by Pace University showed the products resulted in better patient outcomes across several measures, including a reduction in hospitalizations. “And it produces joy and meaningful connections for these patients,” Fischer said.\u003c/p>\n\u003cp>The pharmaceutical industry has racked up a long list of failures in recent years, with many drug candidates following a similar narrative. A promising treatment in early-stage research turns out to be a flop in late-stage trials, putting investors, patients, and caregivers on a roller coaster that always ends in disappointment and a return to the drawing board.\u003c/p>\n\u003cp>Fischer and other technology executives gathered here said their products are neither panaceas nor substitutes for a hoped-for pharmaceutical breakthrough that could reverse or prevent the symptoms of the disease. But they also urged public and private funders to step up investments in technology solutions that, in the short term, represent the best option for patients and families.\u003c/p>\n\u003cp>Carrie Shaw, chief executive of Embodied Labs, said the fear and stigma of Alzheimer’s has undermined the development of tools to help families, clinicians, and payers confront the disease in a meaningful way. “We’re afraid of it, so we’re not addressing it,” she said, adding that more investment is needed to diagnose the onset of the disease at an earlier stage, to ensure more effective treatment.\u003c/p>\n\u003cp>Her company developed a virtual reality program to educate caregivers about the disease and help them understand its impact on their relatives. The product immerses users in various scenarios Alzheimer’s patients and caregivers commonly face — from the loss of cognitive function, to changes in family relationships, to caregiver burnout.\u003c/p>\n\u003cp>“We not only go inside their lives, but inside their bodies, so they actually know what it’s like to have this disease,” Shaw said.\u003c/p>\n\u003cp>Effective training and education for caregivers is especially important as the population ages, dramatically increasing the need for Alzheimer’s treatment as government investment in nursing home beds continues to decline.\u003c/p>\n\u003cp>Riley, the CEO of Seniorlink, said that means care will be increasingly delivered in home settings, where technology can help facilitate access to timely information and care. Seniorlink’s communication platform, called Vela, is a digital messaging service that can be used by all the family members, clinicians, and service providers involved in a patient’s care. Similar to workplace platforms like Slack, it lets the parties communicate in real time to address emergent problems and share information about changes in a patient’s condition and level of need.\u003c/p>\n\u003cp>Riley said the company is using analytics to help recognize patterns in patients’ symptoms, in an effort to flag optimal interventions for caregivers. He cautioned, however, that such technology should be used only to augment human care — not replace it.\u003c/p>\n\u003cp>“Money always rushes to technology,” he said. “But what technology gives you is data that humans still have to act on. And to act on it, they have to be able to trust it.”\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\u003cem>This \u003ca href=\"https://www.statnews.com/2019/01/10/alzheimers-tech-firms-solutions/\">story\u003c/a> was originally published by STAT, an online publication of Boston Globe Media that covers health, medicine, and scientific discovery.\u003c/em>\u003c/p>\n\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/science/1936659/tech-firms-look-to-robotic-pets-music-and-vr-to-help-treat-alzheimers","authors":["byline_science_1936659"],"categories":["science_3151","science_39","science_16","science_40"],"tags":["science_235","science_1785","science_5181","science_3838"],"featImg":"science_1936726","label":"source_science_1936659"},"science_1927274":{"type":"posts","id":"science_1927274","meta":{"index":"posts_1591205157","site":"science","id":"1927274","score":null,"sort":[1531429218000]},"guestAuthors":[],"slug":"late-life-high-blood-pressure-may-harm-the-brain-study-says","title":"Late-Life High Blood Pressure May Harm the Brain, Study Says","publishDate":1531429218,"format":"standard","headTitle":"Late-Life High Blood Pressure May Harm the Brain, Study Says | KQED","labelTerm":{},"content":"\u003cp>Decades ago, hundreds of nuns and priests made an extraordinary decision: They agreed to donate their brains upon death to science, hoping to help solve mysteries about Alzheimer’s and other diseases. Now, a study that used their gifts is giving some clues. It reveals that high blood pressure late in life might harm the brain.\u003c/p>\n\u003cp>Autopsies on nearly 1,300 older people, including about 640 clergy members, found more signs of damage and one of the hallmarks of Alzheimer’s disease in the brains of those with higher blood pressure than among those with pressure closer to normal, researchers reported Wednesday.\u003c/p>\n\u003cp>The \u003ca href=\"http://n.neurology.org/lookup/doi/10.1212/WNL.0000000000005951\">study\u003c/a> does not prove cause and effect, and it does not yet provide a comparison of rates of dementia or its most common form, Alzheimer’s — those results will take longer to parse. But it challenges a theory that high pressure is not as harmful in old age as it is when people are younger.\u003c/p>\n\u003cp>“We can’t be alarmist. This is preliminary data” that needs to be validated by others, said the study leader, Dr. Zoe Arvanitakis of Rush University Medical Center in Chicago. “It’s far too soon to make recommendations about blood pressure in older people based on this study.”\u003c/p>\n\u003cp>The research began in 1994 and combined people from three studies of aging who agreed to donate their brains for autopsy upon their death, including the Religious Orders Study of Catholic clergy throughout the United States. All were over 65 and without known dementia at the start and were followed until they died — at an average age of 89 and after an average of eight years in the study.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>Two-thirds had high blood pressure, defined as a top reading of 140 or more when the study began (it’s now 130 under new guidelines adopted last fall.) Their pressures were measured once a year during the study — a strength of this work over some previous research that just relied on people to say whether they had high pressure or not.\u003c/p>\n\u003cp>After each participant died, researchers examined their brains for areas of dead tissue caused by lack of blood supply. These blighted areas can be tiny and cause no symptoms, so they’re sometimes called evidence of “silent strokes.”\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>About half of the study participants had one or more of these, and the risk was greater for those with higher blood pressure. For example, people with an average top reading of 147 had a 46 percent greater risk of having one or more of the bad spots than those with an average top reading of 134. People with higher bottom blood pressure readings also had a greater risk for this problem.\u003c/p>\n\u003cdiv id=\"div-gpt-ad-1470255291270-1\" class=\"ad-placeholder\">\n\u003cp>Researchers also found a link between higher pressure and one of the signs of Alzheimer’s — tangles of a protein called tau — but not another Alzheimer’s hallmark, amyloid plaques. This needs further research to understand the implications, Arvanitakis said.\u003c/p>\n\u003cp>“It’s a pretty strong study,” said James Hendrix, director of global science initiatives at the Alzheimer’s Association. “Autopsy data is really powerful” and has been the gold standard for diagnosing Alzheimer’s for many years, he said.\u003c/p>\n\u003cp>With Alzheimer’s, changes in the brain occur a decade or more before symptoms do, so high blood pressure may have been doing damage well before the age when these people enrolled in the study, he said.\u003c/p>\n\u003cp>How might high pressure do harm?\u003c/p>\n\u003cp>“Lower blood pressure reduces the risk of those blood vessel blockages” that can cause a silent stroke, said another independent expert, the Mayo Clinic’s Dr. David Knopman. The work shows that “treating blood pressure throughout the lifespan is important.”\u003c/p>\n\u003cp>Knopman is a spokesman for the American Academy of Neurology, whose journal, Neurology, published the study. Federal grants paid for the work.\u003c/p>\n\u003c/div>\n\n","blocks":[],"excerpt":"Autopsies on nearly 1,300 older people found more signs of damage and one of the hallmarks of Alzheimer’s disease in the brains of those with higher blood pressure.","status":"publish","parent":0,"modified":1704927700,"stats":{"hasAudio":false,"hasVideo":false,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":16,"wordCount":668},"headData":{"title":"Late-Life High Blood Pressure May Harm the Brain, Study Says | KQED","description":"Autopsies on nearly 1,300 older people found more signs of damage and one of the hallmarks of Alzheimer’s disease in the brains of those with higher blood pressure.","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":"","schema":{"@context":"http://schema.org","@type":"Article","headline":"Late-Life High Blood Pressure May Harm the Brain, Study Says","datePublished":"2018-07-12T21:00:18.000Z","dateModified":"2024-01-10T23:01:40.000Z","image":"https://cdn.kqed.org/wp-content/uploads/2020/02/KQED-OG-Image@1x.png"}},"source":"Health","sticky":false,"nprByline":"Marilynn Marchione\u003cbr />The Associated Press","path":"/science/1927274/late-life-high-blood-pressure-may-harm-the-brain-study-says","audioTrackLength":null,"parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003cp>Decades ago, hundreds of nuns and priests made an extraordinary decision: They agreed to donate their brains upon death to science, hoping to help solve mysteries about Alzheimer’s and other diseases. Now, a study that used their gifts is giving some clues. It reveals that high blood pressure late in life might harm the brain.\u003c/p>\n\u003cp>Autopsies on nearly 1,300 older people, including about 640 clergy members, found more signs of damage and one of the hallmarks of Alzheimer’s disease in the brains of those with higher blood pressure than among those with pressure closer to normal, researchers reported Wednesday.\u003c/p>\n\u003cp>The \u003ca href=\"http://n.neurology.org/lookup/doi/10.1212/WNL.0000000000005951\">study\u003c/a> does not prove cause and effect, and it does not yet provide a comparison of rates of dementia or its most common form, Alzheimer’s — those results will take longer to parse. But it challenges a theory that high pressure is not as harmful in old age as it is when people are younger.\u003c/p>\n\u003cp>“We can’t be alarmist. This is preliminary data” that needs to be validated by others, said the study leader, Dr. Zoe Arvanitakis of Rush University Medical Center in Chicago. “It’s far too soon to make recommendations about blood pressure in older people based on this study.”\u003c/p>\n\u003cp>The research began in 1994 and combined people from three studies of aging who agreed to donate their brains for autopsy upon their death, including the Religious Orders Study of Catholic clergy throughout the United States. All were over 65 and without known dementia at the start and were followed until they died — at an average age of 89 and after an average of eight years in the study.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>","attributes":{"named":{},"numeric":[]}},{"type":"component","content":"","name":"ad","attributes":{"named":{"label":"fullwidth"},"numeric":["fullwidth"]}},{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>Two-thirds had high blood pressure, defined as a top reading of 140 or more when the study began (it’s now 130 under new guidelines adopted last fall.) Their pressures were measured once a year during the study — a strength of this work over some previous research that just relied on people to say whether they had high pressure or not.\u003c/p>\n\u003cp>After each participant died, researchers examined their brains for areas of dead tissue caused by lack of blood supply. These blighted areas can be tiny and cause no symptoms, so they’re sometimes called evidence of “silent strokes.”\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>About half of the study participants had one or more of these, and the risk was greater for those with higher blood pressure. For example, people with an average top reading of 147 had a 46 percent greater risk of having one or more of the bad spots than those with an average top reading of 134. People with higher bottom blood pressure readings also had a greater risk for this problem.\u003c/p>\n\u003cdiv id=\"div-gpt-ad-1470255291270-1\" class=\"ad-placeholder\">\n\u003cp>Researchers also found a link between higher pressure and one of the signs of Alzheimer’s — tangles of a protein called tau — but not another Alzheimer’s hallmark, amyloid plaques. This needs further research to understand the implications, Arvanitakis said.\u003c/p>\n\u003cp>“It’s a pretty strong study,” said James Hendrix, director of global science initiatives at the Alzheimer’s Association. “Autopsy data is really powerful” and has been the gold standard for diagnosing Alzheimer’s for many years, he said.\u003c/p>\n\u003cp>With Alzheimer’s, changes in the brain occur a decade or more before symptoms do, so high blood pressure may have been doing damage well before the age when these people enrolled in the study, he said.\u003c/p>\n\u003cp>How might high pressure do harm?\u003c/p>\n\u003cp>“Lower blood pressure reduces the risk of those blood vessel blockages” that can cause a silent stroke, said another independent expert, the Mayo Clinic’s Dr. David Knopman. The work shows that “treating blood pressure throughout the lifespan is important.”\u003c/p>\n\u003cp>Knopman is a spokesman for the American Academy of Neurology, whose journal, Neurology, published the study. Federal grants paid for the work.\u003c/p>\n\u003c/div>\n\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/science/1927274/late-life-high-blood-pressure-may-harm-the-brain-study-says","authors":["byline_science_1927274"],"categories":["science_30","science_39","science_40"],"tags":["science_235","science_1785","science_5181"],"featImg":"science_1927277","label":"source_science_1927274"},"science_1274894":{"type":"posts","id":"science_1274894","meta":{"index":"posts_1591205157","site":"science","id":"1274894","score":null,"sort":[1482866872000]},"guestAuthors":[],"slug":"early-alzheimers-jalisco-mutation-is-a-curse-for-families","title":"Early Alzheimer's 'Jalisco' Mutation Is A Curse For Families","publishDate":1482866872,"format":"standard","headTitle":"Early Alzheimer’s ‘Jalisco’ Mutation Is A Curse For Families | KQED","labelTerm":{"site":"science"},"content":"\u003cp>Rosemary Navarro was living in Mexico when her brother called from California.\u003c/p>\n\u003cp>Something wasn’t right with their mom, then in her early 40s. She was having trouble paying bills and keeping jobs as a food preparer in convalescent homes.\u003c/p>\n\u003cp>Navarro, then 22, sold her furniture to pay for a trip back to the U.S. for herself and her two young children. Almost as soon as she arrived, she knew her mother wasn’t the same person. “She was there but sometimes she wasn’t there,” she said. “I thought, ‘Oh man, this isn’t going to be good.’ ”\u003c/p>\n\u003cp>Before long, Navarro was feeding her mom, then changing her diapers. She put a special lock on the door to keep her from straying outside. Unable to continue caring for her, Navarro eventually moved her mom to a nursing home, where she spent eight years.\u003c/p>\n\u003cp>Near the end, her mom, a quiet woman who had immigrated to the U.S. as a teenager and loved \u003cem>telenovelas\u003c/em>, could communicate only by laughing or crying. Navarro was there when she took her last breath in 2009, at age 53. “What I went through with my mom I wouldn’t wish on anyone,” she said.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>It has happened again and again in her family — relatives struck by the same terrible disease, most without any clue what it was. An aunt, an uncle, a cousin, a grandfather, a great grandfather. “Too many have died,” Navarro said. All in their early 50s.\u003c/p>\n\u003cp>Now the family knows the reason for their curse: It’s a rare type of early-onset Alzheimer’s disease, caused by what’s come to be known as the “Jalisco” genetic mutation. Doctors today can tell someone they have it but they can’t stop its destructive march.\u003c/p>\n\u003cp>For Navarro, watching her relatives succumb is like looking into a crystal ball, one she wants to hurl across the room. She, too, has the mutation.\u003c/p>\n\u003caside class=\"pullquote alignright\">‘They are all desperately fearful that they themselves have inherited a mutation. But what they are really fearful about is that they will pass it along to their children.’\u003ccite>John C. Morris, Alzheimer’s Disease Research Center\u003c/cite>\u003c/aside>\n\u003cp>It’s getting harder to stifle her fear. This year, she turned 40 — the same age her mother was when she started wandering off and forgetting simple things.\u003c/p>\n\u003cp>“I don’t look forward to birthdays,” she said. “I didn’t want to celebrate 40, much less 41.”\u003c/p>\n\u003cp>\u003cstrong>Sparing The Next Generation\u003c/strong>\u003c/p>\n\u003cp>Navarro, who lives in La Habra, Calif., belongs to an exclusive but unenviable club whose members are genetically programmed for early memory loss and death.\u003c/p>\n\u003cp>Of the more than 5 million people across the U.S. who have Alzheimer’s, 5 percent are believed to have the early-onset form, striking people under the age of 65. Fewer still — about one percent — have genetic mutations that are known to cause the disease.\u003c/p>\n\u003cp>Navarro’s gene is known as the Jalisco mutation because it is believed to have surfaced first in that Mexican state. Over time, it likely was carried by immigrants across the Mexican border into California and other states. In Mexico and the U.S., roughly 50 families are known to have it.\u003c/p>\n\u003cp>Cases like Navarro’s are of great interest to Alzheimer’s researchers. Studying this unique population with genetic mutations, they say, could help unlock some of the biggest mysteries of the more common form of the disease: How does it develop? How can it be diagnosed earlier? What can be done to stop it?\u003c/p>\n\u003cfigure id=\"attachment_1275007\" class=\"wp-caption aligncenter\" style=\"max-width: 800px\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-medium wp-image-1275007\" src=\"http://ww2.kqed.org/science/wp-content/uploads/sites/35/2016/12/alzheimer2-800x538.jpg\" alt=\"Rosemary Navarro (left) discovered that she carries a rare gene for early-onset Alzheimer's disease. Navarro's mother (right) died from the disease in 2009. "What I went through with my mom I wouldn't wish on anyone," Navarro said. \" width=\"800\" height=\"538\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer2.jpg 800w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer2-160x108.jpg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer2-768x516.jpg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer2-240x161.jpg 240w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer2-375x252.jpg 375w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer2-520x350.jpg 520w\" sizes=\"(max-width: 800px) 100vw, 800px\">\u003cfigcaption class=\"wp-caption-text\">Rosemary Navarro (left) discovered that she carries a rare gene for early-onset Alzheimer’s disease. Navarro’s mother (right) died from the disease in 2009. “What I went through with my mom I wouldn’t wish on anyone,” Navarro said. \u003ccite>(Heidi de Marco/Kaiser Health News)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>Ordinarily, it’s difficult — if not impossible — to predict Alzheimer’s. But with these families, researchers know the mutation carriers \u003cem>will\u003c/em> get the disease. They also know approximately \u003cem>when \u003c/em>symptoms will appear. So they can get a real-time look at how the disease develops — and can measure when the brain starts changing relative to expected onset. Perhaps most important, they can design drugs to target the disease before patients lose their memory.\u003c/p>\n\u003cp>“If you know from age 18 or even from birth whether someone is going to develop the disease or not, you have got a big window to intervene,” Navarro’s doctor, \u003ca href=\"http://keck.usc.edu/faculty/john-m-ringman/\">John Ringman\u003c/a>, a neurology professor at the Keck School of Medicine of the University of Southern California. “We don’t have a way to repair or bring back lost brain cells.”\u003c/p>\n\u003cp>Patients with a familial Alzheimer’s mutation “are sort of a model for how the disease progresses, because they are easier to recognize and easier to study,” said Bruce Miller, a longtime Alzheimer’s researcher who directs the memory and aging center at the University of California, San Francisco.\u003c/p>\n\u003cp>Around the world, hundreds of people whose families are afflicted with a variety of early-onset mutations are subjecting themselves to medical tests — spinal taps, memory quizzes, MRIs and other brain imaging, hoping scientists can develop therapies to prevent and treat Alzheimer’s.\u003c/p>\n\u003cp>But their participation often comes with the sad realization that resulting treatments may come too late for them. Ringman is studying about 100 patients at USC. Navarro is among about 30 with the Jalisco mutation.\u003c/p>\n\u003cp>More than 450 people are part of an international network of research being led by Washington University School of Medicine in St. Louis. Each has a parent with an early-onset gene mutation. If the research doesn’t help them, they tell researchers, maybe it will help the next generation.\u003c/p>\n\u003cp>“They are all desperately fearful that they themselves have inherited a mutation,” said John C. Morris, director of the school’s Alzheimer’s Disease Research Center. “But what they are really fearful about is that if they did, that they will pass it along to their children.”\u003c/p>\n\u003cp>Children have a 50 percent chance of inheriting the mutation from a parent who carries it.\u003c/p>\n\u003cp>Navarro, whose children are now young adults, is well aware of the statistics. She has joined the network’s research effort, of which Ringman is a part.\u003c/p>\n\u003cp>In 2014, she went for a brain scan. She had no overt symptoms, but the results told a different story. Her brain had already started to shrink — a sign that the disease was taking hold.\u003c/p>\n\u003cp>\u003cstrong>‘At Least We Know Now’\u003c/strong>\u003c/p>\n\u003cp>In November 2015, Ringman drove to Colton, Calif. — 60 miles east of Los Angeles — to meet with the large and close-knit Kitchen family. Jay Kitchen and his younger brother John were referred to him after each suffered a series of baffling symptoms.\u003c/p>\n\u003cp>It had started about four years earlier. Jay, then a 44-year-old sports writer, began having difficulty speaking. He felt off balance, was forgetting things and having difficulty paying bills.\u003c/p>\n\u003cp>Soon afterward, his younger brother, John, a high school history teacher, started becoming easily confused. He would forget what day it was and how to get to the market.\u003c/p>\n\u003cfigure id=\"attachment_1275008\" class=\"wp-caption aligncenter\" style=\"max-width: 800px\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-medium wp-image-1275008\" src=\"http://ww2.kqed.org/science/wp-content/uploads/sites/35/2016/12/alzheimer3-800x599.jpg\" alt=\"John (left) and Jay Kitchen with their father in Colton, Calif., in late 2015. \" width=\"800\" height=\"599\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer3.jpg 800w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer3-160x120.jpg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer3-768x575.jpg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer3-240x180.jpg 240w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer3-375x281.jpg 375w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer3-520x389.jpg 520w\" sizes=\"(max-width: 800px) 100vw, 800px\">\u003cfigcaption class=\"wp-caption-text\">John (left) and Jay Kitchen with their father in Colton, Calif., in late 2015. \u003ccite>(Heidi de Marco/Kaiser Health News)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>It struck me as really odd,” said John’s wife, Michelle Lopez. “Nobody could forget the store that was around the corner from the house you lived in for 12 years.”\u003c/p>\n\u003cp>Jay was the first to seek help. He went to an emergency room, then several specialists. One suspected a stroke. Another suggested mental illness. Test after test came back negative or inconclusive.\u003c/p>\n\u003cp>“It has been a long haul trying to get a diagnosis,” said the brothers’ aunt, Linda Ramos, who took Jay to most of the appointments. Doctors constantly were “scratching their heads trying to figure out what was wrong.”\u003c/p>\n\u003cp>In late 2015, a neurologist referred the brothers to Ringman, who ordered a blood test.\u003c/p>\n\u003cp>On the November morning in Colton, Ringman arrived at Ramos’ home where the extended family was gathered. He pulled the brothers and a few others aside to deliver his grim news: Both men had the Jalisco mutation. Ramos said the brothers sat in near silence. She doesn’t think Jay understood, and John, already a quiet man, just seemed scared.\u003c/p>\n\u003cp>Later that morning, a larger group of family members met with Ringman around a long dining room table: the Kitchens’ father, aunts and uncles; Lopez and Jay’s ex-wife. Jay’s son came with his newborn, who fussed in a stroller.\u003c/p>\n\u003cp>Projecting pictures and diagrams on the wall, the doctor explained the basics of early-onset Alzheimer’s disease and the different mutations that can cause it.\u003c/p>\n\u003cfigure id=\"attachment_1275009\" class=\"wp-caption aligncenter\" style=\"max-width: 800px\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-medium wp-image-1275009\" src=\"http://ww2.kqed.org/science/wp-content/uploads/sites/35/2016/12/alzheimer4-800x533.jpg\" alt=\"John Ringman, a neurologist at the University of Southern California, describes inheritance of genetic disease to John and Jay Kitchen's family in Riverside, Calif. Ringman has devoted much of his career to studying families with a mutation linked to early-onset Alzheimer's. \" width=\"800\" height=\"533\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer4.jpg 800w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer4-160x107.jpg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer4-768x512.jpg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer4-240x160.jpg 240w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer4-375x250.jpg 375w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer4-520x346.jpg 520w\" sizes=\"(max-width: 800px) 100vw, 800px\">\u003cfigcaption class=\"wp-caption-text\">John Ringman, a neurologist at the University of Southern California, describes inheritance of genetic disease to John and Jay Kitchen’s family in Riverside, Calif. Ringman has devoted much of his career to studying families with a mutation linked to early-onset Alzheimer’s. \u003ccite>(Heidi de Marco/Kaiser Health News )\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>Medications available today only address the symptoms, not the disease itself, Ringman said. Drugs may improve people’s thinking but don’t stop the progression.\u003c/p>\n\u003cp>“This is something we are going to crack eventually,” he said.\u003c/p>\n\u003cp>Like many families Ringman encounters, the relatives in the dining room absorbed the news with little emotion or surprise, as though the doctor were confirming nameless fears.\u003c/p>\n\u003cp>Ramos had watched the Kitchens’ mother, Olivia, lose the ability to walk and speak and eventually die in 2002. At the time, they were told she had multiple sclerosis. Now she wasn’t so sure.\u003c/p>\n\u003cp>John Kitchen asked if there was any connection to \u003ca href=\"https://ghr.nlm.nih.gov/condition/huntington-disease\">Huntington’s disease\u003c/a>, which the family had been told his grandfather had.\u003c/p>\n\u003cp>“Probably he didn’t have Huntington’s,” Ringman responded, adding that doctors often get the diagnosis wrong.\u003c/p>\n\u003cp>Ramos recalls feeling somewhat relieved that day.\u003c/p>\n\u003cp>“My thought was, ‘At least we know now. Finally, we know.’ Thank God we have a name [for it] and maybe we can do something for their kids.”\u003c/p>\n\u003cp>\u003cstrong>One Family Leads To Another\u003c/strong>\u003c/p>\n\u003cp>Ringman, now 51, became interested in neuroscience while in college at the University of California, Berkeley. But he knew lab work wasn’t for him. “I realized all these Ph.D.s study one molecule their entire lives and sit in a laboratory,” he said. “I didn’t want that.”\u003c/p>\n\u003cp>In the late 1990s, after completing medical school and specialty training, he joined the medical staff at the University of California, Irvine, where he saw patients with dementia and Huntington’s disease. He liked the personal interaction, combined with the scientific challenge.\u003c/p>\n\u003cp>In 1999, a 42-year-old woman came to see him, brought in by her young adult daughter. Rosa Maria Navarro had signs of early Alzheimer’s disease. Her daughter Rosemary was distraught, reporting that something similar had afflicted many other relatives. It was the beginning of a long relationship, and a new line of scientific inquiry for Ringman.\u003c/p>\n\u003cp>The young neurologist was aware of recently identified familial Alzheimer’s mutations, and he immediately suspected Rosa Maria had one. He sent her blood sample to get the genetic test, and it came back positive for the A431E mutation of a gene known as \u003ca href=\"https://ghr.nlm.nih.gov/gene/PSEN1\">presenilin 1\u003c/a>.\u003c/p>\n\u003cp>Rosemary Navarro suspects her mother sensed even before then what was wrong, having seen her own father lose his memory and die young. “But she was quiet,” Navarro said. “She never said, ‘I might have this.’ ”\u003c/p>\n\u003cp>Soon afterward, another patient came into Ringman’s office with similar symptoms. That patient tested positive for the same mutation. Both had families originating from Jalisco, Mexico. “I was already getting suspicious,” he said.\u003c/p>\n\u003cp>Familial Alzheimer’s intrigued Ringman. It was a relatively new field. Families with the disease had been known to exist since Alzheimer’s first described the disease in 1906, but the genes weren’t identified until about 90 years later. The research touched on so many parts of science — neurology, biology and psychology.\u003c/p>\n\u003cfigure id=\"attachment_1275010\" class=\"wp-caption aligncenter\" style=\"max-width: 800px\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-medium wp-image-1275010\" src=\"http://ww2.kqed.org/science/wp-content/uploads/sites/35/2016/12/alzheimer5-800x534.jpg\" alt=\"Relatives gathered around a dining room table as neurologist John Ringman gave a presentation about Alzheimer's disease and current research in Riverside, Calif., in 2015. \" width=\"800\" height=\"534\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer5.jpg 800w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer5-160x107.jpg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer5-768x513.jpg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer5-240x160.jpg 240w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer5-375x250.jpg 375w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer5-520x347.jpg 520w\" sizes=\"(max-width: 800px) 100vw, 800px\">\u003cfigcaption class=\"wp-caption-text\">Relatives gathered around a dining room table as neurologist John Ringman gave a presentation about Alzheimer’s disease and current research in Riverside, Calif., in 2015. \u003ccite>(Heidi de Marco/Kaiser Health News )\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>Later, Ringman came across an article co-authored by a Mexican neuropsychologist he had worked with before, Yaneth Rodriguez. It was about four families in Mexico that had early Alzheimer’s disease, and they had symptoms similar to his two patients.\u003c/p>\n\u003cp>In 2000, Ringman traveled to Mexico and met with both Rodriguez and a geneticist, Maria Elisa Alonso. Alonso told him that another family there had tested positive for the A431E mutation. Now, there were three, all of Mexican heritage.\u003c/p>\n\u003cp>Ringman collected DNA samples of members of seven more families who were being treated in Mexico. Test results not only confirmed members of each family had A431E, they indicated the patients all shared the same chunk of DNA. That’s when he knew. They were all related, distant cousins who had never met. [contextly_sidebar id=”coB3mfVYKnusWPldJ7HwVwtS5T7WJFzj”]\u003c/p>\n\u003cp>In 2006, the Mexican geneticist, Alonso, published a \u003ca href=\"http://www.ncbi.nlm.nih.gov/pubmed/16628450\">report\u003c/a> in \u003cem>Neurogenetics\u003c/em>, describing nine families who didn’t know they were related but all shared the A431E mutation. She concluded that the disease likely started with one ancestor in Jalisco. Ringman published a \u003ca href=\"http://www.ncbi.nlm.nih.gov/pubmed/16897084\">response\u003c/a> describing 15 additional families with the same mutation.\u003c/p>\n\u003cp>The findings meant that Ringman’s patients owed their suffering to an unidentified individual who likely lived in Jalisco perhaps hundreds of years ago. Somehow, as his or her DNA copied itself during cell division, a fatal mistake occurred. And now, in places like La Habra and Colton, Calif., whole families were coping with the awful results.\u003c/p>\n\u003cp>Ringman saw the tragedy but also the scientific opportunity in these discoveries. He later joined the Washington University School of Medicine network in its international quest for knowledge and treatment for familial Alzheimer’s disease. The research now includes different sites in Europe, Asia and Australia.\u003c/p>\n\u003cp>Among the network’s early findings: Amyloid plaques characteristic of Alzheimer’s appear decades before the first noticeable signs of memory loss. The research essentially has presented a timeline of brain changes leading up to memory loss and cognitive decline and has helped lead scientists to decide when and where to aim drugs.\u003c/p>\n\u003cp>A promising target is beta-amyloid. Many researchers believe that flaws in how the sticky substance is accumulated and disposed of in the brain can lead to the disease. Scientists now are studying drugs aimed at attacking beta-amyloid and removing it from the brain.\u003c/p>\n\u003cp>Another encouraging finding, the researchers say, is that early-onset and late-onset Alzheimer’s seem to share many characteristics, and findings that help with one disease are likely to help with the other.\u003c/p>\n\u003cp>The Kitchen brothers aren’t participating in the research. Their mental abilities are declining precipitously.\u003c/p>\n\u003cp>“We get a glimmer of hope,” their aunt Ramos said, “but then we think we are foolish for even hoping.”\u003c/p>\n\u003cp>Jay is living in a locked facility, having tried to run away from another place. He can no longer speak in full sentences and only occasionally recognizes family members.\u003c/p>\n\u003cp>John, now 43, can still hold a conversation but struggles to find the right words. Simple tasks elude him — like writing is name. He feels he is losing control of his life and worries about his family. “I want to be around for my son,” he said.\u003c/p>\n\u003cp>His son, 14-year-old Reese, says he sees his father “slowly fading away.” One day, he asked his mother: “Is that going to happen to me?”\u003c/p>\n\u003cp>“That was the worst day of my life,” Lopez said.\u003c/p>\n\u003cp>\u003cstrong>Fear And Faith\u003c/strong>\u003c/p>\n\u003cfigure id=\"attachment_1275011\" class=\"wp-caption aligncenter\" style=\"max-width: 800px\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-medium wp-image-1275011\" src=\"http://ww2.kqed.org/science/wp-content/uploads/sites/35/2016/12/alzheimer6-800x535.jpg\" alt=\"Rosemary Navarro's son, Ricardo, says he won't get tested for the gene. \" width=\"800\" height=\"535\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer6.jpg 800w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer6-160x107.jpg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer6-768x514.jpg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer6-240x161.jpg 240w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer6-375x251.jpg 375w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer6-520x348.jpg 520w\" sizes=\"(max-width: 800px) 100vw, 800px\">\u003cfigcaption class=\"wp-caption-text\">Rosemary Navarro’s son, Ricardo, says he won’t get tested for the gene. \u003ccite>(Heidi de Marco/Kaiser Health News )\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>Navarro’s 19-year-old daughter, Lizeth, and her 22-year-old son, Ricardo, live with her in a three-bedroom trailer in La Habra.\u003c/p>\n\u003cp>Both say said their mom has started forgetting little things — the movie they saw last week or what they need from the grocery store. “I usually have to say things more than once,” said Lizeth Navarro.\u003c/p>\n\u003cp>Lizeth, a chemical engineering major, decided to attend college nearby partly just to keep an eye on her mother. She hasn’t decided whether to get tested for the mutation herself. But her brother said he won’t.\u003c/p>\n\u003cp>“I would rather live my life not knowing,” said Ricardo Navarro, who is studying broadcast journalism at California State University, Fullerton.\u003c/p>\n\u003cp>Their mother meanwhile, works as a temp in customer service and doesn’t make a point of telling the agency or the employers. At a recent job, she had trouble focusing and remembering some of the things her trainers taught her. She didn’t get hired on permanently.\u003c/p>\n\u003cp>She tries to focus on her family rather than the disease. “I can’t let it overcome me,” she said.\u003c/p>\n\u003cp>She puts a lot of faith in a drug trial out of Washington University. Each month, a nurse visits her in La Habra and injects a medication, which she’s pretty sure is not a placebo.\u003c/p>\n\u003cp>“I have to have faith in the drug,” she said. “That’s my only solution for now.”\u003c/p>\n\u003cp>“Otherwise …”\u003c/p>\n\u003cp>She doesn’t finish her thought.\u003c/p>\n\u003cp>[ad floatright]\u003c/p>\n\u003cp>\u003ca href=\"http://www.kaiserhealthnews.org/\">Kaiser Health News\u003c/a>\u003cem> is an editorially independent program of the Henry J. Kaiser Family Foundation, a nonprofit, nonpartisan health policy research and communication organization not affiliated with Kaiser Permanente. You can follow Anna Gorman on Twitter: \u003c/em>\u003ca href=\"https://twitter.com/annagorman\">@annagorman\u003c/a>.\u003c/p>\n\n","blocks":[],"excerpt":"A handful of American families have an inherited early-onset Alzheimer's gene that makes it possible for scientists to predict and potentially treat. ","status":"publish","parent":0,"modified":1704929263,"stats":{"hasAudio":false,"hasVideo":false,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":81,"wordCount":3082},"headData":{"title":"Early Alzheimer's 'Jalisco' Mutation Is A Curse For Families | KQED","description":"A handful of American families have an inherited early-onset Alzheimer's gene that makes it possible for scientists to predict and potentially treat. ","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":"","schema":{"@context":"http://schema.org","@type":"Article","headline":"Early Alzheimer's 'Jalisco' Mutation Is A Curse For Families","datePublished":"2016-12-27T19:27:52.000Z","dateModified":"2024-01-10T23:27:43.000Z","image":"https://cdn.kqed.org/wp-content/uploads/2020/02/KQED-OG-Image@1x.png"}},"sticky":false,"nprByline":"Anna Gorman \u003c/br> Kaiser Health News","path":"/science/1274894/early-alzheimers-jalisco-mutation-is-a-curse-for-families","audioTrackLength":null,"parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003cp>Rosemary Navarro was living in Mexico when her brother called from California.\u003c/p>\n\u003cp>Something wasn’t right with their mom, then in her early 40s. She was having trouble paying bills and keeping jobs as a food preparer in convalescent homes.\u003c/p>\n\u003cp>Navarro, then 22, sold her furniture to pay for a trip back to the U.S. for herself and her two young children. Almost as soon as she arrived, she knew her mother wasn’t the same person. “She was there but sometimes she wasn’t there,” she said. “I thought, ‘Oh man, this isn’t going to be good.’ ”\u003c/p>\n\u003cp>Before long, Navarro was feeding her mom, then changing her diapers. She put a special lock on the door to keep her from straying outside. Unable to continue caring for her, Navarro eventually moved her mom to a nursing home, where she spent eight years.\u003c/p>\n\u003cp>Near the end, her mom, a quiet woman who had immigrated to the U.S. as a teenager and loved \u003cem>telenovelas\u003c/em>, could communicate only by laughing or crying. Navarro was there when she took her last breath in 2009, at age 53. “What I went through with my mom I wouldn’t wish on anyone,” she said.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>","attributes":{"named":{},"numeric":[]}},{"type":"component","content":"","name":"ad","attributes":{"named":{"label":"fullwidth"},"numeric":["fullwidth"]}},{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>It has happened again and again in her family — relatives struck by the same terrible disease, most without any clue what it was. An aunt, an uncle, a cousin, a grandfather, a great grandfather. “Too many have died,” Navarro said. All in their early 50s.\u003c/p>\n\u003cp>Now the family knows the reason for their curse: It’s a rare type of early-onset Alzheimer’s disease, caused by what’s come to be known as the “Jalisco” genetic mutation. Doctors today can tell someone they have it but they can’t stop its destructive march.\u003c/p>\n\u003cp>For Navarro, watching her relatives succumb is like looking into a crystal ball, one she wants to hurl across the room. She, too, has the mutation.\u003c/p>\n\u003caside class=\"pullquote alignright\">‘They are all desperately fearful that they themselves have inherited a mutation. But what they are really fearful about is that they will pass it along to their children.’\u003ccite>John C. Morris, Alzheimer’s Disease Research Center\u003c/cite>\u003c/aside>\n\u003cp>It’s getting harder to stifle her fear. This year, she turned 40 — the same age her mother was when she started wandering off and forgetting simple things.\u003c/p>\n\u003cp>“I don’t look forward to birthdays,” she said. “I didn’t want to celebrate 40, much less 41.”\u003c/p>\n\u003cp>\u003cstrong>Sparing The Next Generation\u003c/strong>\u003c/p>\n\u003cp>Navarro, who lives in La Habra, Calif., belongs to an exclusive but unenviable club whose members are genetically programmed for early memory loss and death.\u003c/p>\n\u003cp>Of the more than 5 million people across the U.S. who have Alzheimer’s, 5 percent are believed to have the early-onset form, striking people under the age of 65. Fewer still — about one percent — have genetic mutations that are known to cause the disease.\u003c/p>\n\u003cp>Navarro’s gene is known as the Jalisco mutation because it is believed to have surfaced first in that Mexican state. Over time, it likely was carried by immigrants across the Mexican border into California and other states. In Mexico and the U.S., roughly 50 families are known to have it.\u003c/p>\n\u003cp>Cases like Navarro’s are of great interest to Alzheimer’s researchers. Studying this unique population with genetic mutations, they say, could help unlock some of the biggest mysteries of the more common form of the disease: How does it develop? How can it be diagnosed earlier? What can be done to stop it?\u003c/p>\n\u003cfigure id=\"attachment_1275007\" class=\"wp-caption aligncenter\" style=\"max-width: 800px\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-medium wp-image-1275007\" src=\"http://ww2.kqed.org/science/wp-content/uploads/sites/35/2016/12/alzheimer2-800x538.jpg\" alt=\"Rosemary Navarro (left) discovered that she carries a rare gene for early-onset Alzheimer's disease. Navarro's mother (right) died from the disease in 2009. "What I went through with my mom I wouldn't wish on anyone," Navarro said. \" width=\"800\" height=\"538\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer2.jpg 800w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer2-160x108.jpg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer2-768x516.jpg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer2-240x161.jpg 240w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer2-375x252.jpg 375w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer2-520x350.jpg 520w\" sizes=\"(max-width: 800px) 100vw, 800px\">\u003cfigcaption class=\"wp-caption-text\">Rosemary Navarro (left) discovered that she carries a rare gene for early-onset Alzheimer’s disease. Navarro’s mother (right) died from the disease in 2009. “What I went through with my mom I wouldn’t wish on anyone,” Navarro said. \u003ccite>(Heidi de Marco/Kaiser Health News)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>Ordinarily, it’s difficult — if not impossible — to predict Alzheimer’s. But with these families, researchers know the mutation carriers \u003cem>will\u003c/em> get the disease. They also know approximately \u003cem>when \u003c/em>symptoms will appear. So they can get a real-time look at how the disease develops — and can measure when the brain starts changing relative to expected onset. Perhaps most important, they can design drugs to target the disease before patients lose their memory.\u003c/p>\n\u003cp>“If you know from age 18 or even from birth whether someone is going to develop the disease or not, you have got a big window to intervene,” Navarro’s doctor, \u003ca href=\"http://keck.usc.edu/faculty/john-m-ringman/\">John Ringman\u003c/a>, a neurology professor at the Keck School of Medicine of the University of Southern California. “We don’t have a way to repair or bring back lost brain cells.”\u003c/p>\n\u003cp>Patients with a familial Alzheimer’s mutation “are sort of a model for how the disease progresses, because they are easier to recognize and easier to study,” said Bruce Miller, a longtime Alzheimer’s researcher who directs the memory and aging center at the University of California, San Francisco.\u003c/p>\n\u003cp>Around the world, hundreds of people whose families are afflicted with a variety of early-onset mutations are subjecting themselves to medical tests — spinal taps, memory quizzes, MRIs and other brain imaging, hoping scientists can develop therapies to prevent and treat Alzheimer’s.\u003c/p>\n\u003cp>But their participation often comes with the sad realization that resulting treatments may come too late for them. Ringman is studying about 100 patients at USC. Navarro is among about 30 with the Jalisco mutation.\u003c/p>\n\u003cp>More than 450 people are part of an international network of research being led by Washington University School of Medicine in St. Louis. Each has a parent with an early-onset gene mutation. If the research doesn’t help them, they tell researchers, maybe it will help the next generation.\u003c/p>\n\u003cp>“They are all desperately fearful that they themselves have inherited a mutation,” said John C. Morris, director of the school’s Alzheimer’s Disease Research Center. “But what they are really fearful about is that if they did, that they will pass it along to their children.”\u003c/p>\n\u003cp>Children have a 50 percent chance of inheriting the mutation from a parent who carries it.\u003c/p>\n\u003cp>Navarro, whose children are now young adults, is well aware of the statistics. She has joined the network’s research effort, of which Ringman is a part.\u003c/p>\n\u003cp>In 2014, she went for a brain scan. She had no overt symptoms, but the results told a different story. Her brain had already started to shrink — a sign that the disease was taking hold.\u003c/p>\n\u003cp>\u003cstrong>‘At Least We Know Now’\u003c/strong>\u003c/p>\n\u003cp>In November 2015, Ringman drove to Colton, Calif. — 60 miles east of Los Angeles — to meet with the large and close-knit Kitchen family. Jay Kitchen and his younger brother John were referred to him after each suffered a series of baffling symptoms.\u003c/p>\n\u003cp>It had started about four years earlier. Jay, then a 44-year-old sports writer, began having difficulty speaking. He felt off balance, was forgetting things and having difficulty paying bills.\u003c/p>\n\u003cp>Soon afterward, his younger brother, John, a high school history teacher, started becoming easily confused. He would forget what day it was and how to get to the market.\u003c/p>\n\u003cfigure id=\"attachment_1275008\" class=\"wp-caption aligncenter\" style=\"max-width: 800px\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-medium wp-image-1275008\" src=\"http://ww2.kqed.org/science/wp-content/uploads/sites/35/2016/12/alzheimer3-800x599.jpg\" alt=\"John (left) and Jay Kitchen with their father in Colton, Calif., in late 2015. \" width=\"800\" height=\"599\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer3.jpg 800w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer3-160x120.jpg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer3-768x575.jpg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer3-240x180.jpg 240w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer3-375x281.jpg 375w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer3-520x389.jpg 520w\" sizes=\"(max-width: 800px) 100vw, 800px\">\u003cfigcaption class=\"wp-caption-text\">John (left) and Jay Kitchen with their father in Colton, Calif., in late 2015. \u003ccite>(Heidi de Marco/Kaiser Health News)\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>It struck me as really odd,” said John’s wife, Michelle Lopez. “Nobody could forget the store that was around the corner from the house you lived in for 12 years.”\u003c/p>\n\u003cp>Jay was the first to seek help. He went to an emergency room, then several specialists. One suspected a stroke. Another suggested mental illness. Test after test came back negative or inconclusive.\u003c/p>\n\u003cp>“It has been a long haul trying to get a diagnosis,” said the brothers’ aunt, Linda Ramos, who took Jay to most of the appointments. Doctors constantly were “scratching their heads trying to figure out what was wrong.”\u003c/p>\n\u003cp>In late 2015, a neurologist referred the brothers to Ringman, who ordered a blood test.\u003c/p>\n\u003cp>On the November morning in Colton, Ringman arrived at Ramos’ home where the extended family was gathered. He pulled the brothers and a few others aside to deliver his grim news: Both men had the Jalisco mutation. Ramos said the brothers sat in near silence. She doesn’t think Jay understood, and John, already a quiet man, just seemed scared.\u003c/p>\n\u003cp>Later that morning, a larger group of family members met with Ringman around a long dining room table: the Kitchens’ father, aunts and uncles; Lopez and Jay’s ex-wife. Jay’s son came with his newborn, who fussed in a stroller.\u003c/p>\n\u003cp>Projecting pictures and diagrams on the wall, the doctor explained the basics of early-onset Alzheimer’s disease and the different mutations that can cause it.\u003c/p>\n\u003cfigure id=\"attachment_1275009\" class=\"wp-caption aligncenter\" style=\"max-width: 800px\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-medium wp-image-1275009\" src=\"http://ww2.kqed.org/science/wp-content/uploads/sites/35/2016/12/alzheimer4-800x533.jpg\" alt=\"John Ringman, a neurologist at the University of Southern California, describes inheritance of genetic disease to John and Jay Kitchen's family in Riverside, Calif. Ringman has devoted much of his career to studying families with a mutation linked to early-onset Alzheimer's. \" width=\"800\" height=\"533\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer4.jpg 800w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer4-160x107.jpg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer4-768x512.jpg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer4-240x160.jpg 240w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer4-375x250.jpg 375w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer4-520x346.jpg 520w\" sizes=\"(max-width: 800px) 100vw, 800px\">\u003cfigcaption class=\"wp-caption-text\">John Ringman, a neurologist at the University of Southern California, describes inheritance of genetic disease to John and Jay Kitchen’s family in Riverside, Calif. Ringman has devoted much of his career to studying families with a mutation linked to early-onset Alzheimer’s. \u003ccite>(Heidi de Marco/Kaiser Health News )\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>Medications available today only address the symptoms, not the disease itself, Ringman said. Drugs may improve people’s thinking but don’t stop the progression.\u003c/p>\n\u003cp>“This is something we are going to crack eventually,” he said.\u003c/p>\n\u003cp>Like many families Ringman encounters, the relatives in the dining room absorbed the news with little emotion or surprise, as though the doctor were confirming nameless fears.\u003c/p>\n\u003cp>Ramos had watched the Kitchens’ mother, Olivia, lose the ability to walk and speak and eventually die in 2002. At the time, they were told she had multiple sclerosis. Now she wasn’t so sure.\u003c/p>\n\u003cp>John Kitchen asked if there was any connection to \u003ca href=\"https://ghr.nlm.nih.gov/condition/huntington-disease\">Huntington’s disease\u003c/a>, which the family had been told his grandfather had.\u003c/p>\n\u003cp>“Probably he didn’t have Huntington’s,” Ringman responded, adding that doctors often get the diagnosis wrong.\u003c/p>\n\u003cp>Ramos recalls feeling somewhat relieved that day.\u003c/p>\n\u003cp>“My thought was, ‘At least we know now. Finally, we know.’ Thank God we have a name [for it] and maybe we can do something for their kids.”\u003c/p>\n\u003cp>\u003cstrong>One Family Leads To Another\u003c/strong>\u003c/p>\n\u003cp>Ringman, now 51, became interested in neuroscience while in college at the University of California, Berkeley. But he knew lab work wasn’t for him. “I realized all these Ph.D.s study one molecule their entire lives and sit in a laboratory,” he said. “I didn’t want that.”\u003c/p>\n\u003cp>In the late 1990s, after completing medical school and specialty training, he joined the medical staff at the University of California, Irvine, where he saw patients with dementia and Huntington’s disease. He liked the personal interaction, combined with the scientific challenge.\u003c/p>\n\u003cp>In 1999, a 42-year-old woman came to see him, brought in by her young adult daughter. Rosa Maria Navarro had signs of early Alzheimer’s disease. Her daughter Rosemary was distraught, reporting that something similar had afflicted many other relatives. It was the beginning of a long relationship, and a new line of scientific inquiry for Ringman.\u003c/p>\n\u003cp>The young neurologist was aware of recently identified familial Alzheimer’s mutations, and he immediately suspected Rosa Maria had one. He sent her blood sample to get the genetic test, and it came back positive for the A431E mutation of a gene known as \u003ca href=\"https://ghr.nlm.nih.gov/gene/PSEN1\">presenilin 1\u003c/a>.\u003c/p>\n\u003cp>Rosemary Navarro suspects her mother sensed even before then what was wrong, having seen her own father lose his memory and die young. “But she was quiet,” Navarro said. “She never said, ‘I might have this.’ ”\u003c/p>\n\u003cp>Soon afterward, another patient came into Ringman’s office with similar symptoms. That patient tested positive for the same mutation. Both had families originating from Jalisco, Mexico. “I was already getting suspicious,” he said.\u003c/p>\n\u003cp>Familial Alzheimer’s intrigued Ringman. It was a relatively new field. Families with the disease had been known to exist since Alzheimer’s first described the disease in 1906, but the genes weren’t identified until about 90 years later. The research touched on so many parts of science — neurology, biology and psychology.\u003c/p>\n\u003cfigure id=\"attachment_1275010\" class=\"wp-caption aligncenter\" style=\"max-width: 800px\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-medium wp-image-1275010\" src=\"http://ww2.kqed.org/science/wp-content/uploads/sites/35/2016/12/alzheimer5-800x534.jpg\" alt=\"Relatives gathered around a dining room table as neurologist John Ringman gave a presentation about Alzheimer's disease and current research in Riverside, Calif., in 2015. \" width=\"800\" height=\"534\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer5.jpg 800w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer5-160x107.jpg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer5-768x513.jpg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer5-240x160.jpg 240w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer5-375x250.jpg 375w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer5-520x347.jpg 520w\" sizes=\"(max-width: 800px) 100vw, 800px\">\u003cfigcaption class=\"wp-caption-text\">Relatives gathered around a dining room table as neurologist John Ringman gave a presentation about Alzheimer’s disease and current research in Riverside, Calif., in 2015. \u003ccite>(Heidi de Marco/Kaiser Health News )\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>Later, Ringman came across an article co-authored by a Mexican neuropsychologist he had worked with before, Yaneth Rodriguez. It was about four families in Mexico that had early Alzheimer’s disease, and they had symptoms similar to his two patients.\u003c/p>\n\u003cp>In 2000, Ringman traveled to Mexico and met with both Rodriguez and a geneticist, Maria Elisa Alonso. Alonso told him that another family there had tested positive for the A431E mutation. Now, there were three, all of Mexican heritage.\u003c/p>\n\u003cp>Ringman collected DNA samples of members of seven more families who were being treated in Mexico. Test results not only confirmed members of each family had A431E, they indicated the patients all shared the same chunk of DNA. That’s when he knew. They were all related, distant cousins who had never met. \u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>In 2006, the Mexican geneticist, Alonso, published a \u003ca href=\"http://www.ncbi.nlm.nih.gov/pubmed/16628450\">report\u003c/a> in \u003cem>Neurogenetics\u003c/em>, describing nine families who didn’t know they were related but all shared the A431E mutation. She concluded that the disease likely started with one ancestor in Jalisco. Ringman published a \u003ca href=\"http://www.ncbi.nlm.nih.gov/pubmed/16897084\">response\u003c/a> describing 15 additional families with the same mutation.\u003c/p>\n\u003cp>The findings meant that Ringman’s patients owed their suffering to an unidentified individual who likely lived in Jalisco perhaps hundreds of years ago. Somehow, as his or her DNA copied itself during cell division, a fatal mistake occurred. And now, in places like La Habra and Colton, Calif., whole families were coping with the awful results.\u003c/p>\n\u003cp>Ringman saw the tragedy but also the scientific opportunity in these discoveries. He later joined the Washington University School of Medicine network in its international quest for knowledge and treatment for familial Alzheimer’s disease. The research now includes different sites in Europe, Asia and Australia.\u003c/p>\n\u003cp>Among the network’s early findings: Amyloid plaques characteristic of Alzheimer’s appear decades before the first noticeable signs of memory loss. The research essentially has presented a timeline of brain changes leading up to memory loss and cognitive decline and has helped lead scientists to decide when and where to aim drugs.\u003c/p>\n\u003cp>A promising target is beta-amyloid. Many researchers believe that flaws in how the sticky substance is accumulated and disposed of in the brain can lead to the disease. Scientists now are studying drugs aimed at attacking beta-amyloid and removing it from the brain.\u003c/p>\n\u003cp>Another encouraging finding, the researchers say, is that early-onset and late-onset Alzheimer’s seem to share many characteristics, and findings that help with one disease are likely to help with the other.\u003c/p>\n\u003cp>The Kitchen brothers aren’t participating in the research. Their mental abilities are declining precipitously.\u003c/p>\n\u003cp>“We get a glimmer of hope,” their aunt Ramos said, “but then we think we are foolish for even hoping.”\u003c/p>\n\u003cp>Jay is living in a locked facility, having tried to run away from another place. He can no longer speak in full sentences and only occasionally recognizes family members.\u003c/p>\n\u003cp>John, now 43, can still hold a conversation but struggles to find the right words. Simple tasks elude him — like writing is name. He feels he is losing control of his life and worries about his family. “I want to be around for my son,” he said.\u003c/p>\n\u003cp>His son, 14-year-old Reese, says he sees his father “slowly fading away.” One day, he asked his mother: “Is that going to happen to me?”\u003c/p>\n\u003cp>“That was the worst day of my life,” Lopez said.\u003c/p>\n\u003cp>\u003cstrong>Fear And Faith\u003c/strong>\u003c/p>\n\u003cfigure id=\"attachment_1275011\" class=\"wp-caption aligncenter\" style=\"max-width: 800px\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-medium wp-image-1275011\" src=\"http://ww2.kqed.org/science/wp-content/uploads/sites/35/2016/12/alzheimer6-800x535.jpg\" alt=\"Rosemary Navarro's son, Ricardo, says he won't get tested for the gene. \" width=\"800\" height=\"535\" srcset=\"https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer6.jpg 800w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer6-160x107.jpg 160w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer6-768x514.jpg 768w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer6-240x161.jpg 240w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer6-375x251.jpg 375w, https://cdn.kqed.org/wp-content/uploads/sites/35/2016/12/alzheimer6-520x348.jpg 520w\" sizes=\"(max-width: 800px) 100vw, 800px\">\u003cfigcaption class=\"wp-caption-text\">Rosemary Navarro’s son, Ricardo, says he won’t get tested for the gene. \u003ccite>(Heidi de Marco/Kaiser Health News )\u003c/cite>\u003c/figcaption>\u003c/figure>\n\u003cp>Navarro’s 19-year-old daughter, Lizeth, and her 22-year-old son, Ricardo, live with her in a three-bedroom trailer in La Habra.\u003c/p>\n\u003cp>Both say said their mom has started forgetting little things — the movie they saw last week or what they need from the grocery store. “I usually have to say things more than once,” said Lizeth Navarro.\u003c/p>\n\u003cp>Lizeth, a chemical engineering major, decided to attend college nearby partly just to keep an eye on her mother. She hasn’t decided whether to get tested for the mutation herself. But her brother said he won’t.\u003c/p>\n\u003cp>“I would rather live my life not knowing,” said Ricardo Navarro, who is studying broadcast journalism at California State University, Fullerton.\u003c/p>\n\u003cp>Their mother meanwhile, works as a temp in customer service and doesn’t make a point of telling the agency or the employers. At a recent job, she had trouble focusing and remembering some of the things her trainers taught her. She didn’t get hired on permanently.\u003c/p>\n\u003cp>She tries to focus on her family rather than the disease. “I can’t let it overcome me,” she said.\u003c/p>\n\u003cp>She puts a lot of faith in a drug trial out of Washington University. Each month, a nurse visits her in La Habra and injects a medication, which she’s pretty sure is not a placebo.\u003c/p>\n\u003cp>“I have to have faith in the drug,” she said. “That’s my only solution for now.”\u003c/p>\n\u003cp>“Otherwise …”\u003c/p>\n\u003cp>She doesn’t finish her thought.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>","attributes":{"named":{},"numeric":[]}},{"type":"component","content":"","name":"ad","attributes":{"named":{"label":"floatright"},"numeric":["floatright"]}},{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>\u003ca href=\"http://www.kaiserhealthnews.org/\">Kaiser Health News\u003c/a>\u003cem> is an editorially independent program of the Henry J. Kaiser Family Foundation, a nonprofit, nonpartisan health policy research and communication organization not affiliated with Kaiser Permanente. You can follow Anna Gorman on Twitter: \u003c/em>\u003ca href=\"https://twitter.com/annagorman\">@annagorman\u003c/a>.\u003c/p>\n\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/science/1274894/early-alzheimers-jalisco-mutation-is-a-curse-for-families","authors":["byline_science_1274894"],"categories":["science_39"],"tags":["science_235","science_2936"],"featImg":"science_1275006","label":"science"},"science_18728":{"type":"posts","id":"science_18728","meta":{"index":"posts_1591205157","site":"science","id":"18728","score":null,"sort":[1404136827000]},"guestAuthors":[],"slug":"you-can-transform-your-genetic-ancestry-data-into-health-info-but-your-results-may-vary","title":"You Can Transform Your Genetic Ancestry Data Into Health Info, But Your Results May Vary","publishDate":1404136827,"format":"aside","headTitle":"You Can Transform Your Genetic Ancestry Data Into Health Info, But Your Results May Vary | KQED","labelTerm":{"site":"science"},"content":"\u003cfigure id=\"attachment_18733\" class=\"wp-caption aligncenter\" style=\"max-width: 640px\">\u003ca href=\"http://ww2.kqed.org/science/wp-content/uploads/sites/35/2014/06/MyEthnicityData23andMe.jpg\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-full wp-image-18733\" src=\"http://ww2.kqed.org/science/wp-content/uploads/sites/35/2014/06/MyEthnicityData23andMe.jpg\" alt=\"Promethease can convert ancestry data like this into health data.\" width=\"640\" height=\"341\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">Promethease can convert ancestry data like this into health data.\u003c/figcaption>\u003c/figure>\n\u003cp>DNA ancestry tests like those offered by \u003ca href=\"https://www.23andme.com/\">23andMe\u003c/a> or \u003ca href=\"http://home.ancestry.com/\">ancestry.com\u003c/a> are a lot of fun and in some cases can be incredibly useful. For example, if you’re adopted, you can find out things about your past you had no way of finding out before. You can also find long lost relatives or confirm relationships you weren’t sure about. (Click \u003ca href=\"http://genetics.thetech.org/ask-a-geneticist/dna-testing-first-cousins\">here \u003c/a>for a great example of a person confirming that someone he thought was a first cousin really was.) And of course, it is just plain fun to find out your family history.\u003c/p>\n\u003cp>But this isn’t enough for everyone. After finding a seemingly endless supply of fifth cousins, you may now want to get more out of your DNA test. You may want to learn a bit about what your DNA can say about your current and future health and maybe even about your earwax and why your pee smells funny whenever you eat asparagus.\u003c/p>\n\u003cp>If this were 2012 or even most of 2013, you’d have no trouble at all finding out about this stuff. You would have seen all this information and more from a \u003ca href=\"https://www.23andme.com/\">23andMe\u003c/a> test.\u003c/p>\n\u003cp>This all changed in November of 2013 when the Federal Drug Administration (FDA)\u003ca href=\"http://ww2.kqed.org/science/2013/12/09/consumer-genetic-testing-company-23andme-faces-its-own-test-from-the-fda/\"> forced 23andMe to stop giving out these types of results\u003c/a>. Now it may seem like that until the FDA and 23andMe work out their differences, there simply isn’t any way to get a hold of the kind of data you used to be able to get. But there actually is with an online resource called \u003ca href=\"http://www.snpedia.com/index.php/Promethease\">Promethease\u003c/a>.\u003c/p>\n\u003cp>\u003cstrong>Promethease to the Rescue (?)\u003c/strong>\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>For just $5, Promethease can turn ancestry/family DNA data from companies like \u003ca href=\"https://www.23andme.com/\">23andMe\u003c/a>, \u003ca href=\"https://www.familytreedna.com/\">FamilyTreeDNA\u003c/a>, and/or \u003ca href=\"http://home.ancestry.com/\">ancestry.com\u003c/a> into DNA health data. The link \u003ca href=\"http://www.snpedia.com/index.php/Promethease\">here \u003c/a>has step-by-step instructions about how to get your raw data from each of these companies and how to use Promethease to learn about your disease risks, which medicines may give you trouble and even which bits of DNA contributed to those blue eyes.\u003c/p>\n\u003cp>One nice feature is that after 45 days, all the online traces of your report disappear a la \u003ca href=\"http://www.snapchat.com/\">Snapchat\u003c/a>. In other words, there is no record of your health data floating around the internet for bad folks to somehow use against you. (You can download a hard copy to your computer and should within the 45 days.)\u003c/p>\n\u003cp>Sounds like a perfect way to convert your ancestry data into health data! Except, of course, that you need to be careful about the data you get and what you do about it.\u003c/p>\n\u003cp>Remember, genetic tests in general can only tell you what scientists know about the DNA these tests look at. They obviously can’t tell you anything about the DNA the test doesn’t cover nor things hidden in the DNA that scientists haven’t figured out yet. Your results will be constrained both by what we don’t yet know and by the DNA the companies happen to test.\u003c/p>\n\u003cp>Now none of this says anything about Promethease at all. They do a great job at providing the most up-to-date information based on the literature that is available for various DNA differences that result in increased disease risk, eye color prediction and so on. It is just that the picture you will get will be incomplete. And different based on the test results you use.\u003c/p>\n\u003cp>This may all sound pretty abstract but this stuff matters. To show you how, I’ll use my Alzheimer’s risk as an example.\u003c/p>\n\u003cp>As you’ll see, my original results from 23andMe are different from the Promethease results I get from the same 23andMe data. And the results from my ancestry.com data are different from both of these.\u003c/p>\n\u003cp>\u003cstrong>Increased and Decreased Risk for Alzheimer’s\u003c/strong>\u003c/p>\n\u003cfigure id=\"attachment_18731\" class=\"wp-caption alignright\" style=\"max-width: 236px\">\u003ca href=\"http://ww2.kqed.org/science/wp-content/uploads/sites/35/2014/06/BarryAlz23andMeOfficialSmall.jpg\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-full wp-image-18731\" src=\"http://ww2.kqed.org/science/wp-content/uploads/sites/35/2014/06/BarryAlz23andMeOfficialSmall.jpg\" alt=\"My reported lowered risk is almost entirely due to my having two copies of APOE2.\" width=\"236\" height=\"239\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">My reported lowered risk is almost entirely due to my having two copies of APOE2.\u003c/figcaption>\u003c/figure>\n\u003cp>I got my 23andMe test before the FDA (temporarily) halted them from giving out health data. As you can see at the right, my risk for Alzheimer’s is, according to the test, much lower than average.\u003c/p>\n\u003cp>This decreased risk is almost completely determined by my having two copies of the APOE2 version of the APOE gene. Now of course there are many other genes that will affect this number either positively or negatively. But APOE is the most important gene scientists have identified so far.\u003c/p>\n\u003cp>When I send my 23andMe data through Promethease, I do not get my results distilled this way. I see a much longer list that includes many findings that 23andMe probably correctly chose not to include because the results are too new, not significant enough, not done with enough participants or any other number of potential problems. This makes the report harder to interpret as I don’t know which results are the most important (although the report does give me some idea).\u003c/p>\n\u003cp>What this means is that I see lots of reports based on different parts of my DNA. A quick look suggests a wash—the different bits of DNA I have that contribute to my Alzheimer’s risk seem to all cancel out. With more digging I would be able to glean the fact that my APOE2 is the key part of my test results and that I have a lowered risk based on the DNA they tested and by what we know about Alzheimer’s and genes right now. But it would take a lot of time and not necessarily be easy (especially if I weren’t already a scientist).\u003c/p>\n\u003cp>My Alzheimer’s risk is very different when I look at my ancestry.com results because they happen not to include the APOE2 marker. Because of this, I end up looking like I am at a higher risk for Alzheimer’s because of all of those other, less significant markers.\u003c/p>\n\u003cp>If I were just to use my ancestry.com results, I would come to a completely different conclusion about my chances for getting Alzheimer’s.This result would matter a whole lot more if instead of two copies of APOE2, I had two copies of APOE4. Then I would be at a significantly higher risk for Alzheimer’s but this would be invisible to my ancestry.com results.\u003c/p>\n\u003cp>None of this says anything bad about ancestry.com. They presumably chose the DNA they wanted to focus on based on what would give them the best results for ancestry and there is no reason to think they chose poorly. It is just they did not happen to choose the specific bit of DNA that indicated I had a lowered risk for Alzheimer’s.\u003c/p>\n\u003cp>[ad floatright]\u003c/p>\n\u003cp>This all points to the bigger problem with trying to predict disease risk for complicated diseases with an incomplete understanding of our genome. Even if we sequenced every last A, T, C, and G, we still might not get an accurate read on our risks for having a heart attack or ending up with diabetes.\u003c/p>\n\n","blocks":[],"excerpt":"An online service called Promethease allows you to convert your genetic ancestry data into health data. If you do, keep in mind that you may miss key health data because your ancestry test might not have been designed to find important health markers.","status":"publish","parent":0,"modified":1704933412,"stats":{"hasAudio":false,"hasVideo":false,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":23,"wordCount":1227},"headData":{"title":"You Can Transform Your Genetic Ancestry Data Into Health Info, But Your Results May Vary | KQED","description":"An online service called Promethease allows you to convert your genetic ancestry data into health data. If you do, keep in mind that you may miss key health data because your ancestry test might not have been designed to find important health markers.","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":"","schema":{"@context":"http://schema.org","@type":"Article","headline":"You Can Transform Your Genetic Ancestry Data Into Health Info, But Your Results May Vary","datePublished":"2014-06-30T14:00:27.000Z","dateModified":"2024-01-11T00:36:52.000Z","image":"https://cdn.kqed.org/wp-content/uploads/2020/02/KQED-OG-Image@1x.png"}},"sticky":false,"path":"/science/18728/you-can-transform-your-genetic-ancestry-data-into-health-info-but-your-results-may-vary","audioTrackLength":null,"parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003cfigure id=\"attachment_18733\" class=\"wp-caption aligncenter\" style=\"max-width: 640px\">\u003ca href=\"http://ww2.kqed.org/science/wp-content/uploads/sites/35/2014/06/MyEthnicityData23andMe.jpg\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-full wp-image-18733\" src=\"http://ww2.kqed.org/science/wp-content/uploads/sites/35/2014/06/MyEthnicityData23andMe.jpg\" alt=\"Promethease can convert ancestry data like this into health data.\" width=\"640\" height=\"341\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">Promethease can convert ancestry data like this into health data.\u003c/figcaption>\u003c/figure>\n\u003cp>DNA ancestry tests like those offered by \u003ca href=\"https://www.23andme.com/\">23andMe\u003c/a> or \u003ca href=\"http://home.ancestry.com/\">ancestry.com\u003c/a> are a lot of fun and in some cases can be incredibly useful. For example, if you’re adopted, you can find out things about your past you had no way of finding out before. You can also find long lost relatives or confirm relationships you weren’t sure about. (Click \u003ca href=\"http://genetics.thetech.org/ask-a-geneticist/dna-testing-first-cousins\">here \u003c/a>for a great example of a person confirming that someone he thought was a first cousin really was.) And of course, it is just plain fun to find out your family history.\u003c/p>\n\u003cp>But this isn’t enough for everyone. After finding a seemingly endless supply of fifth cousins, you may now want to get more out of your DNA test. You may want to learn a bit about what your DNA can say about your current and future health and maybe even about your earwax and why your pee smells funny whenever you eat asparagus.\u003c/p>\n\u003cp>If this were 2012 or even most of 2013, you’d have no trouble at all finding out about this stuff. You would have seen all this information and more from a \u003ca href=\"https://www.23andme.com/\">23andMe\u003c/a> test.\u003c/p>\n\u003cp>This all changed in November of 2013 when the Federal Drug Administration (FDA)\u003ca href=\"http://ww2.kqed.org/science/2013/12/09/consumer-genetic-testing-company-23andme-faces-its-own-test-from-the-fda/\"> forced 23andMe to stop giving out these types of results\u003c/a>. Now it may seem like that until the FDA and 23andMe work out their differences, there simply isn’t any way to get a hold of the kind of data you used to be able to get. But there actually is with an online resource called \u003ca href=\"http://www.snpedia.com/index.php/Promethease\">Promethease\u003c/a>.\u003c/p>\n\u003cp>\u003cstrong>Promethease to the Rescue (?)\u003c/strong>\u003c/p>\n\u003cp>\u003c/p>\u003c/div>","attributes":{"named":{},"numeric":[]}},{"type":"component","content":"","name":"ad","attributes":{"named":{"label":"fullwidth"},"numeric":["fullwidth"]}},{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>For just $5, Promethease can turn ancestry/family DNA data from companies like \u003ca href=\"https://www.23andme.com/\">23andMe\u003c/a>, \u003ca href=\"https://www.familytreedna.com/\">FamilyTreeDNA\u003c/a>, and/or \u003ca href=\"http://home.ancestry.com/\">ancestry.com\u003c/a> into DNA health data. The link \u003ca href=\"http://www.snpedia.com/index.php/Promethease\">here \u003c/a>has step-by-step instructions about how to get your raw data from each of these companies and how to use Promethease to learn about your disease risks, which medicines may give you trouble and even which bits of DNA contributed to those blue eyes.\u003c/p>\n\u003cp>One nice feature is that after 45 days, all the online traces of your report disappear a la \u003ca href=\"http://www.snapchat.com/\">Snapchat\u003c/a>. In other words, there is no record of your health data floating around the internet for bad folks to somehow use against you. (You can download a hard copy to your computer and should within the 45 days.)\u003c/p>\n\u003cp>Sounds like a perfect way to convert your ancestry data into health data! Except, of course, that you need to be careful about the data you get and what you do about it.\u003c/p>\n\u003cp>Remember, genetic tests in general can only tell you what scientists know about the DNA these tests look at. They obviously can’t tell you anything about the DNA the test doesn’t cover nor things hidden in the DNA that scientists haven’t figured out yet. Your results will be constrained both by what we don’t yet know and by the DNA the companies happen to test.\u003c/p>\n\u003cp>Now none of this says anything about Promethease at all. They do a great job at providing the most up-to-date information based on the literature that is available for various DNA differences that result in increased disease risk, eye color prediction and so on. It is just that the picture you will get will be incomplete. And different based on the test results you use.\u003c/p>\n\u003cp>This may all sound pretty abstract but this stuff matters. To show you how, I’ll use my Alzheimer’s risk as an example.\u003c/p>\n\u003cp>As you’ll see, my original results from 23andMe are different from the Promethease results I get from the same 23andMe data. And the results from my ancestry.com data are different from both of these.\u003c/p>\n\u003cp>\u003cstrong>Increased and Decreased Risk for Alzheimer’s\u003c/strong>\u003c/p>\n\u003cfigure id=\"attachment_18731\" class=\"wp-caption alignright\" style=\"max-width: 236px\">\u003ca href=\"http://ww2.kqed.org/science/wp-content/uploads/sites/35/2014/06/BarryAlz23andMeOfficialSmall.jpg\">\u003cimg loading=\"lazy\" decoding=\"async\" class=\"size-full wp-image-18731\" src=\"http://ww2.kqed.org/science/wp-content/uploads/sites/35/2014/06/BarryAlz23andMeOfficialSmall.jpg\" alt=\"My reported lowered risk is almost entirely due to my having two copies of APOE2.\" width=\"236\" height=\"239\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">My reported lowered risk is almost entirely due to my having two copies of APOE2.\u003c/figcaption>\u003c/figure>\n\u003cp>I got my 23andMe test before the FDA (temporarily) halted them from giving out health data. As you can see at the right, my risk for Alzheimer’s is, according to the test, much lower than average.\u003c/p>\n\u003cp>This decreased risk is almost completely determined by my having two copies of the APOE2 version of the APOE gene. Now of course there are many other genes that will affect this number either positively or negatively. But APOE is the most important gene scientists have identified so far.\u003c/p>\n\u003cp>When I send my 23andMe data through Promethease, I do not get my results distilled this way. I see a much longer list that includes many findings that 23andMe probably correctly chose not to include because the results are too new, not significant enough, not done with enough participants or any other number of potential problems. This makes the report harder to interpret as I don’t know which results are the most important (although the report does give me some idea).\u003c/p>\n\u003cp>What this means is that I see lots of reports based on different parts of my DNA. A quick look suggests a wash—the different bits of DNA I have that contribute to my Alzheimer’s risk seem to all cancel out. With more digging I would be able to glean the fact that my APOE2 is the key part of my test results and that I have a lowered risk based on the DNA they tested and by what we know about Alzheimer’s and genes right now. But it would take a lot of time and not necessarily be easy (especially if I weren’t already a scientist).\u003c/p>\n\u003cp>My Alzheimer’s risk is very different when I look at my ancestry.com results because they happen not to include the APOE2 marker. Because of this, I end up looking like I am at a higher risk for Alzheimer’s because of all of those other, less significant markers.\u003c/p>\n\u003cp>If I were just to use my ancestry.com results, I would come to a completely different conclusion about my chances for getting Alzheimer’s.This result would matter a whole lot more if instead of two copies of APOE2, I had two copies of APOE4. Then I would be at a significantly higher risk for Alzheimer’s but this would be invisible to my ancestry.com results.\u003c/p>\n\u003cp>None of this says anything bad about ancestry.com. They presumably chose the DNA they wanted to focus on based on what would give them the best results for ancestry and there is no reason to think they chose poorly. It is just they did not happen to choose the specific bit of DNA that indicated I had a lowered risk for Alzheimer’s.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>","attributes":{"named":{},"numeric":[]}},{"type":"component","content":"","name":"ad","attributes":{"named":{"label":"floatright"},"numeric":["floatright"]}},{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>This all points to the bigger problem with trying to predict disease risk for complicated diseases with an incomplete understanding of our genome. Even if we sequenced every last A, T, C, and G, we still might not get an accurate read on our risks for having a heart attack or ending up with diabetes.\u003c/p>\n\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/science/18728/you-can-transform-your-genetic-ancestry-data-into-health-info-but-your-results-may-vary","authors":["6177"],"categories":["science_30","science_39"],"tags":["science_235","science_5181"],"featImg":"science_18733","label":"science"},"science_3707":{"type":"posts","id":"science_3707","meta":{"index":"posts_1591205157","site":"science","id":"3707","score":null,"sort":[1370040384000]},"guestAuthors":[],"slug":"when-will-mental-illness-be-diagnosed-with-a-lab-test","title":"When Will Mental Illness Be Diagnosed With a Lab Test?","publishDate":1370040384,"format":"aside","headTitle":"When Will Mental Illness Be Diagnosed With a Lab Test? | KQED","labelTerm":{"site":"science"},"content":"\u003cdiv class=\"audio-wrap\">\n\u003ch2>Listen:\u003c/h2>\n\u003cp>http://kqed02.streamguys.us/anon.kqed/radio/science/2013/06/2013-06-03-science.mp3\u003c/p>\n\u003c/div>\n\u003cfigure id=\"attachment_3769\" class=\"wp-caption alignnone\" style=\"max-width: 640px\">\u003ca href=\"http://ww2.kqed.org/science/wp-content/uploads/sites/35/2013/05/KQED_CN-PTSD-AD_dts_Scaled.jpg\" rel=\"attachment wp-att-3769\">\u003cimg loading=\"lazy\" decoding=\"async\" src=\"http://ww2.kqed.org/science/wp-content/uploads/sites/35/2013/05/KQED_CN-PTSD-AD_dts_Scaled.jpg\" alt=\"MRIs of two brains show a slightly smaller amygdala in the brain of a man with PTSD. (Photo courtesy Michael Weiner)\" width=\"640\" height=\"360\" class=\"size-full wp-image-3769\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">Two MRI scans show a slightly smaller amygdala in the brain of a man with PTSD. (Photo courtesy Michael Weiner)\u003c/figcaption>\u003c/figure>\n\u003cp>Say you’re a doctor and a patient comes in complaining of chest pains. You’d want to know what was causing them. So you’d run lab tests, looking for signs of a heart attack or some other problem.\u003c/p>\n\u003cp>That’s standard procedure across medicine, except in the case of mental illness. It’s the last area of medicine where there are virtually no lab tests to indicate what’s wrong. \u003c/p>\n\u003cp>This has become a major challenge across the field of psychiatry: to give those who suffer from mental illnesses like schizophrenia and depression the same sort of scientific certainty doctors have recently begun to provide to people with Alzheimer’s disease. \u003c/p>\n\u003cp>People like Robin Jones.\u003cbr>\n\u003cstrong>\u003cbr>\n“Something is different.”\u003c/strong>\u003c/p>\n\u003cp>In 2007, Jones found himself in a parking lot. He had no idea where his car was. This was unlike him. Jones is a scientist who used to work on nuclear power plants. He’s always been good with details. \u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>“I’m the one who parked it there!” Jones recalls thinking. “Why can’t I remember?”\u003c/p>\n\u003cp>At work, he had a hard time finding the right words and making persuasive arguments to his colleagues. He’d come home and tell his wife, Anne, “Something’s different.” \u003c/p>\n\u003cp>“He would say his brain didn’t feel like it was working the same way it used to,” she recalls. “We said, ‘Well, why not talk to your primary care physician about it?’ And that started a cascade of events.”\u003c/p>\n\u003cp>Eventually, the Joneses made it to the \u003ca href=\"http://neurology.stanford.edu/memory/\">Stanford Center for Memory Disorders\u003c/a>, where Robin went through the standard run-up for Alzheimer’s disease, memorizing lists of words, and so on. But he did pretty well on them, says Mike Greicius, the center’s medical director, better than you’d expect from someone in the early stages of the disease. \u003c/p>\n\u003cp>“He didn’t fit neatly into this classic presentation of Alzheimer’s disease,” says Greicius. “That’s one of the reasons that, fairly early on, we started talking about biomarkers.”\u003c/p>\n\u003cp>These biomarkers refer to lab tests, and they’re a very recent development in Alzheimer’s disease care.\u003c/p>\n\u003cp>One test uses a PET scan that can detect amyloid, a protein that takes on an abnormal shape in the brains of Alzheimer’s patients. The second test requires a lumbar puncture to look for traces of amyloid and tau, another protein associated with Alzheimer’s disease, in the patient’s spinal fluid. \u003c/p>\n\u003cp>Robin chose the spinal fluid test. “It seemed to me it would sharpen up my understanding of what was happening,” he says.\u003cbr>\n\u003cstrong>\u003cbr>\nTests for Alzheimer’s disease signal changes across mental health\u003c/strong>\u003c/p>\n\u003cp>Until very recently, Alzheimer’s was diagnosed more or less the same way other mental illnesses, such as autism or schizophrenia, are diagnosed: by asking patients how they feel and observing how they behave. \u003c/p>\n\u003cp>That all changed when scientists discovered biomarkers for Alzheimer’s: the tau and amyloid proteins that are signatures of the disease. \u003c/p>\n\u003cp>Then, it was a matter of finding tests that could pick up those biomarkers. \u003c/p>\n\u003cp>Michael Weiner, who directs the \u003ca href=\"http://www.radiology.ucsf.edu/cind\">Center for Imaging of Neurodegenerative Diseases\u003c/a> at San Francisco’s VA Medical Center, says the same thing happened with heart disease a generation ago. \u003c/p>\n\u003cp>“When I was a medical student 40 years ago, patients would come in with chest pains and we’d spend a lot of time talking to them,” Weiner says. “‘Where is the pain in the chest? What’s going on? How does it radiate in your arm?’” \u003c/p>\n\u003cp>That whole process changed when scientists discovered biomarkers of heart disease, for example, certain enzymes that leak into the bloodstream when the heart is damaged. \u003c/p>\n\u003cp>“Nowadays,” says Weiner, “you draw blood enzymes. And if a person has a rise in certain enzymes, we say they had a heart attack. And if they didn’t, we say you didn’t have a heart attack.” \u003c/p>\n\u003cp>This is the name of the game in psychiatry today: to understand the underlying brain diseases behind mental illness and find ways to test for them.\u003cbr>\n\u003cstrong>\u003cbr>\nBetter tools for diagnosing PTSD\u003c/strong>\u003c/p>\n\u003cp>One of the biggest efforts is directed out of NYU’s \u003ca href=\"http://www.med.nyu.edu/\">Langone Medical Center\u003c/a>, where Charles Marmar chairs the psychiatry department and leads a $28 million dollar effort to look for biomarkers of post traumatic stress disorder and traumatic brain damage, diseases that are often under-reported and under-treated. \u003c/p>\n\u003cp>Marmar believes that one day — maybe within a decade or two — simple tests, much like home pregnancy tests, will indicate whether people are suffering from PTSD or possibly even autism or schizophrenia. \u003c/p>\n\u003cp>“Blood, urine and cerebral spinal fluid will, over time, have something very important to say about risks for psychiatric illness, the presence or absence of illness and the prognosis of a given depressive illness,” says Marmar. \u003c/p>\n\u003cp>And, importantly, he says, whether a treatment – be it talk therapy or drugs – is working. \u003c/p>\n\u003cp>In the case of PTSD, he says, the first step is to look for biomarkers, what he calls the “biological footprint of learned fear,” that could be detectable in a lab test. \u003c/p>\n\u003cp>\u003cstrong>Voice as a diagnostic tool\u003c/strong>\u003c/p>\n\u003cp>But these diseases may announce themselves in other ways, too, for example, in the way people talk. \u003c/p>\n\u003cp>At \u003ca href=\"http://www.sri.com/\">SRI International\u003c/a>, a non-profit research group in Menlo Park, scientists are developing computer algorithms to look for voice signatures of people with PTSD. \u003c/p>\n\u003cp>SRI’s Dimitra Vergyri plays a recording of three voices saying the word “no.” The first sounds disappointed, the second impatient, the third – with a happy laugh – sounds “entertained,” she explains.\u003c/p>\n\u003cp>\u003c!-- iframe plugin v.4.3 wordpress.org/plugins/iframe/ -->\u003cbr>\n\u003ciframe loading=\"lazy\" width=\"100%\" height=\"166\" scrolling=\"no\" frameborder=\"no\" src=\"https://w.soundcloud.com/player/?url=http%3A%2F%2Fapi.soundcloud.com%2Ftracks%2F94724399\" class=\"iframe-class\">\u003c/iframe>\u003c/p>\n\u003cp>“We want to show that there are features that we can extract automatically, measure them, and they can be an indicator of a very specific emotional state,” she says. \u003c/p>\n\u003cp>The idea here is that you could take voice recordings of, say, returning soldiers, and use the algorithm to flag which of them might be more at risk for psychological problems. Then, make sure they don’t slip through the cracks. \u003c/p>\n\u003cp>Charles Marmar, head of the NYU effort, believes tests like these will change the field of psychiatry.\u003c/p>\n\u003cp>“As we advance biomarkers, we will demystify and de-stigmatize psychiatric illness,” says Marmar. “We will make [mental health] part of normal care.”\u003c/p>\n\u003cp>\u003cstrong>The results come back \u003c/strong>\u003c/p>\n\u003cp>Slowly, that is what’s happening in Alzheimer’s disease, and in the case of Robin Jones. \u003c/p>\n\u003cp>Robin’s wife, Anne, was the first to learn the results of his Alzheimer’s test, which came back positive. \u003c/p>\n\u003cp>Her first reaction, she says, was simply sadness. But after that came “a certain amount of relief.” \u003c/p>\n\u003cp>“There’s relief knowing why your arm hurts, or why you have a bad cough. Knowing how to chart out the rest of our time together.” \u003c/p>\n\u003cp>Recently, Anne took a trip alone to Florence to see the great works of art she studied as an art history major in college. She left a note for Robin, reminding him where she had gone and thanking him for the opportunity. \u003c/p>\n\u003cp>Having a concrete diagnosis, she says, helped her recognize a window for such adventures, before her care-taking responsibilities begin to keep her closer to home. \u003c/p>\n\u003cp>[ad floatright]\u003c/p>\n\u003cp>The test, she says, gave them both certainty and the ability to focus on what lies ahead. \u003c/p>\n\n","blocks":[],"excerpt":"Mental illness is the last area of medicine where there are virtually no lab tests to indicate what’s wrong. This has become a major challenge across the field of psychiatry: to give those who suffer from mental illnesses like schizophrenia and depression the same sort of scientific certainty doctors have recently begun to provide to people with Alzheimer’s disease. ","status":"publish","parent":0,"modified":1704935683,"stats":{"hasAudio":true,"hasVideo":false,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":45,"wordCount":1334},"headData":{"title":"When Will Mental Illness Be Diagnosed With a Lab Test? | KQED","description":"Mental illness is the last area of medicine where there are virtually no lab tests to indicate what’s wrong. This has become a major challenge across the field of psychiatry: to give those who suffer from mental illnesses like schizophrenia and depression the same sort of scientific certainty doctors have recently begun to provide to people with Alzheimer’s disease. ","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":"","schema":{"@context":"http://schema.org","@type":"Article","headline":"When Will Mental Illness Be Diagnosed With a Lab Test?","datePublished":"2013-05-31T22:46:24.000Z","dateModified":"2024-01-11T01:14:43.000Z","image":"https://cdn.kqed.org/wp-content/uploads/2020/02/KQED-OG-Image@1x.png"}},"audioUrl":"http://kqed02.streamguys.us/anon.kqed/radio/science/2013/06/2013-06-03-science.mp3","sticky":false,"path":"/science/3707/when-will-mental-illness-be-diagnosed-with-a-lab-test","audioTrackLength":null,"parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003cdiv class=\"audio-wrap\">\n\u003ch2>Listen:\u003c/h2>\n\u003cp>http://kqed02.streamguys.us/anon.kqed/radio/science/2013/06/2013-06-03-science.mp3\u003c/p>\n\u003c/div>\n\u003cfigure id=\"attachment_3769\" class=\"wp-caption alignnone\" style=\"max-width: 640px\">\u003ca href=\"http://ww2.kqed.org/science/wp-content/uploads/sites/35/2013/05/KQED_CN-PTSD-AD_dts_Scaled.jpg\" rel=\"attachment wp-att-3769\">\u003cimg loading=\"lazy\" decoding=\"async\" src=\"http://ww2.kqed.org/science/wp-content/uploads/sites/35/2013/05/KQED_CN-PTSD-AD_dts_Scaled.jpg\" alt=\"MRIs of two brains show a slightly smaller amygdala in the brain of a man with PTSD. (Photo courtesy Michael Weiner)\" width=\"640\" height=\"360\" class=\"size-full wp-image-3769\">\u003c/a>\u003cfigcaption class=\"wp-caption-text\">Two MRI scans show a slightly smaller amygdala in the brain of a man with PTSD. (Photo courtesy Michael Weiner)\u003c/figcaption>\u003c/figure>\n\u003cp>Say you’re a doctor and a patient comes in complaining of chest pains. You’d want to know what was causing them. So you’d run lab tests, looking for signs of a heart attack or some other problem.\u003c/p>\n\u003cp>That’s standard procedure across medicine, except in the case of mental illness. It’s the last area of medicine where there are virtually no lab tests to indicate what’s wrong. \u003c/p>\n\u003cp>This has become a major challenge across the field of psychiatry: to give those who suffer from mental illnesses like schizophrenia and depression the same sort of scientific certainty doctors have recently begun to provide to people with Alzheimer’s disease. \u003c/p>\n\u003cp>People like Robin Jones.\u003cbr>\n\u003cstrong>\u003cbr>\n“Something is different.”\u003c/strong>\u003c/p>\n\u003cp>In 2007, Jones found himself in a parking lot. He had no idea where his car was. This was unlike him. Jones is a scientist who used to work on nuclear power plants. He’s always been good with details. \u003c/p>\n\u003cp>\u003c/p>\u003c/div>","attributes":{"named":{},"numeric":[]}},{"type":"component","content":"","name":"ad","attributes":{"named":{"label":"fullwidth"},"numeric":["fullwidth"]}},{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>“I’m the one who parked it there!” Jones recalls thinking. “Why can’t I remember?”\u003c/p>\n\u003cp>At work, he had a hard time finding the right words and making persuasive arguments to his colleagues. He’d come home and tell his wife, Anne, “Something’s different.” \u003c/p>\n\u003cp>“He would say his brain didn’t feel like it was working the same way it used to,” she recalls. “We said, ‘Well, why not talk to your primary care physician about it?’ And that started a cascade of events.”\u003c/p>\n\u003cp>Eventually, the Joneses made it to the \u003ca href=\"http://neurology.stanford.edu/memory/\">Stanford Center for Memory Disorders\u003c/a>, where Robin went through the standard run-up for Alzheimer’s disease, memorizing lists of words, and so on. But he did pretty well on them, says Mike Greicius, the center’s medical director, better than you’d expect from someone in the early stages of the disease. \u003c/p>\n\u003cp>“He didn’t fit neatly into this classic presentation of Alzheimer’s disease,” says Greicius. “That’s one of the reasons that, fairly early on, we started talking about biomarkers.”\u003c/p>\n\u003cp>These biomarkers refer to lab tests, and they’re a very recent development in Alzheimer’s disease care.\u003c/p>\n\u003cp>One test uses a PET scan that can detect amyloid, a protein that takes on an abnormal shape in the brains of Alzheimer’s patients. The second test requires a lumbar puncture to look for traces of amyloid and tau, another protein associated with Alzheimer’s disease, in the patient’s spinal fluid. \u003c/p>\n\u003cp>Robin chose the spinal fluid test. “It seemed to me it would sharpen up my understanding of what was happening,” he says.\u003cbr>\n\u003cstrong>\u003cbr>\nTests for Alzheimer’s disease signal changes across mental health\u003c/strong>\u003c/p>\n\u003cp>Until very recently, Alzheimer’s was diagnosed more or less the same way other mental illnesses, such as autism or schizophrenia, are diagnosed: by asking patients how they feel and observing how they behave. \u003c/p>\n\u003cp>That all changed when scientists discovered biomarkers for Alzheimer’s: the tau and amyloid proteins that are signatures of the disease. \u003c/p>\n\u003cp>Then, it was a matter of finding tests that could pick up those biomarkers. \u003c/p>\n\u003cp>Michael Weiner, who directs the \u003ca href=\"http://www.radiology.ucsf.edu/cind\">Center for Imaging of Neurodegenerative Diseases\u003c/a> at San Francisco’s VA Medical Center, says the same thing happened with heart disease a generation ago. \u003c/p>\n\u003cp>“When I was a medical student 40 years ago, patients would come in with chest pains and we’d spend a lot of time talking to them,” Weiner says. “‘Where is the pain in the chest? What’s going on? How does it radiate in your arm?’” \u003c/p>\n\u003cp>That whole process changed when scientists discovered biomarkers of heart disease, for example, certain enzymes that leak into the bloodstream when the heart is damaged. \u003c/p>\n\u003cp>“Nowadays,” says Weiner, “you draw blood enzymes. And if a person has a rise in certain enzymes, we say they had a heart attack. And if they didn’t, we say you didn’t have a heart attack.” \u003c/p>\n\u003cp>This is the name of the game in psychiatry today: to understand the underlying brain diseases behind mental illness and find ways to test for them.\u003cbr>\n\u003cstrong>\u003cbr>\nBetter tools for diagnosing PTSD\u003c/strong>\u003c/p>\n\u003cp>One of the biggest efforts is directed out of NYU’s \u003ca href=\"http://www.med.nyu.edu/\">Langone Medical Center\u003c/a>, where Charles Marmar chairs the psychiatry department and leads a $28 million dollar effort to look for biomarkers of post traumatic stress disorder and traumatic brain damage, diseases that are often under-reported and under-treated. \u003c/p>\n\u003cp>Marmar believes that one day — maybe within a decade or two — simple tests, much like home pregnancy tests, will indicate whether people are suffering from PTSD or possibly even autism or schizophrenia. \u003c/p>\n\u003cp>“Blood, urine and cerebral spinal fluid will, over time, have something very important to say about risks for psychiatric illness, the presence or absence of illness and the prognosis of a given depressive illness,” says Marmar. \u003c/p>\n\u003cp>And, importantly, he says, whether a treatment – be it talk therapy or drugs – is working. \u003c/p>\n\u003cp>In the case of PTSD, he says, the first step is to look for biomarkers, what he calls the “biological footprint of learned fear,” that could be detectable in a lab test. \u003c/p>\n\u003cp>\u003cstrong>Voice as a diagnostic tool\u003c/strong>\u003c/p>\n\u003cp>But these diseases may announce themselves in other ways, too, for example, in the way people talk. \u003c/p>\n\u003cp>At \u003ca href=\"http://www.sri.com/\">SRI International\u003c/a>, a non-profit research group in Menlo Park, scientists are developing computer algorithms to look for voice signatures of people with PTSD. \u003c/p>\n\u003cp>SRI’s Dimitra Vergyri plays a recording of three voices saying the word “no.” The first sounds disappointed, the second impatient, the third – with a happy laugh – sounds “entertained,” she explains.\u003c/p>\n\u003cp>\u003c!-- iframe plugin v.4.3 wordpress.org/plugins/iframe/ -->\u003cbr>\n\u003ciframe loading=\"lazy\" width=\"100%\" height=\"166\" scrolling=\"no\" frameborder=\"no\" src=\"https://w.soundcloud.com/player/?url=http%3A%2F%2Fapi.soundcloud.com%2Ftracks%2F94724399\" class=\"iframe-class\">\u003c/iframe>\u003c/p>\n\u003cp>“We want to show that there are features that we can extract automatically, measure them, and they can be an indicator of a very specific emotional state,” she says. \u003c/p>\n\u003cp>The idea here is that you could take voice recordings of, say, returning soldiers, and use the algorithm to flag which of them might be more at risk for psychological problems. Then, make sure they don’t slip through the cracks. \u003c/p>\n\u003cp>Charles Marmar, head of the NYU effort, believes tests like these will change the field of psychiatry.\u003c/p>\n\u003cp>“As we advance biomarkers, we will demystify and de-stigmatize psychiatric illness,” says Marmar. “We will make [mental health] part of normal care.”\u003c/p>\n\u003cp>\u003cstrong>The results come back \u003c/strong>\u003c/p>\n\u003cp>Slowly, that is what’s happening in Alzheimer’s disease, and in the case of Robin Jones. \u003c/p>\n\u003cp>Robin’s wife, Anne, was the first to learn the results of his Alzheimer’s test, which came back positive. \u003c/p>\n\u003cp>Her first reaction, she says, was simply sadness. But after that came “a certain amount of relief.” \u003c/p>\n\u003cp>“There’s relief knowing why your arm hurts, or why you have a bad cough. Knowing how to chart out the rest of our time together.” \u003c/p>\n\u003cp>Recently, Anne took a trip alone to Florence to see the great works of art she studied as an art history major in college. She left a note for Robin, reminding him where she had gone and thanking him for the opportunity. \u003c/p>\n\u003cp>Having a concrete diagnosis, she says, helped her recognize a window for such adventures, before her care-taking responsibilities begin to keep her closer to home. \u003c/p>\n\u003cp>\u003c/p>\u003c/div>","attributes":{"named":{},"numeric":[]}},{"type":"component","content":"","name":"ad","attributes":{"named":{"label":"floatright"},"numeric":["floatright"]}},{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>The test, she says, gave them both certainty and the ability to focus on what lies ahead. \u003c/p>\n\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/science/3707/when-will-mental-illness-be-diagnosed-with-a-lab-test","authors":["210"],"categories":["science_46","science_30","science_39","science_40","science_43"],"tags":["science_235","science_249"],"featImg":"science_3769","label":"science"}},"programsReducer":{"possible":{"id":"possible","title":"Possible","info":"Possible is hosted by entrepreneur Reid Hoffman and writer Aria Finger. Together in Possible, Hoffman and Finger lead enlightening discussions about building a brighter collective future. The show features interviews with visionary guests like Trevor Noah, Sam Altman and Janette Sadik-Khan. Possible paints an optimistic portrait of the world we can create through science, policy, business, art and our shared humanity. It asks: What if everything goes right for once? How can we get there? Each episode also includes a short fiction story generated by advanced AI GPT-4, serving as a thought-provoking springboard to speculate how humanity could leverage technology for good.","airtime":"SUN 2pm","imageSrc":"https://cdn.kqed.org/wp-content/uploads/2024/04/Possible-Podcast-Tile-360x360-1.jpg","officialWebsiteLink":"https://www.possible.fm/","meta":{"site":"news","source":"Possible"},"link":"/radio/program/possible","subscribe":{"apple":"https://podcasts.apple.com/us/podcast/possible/id1677184070","spotify":"https://open.spotify.com/show/730YpdUSNlMyPQwNnyjp4k"}},"1a":{"id":"1a","title":"1A","info":"1A is home to the national conversation. 1A brings on great guests and frames the best debate in ways that make you think, share and engage.","airtime":"MON-THU 11pm-12am","imageSrc":"https://ww2.kqed.org/radio/wp-content/uploads/sites/50/2018/04/1a.jpg","officialWebsiteLink":"https://the1a.org/","meta":{"site":"news","source":"npr"},"link":"/radio/program/1a","subscribe":{"npr":"https://rpb3r.app.goo.gl/RBrW","apple":"https://itunes.apple.com/WebObjects/MZStore.woa/wa/viewPodcast?s=143441&mt=2&id=1188724250&at=11l79Y&ct=nprdirectory","tuneIn":"https://tunein.com/radio/1A-p947376/","rss":"https://feeds.npr.org/510316/podcast.xml"}},"all-things-considered":{"id":"all-things-considered","title":"All Things Considered","info":"Every weekday, \u003cem>All Things Considered\u003c/em> hosts Robert Siegel, Audie Cornish, Ari Shapiro, and Kelly McEvers present the program's trademark mix of news, interviews, commentaries, reviews, and offbeat features. Michel Martin hosts on the weekends.","airtime":"MON-FRI 1pm-2pm, 4:30pm-6:30pm\u003cbr />SAT-SUN 5pm-6pm","imageSrc":"https://cdn.kqed.org/wp-content/uploads/2024/04/All-Things-Considered-Podcast-Tile-360x360-1.jpg","officialWebsiteLink":"https://www.npr.org/programs/all-things-considered/","meta":{"site":"news","source":"npr"},"link":"/radio/program/all-things-considered"},"american-suburb-podcast":{"id":"american-suburb-podcast","title":"American Suburb: The Podcast","tagline":"The flip side of gentrification, told through one town","info":"Gentrification is changing cities across America, forcing people from neighborhoods they have long called home. Call them the displaced. Now those priced out of the Bay Area are looking for a better life in an unlikely place. American Suburb follows this migration to one California town along the Delta, 45 miles from San Francisco. But is this once sleepy suburb ready for them?","imageSrc":"https://cdn.kqed.org/wp-content/uploads/2024/04/American-Suburb-Podcast-Tile-703x703-1.jpg","officialWebsiteLink":"/news/series/american-suburb-podcast","meta":{"site":"news","source":"kqed","order":"13"},"link":"/news/series/american-suburb-podcast/","subscribe":{"npr":"https://rpb3r.app.goo.gl/RBrW","apple":"https://itunes.apple.com/WebObjects/MZStore.woa/wa/viewPodcast?mt=2&id=1287748328","tuneIn":"https://tunein.com/radio/American-Suburb-p1086805/","rss":"https://ww2.kqed.org/news/series/american-suburb-podcast/feed/podcast","google":"https://podcasts.google.com/feed/aHR0cHM6Ly9mZWVkcy5tZWdhcGhvbmUuZm0vS1FJTkMzMDExODgxNjA5"}},"baycurious":{"id":"baycurious","title":"Bay Curious","tagline":"Exploring the Bay Area, one question at a time","info":"KQED’s new podcast, Bay Curious, gets to the bottom of the mysteries — both profound and peculiar — that give the Bay Area its unique identity. And we’ll do it with your help! You ask the questions. You decide what Bay Curious investigates. 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You can also visit the MindShift website for episodes and supplemental blog posts or tweet us \u003ca href=\"https://twitter.com/MindShiftKQED\">@MindShiftKQED\u003c/a> or visit us at \u003ca href=\"/mindshift\">MindShift.KQED.org\u003c/a>","imageSrc":"https://cdn.kqed.org/wp-content/uploads/2024/04/Mindshift-Podcast-Tile-703x703-1.jpg","imageAlt":"KQED MindShift: How We Will Learn","officialWebsiteLink":"/mindshift/","meta":{"site":"news","source":"kqed","order":"2"},"link":"/podcasts/mindshift","subscribe":{"apple":"https://podcasts.apple.com/us/podcast/mindshift-podcast/id1078765985","google":"https://podcasts.google.com/feed/aHR0cHM6Ly9mZWVkcy5tZWdhcGhvbmUuZm0vS1FJTkM1NzY0NjAwNDI5","npr":"https://www.npr.org/podcasts/464615685/mind-shift-podcast","stitcher":"https://www.stitcher.com/podcast/kqed/stories-teachers-share","spotify":"https://open.spotify.com/show/0MxSpNYZKNprFLCl7eEtyx"}},"morning-edition":{"id":"morning-edition","title":"Morning Edition","info":"\u003cem>Morning Edition\u003c/em> takes listeners around the country and the world with multi-faceted stories and commentaries every weekday. 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On Our Watch brings listeners into the rooms where officers are questioned and witnesses are interrogated to find out who this system is really protecting. 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