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Shift in Treatment","publishDate":1536615990,"format":"standard","headTitle":"KQED Future of You | KQED Science","labelTerm":{},"content":"\u003cp>Dr. Leslie Norins is willing to hand over $1 million of his own money to anyone who can clarify something: Is Alzheimer's disease, the most common form of dementia worldwide, caused by a germ?[contextly_sidebar id=\"MVU0oAlLJAOY5cRLFm8SgRXzH5ufmBIa\"]\u003c/p>\n\u003cp>By \"germ\" he means microbes like bacteria, viruses, fungi and parasites. In other words, Norins, a physician turned publisher, wants to know if Alzheimer's is infectious.\u003c/p>\n\u003cp>It's an idea that just a few years ago would've seemed to many an easy way to drain your research budget on bunk science. Money has poured into Alzheimer's research for years, but until very recently not much of it went toward investigating infection in causing dementia.\u003c/p>\n\u003cp>But this \"germ theory\" of Alzheimer's, as Norins calls it, has been fermenting in the literature for decades. Even early 20th century Czech physician Oskar Fischer — who, along with his German contemporary Dr. Alois Alzheimer, was integral in first describing the condition — noted a possible connection between the newly identified dementia and tuberculosis.\u003c/p>\n\u003cp>If the germ theory gets traction, even in some Alzheimer's patients, it could trigger a seismic shift in how doctors understand and treat the disease.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>For instance, would we see a day when dementia is prevented with a vaccine, or treated with antibiotics and antiviral medications? Norins thinks it's worth looking into.\u003c/p>\n\u003cp>Norins received his medical degree from Duke in the early 1960s, and after a stint at the Centers for Disease Control and Prevention he fell into a lucrative career in medical publishing. He eventually settled in an admittedly aged community in Naples, Fla., where he took an interest in dementia and began reading up on the condition.[contextly_sidebar id=\"Xrb4XR0KXYySlI7ldjHh45GWXuqxKcIS\"]\u003c/p>\n\u003cp>After scouring the medical literature he noticed a pattern.\u003c/p>\n\u003cp>\"It appeared that many of the reported characteristics of Alzheimer's disease were compatible with an infectious process,\" Norins tells NPR. \"I thought for sure this must have already been investigated, because \u003ca href=\"http://act.alz.org/site/DocServer/2015_Appropriations_Fact_Sheet__FY16_.pdf?docID=3641\" target=\"_blank\" rel=\"noopener\">millions and millions of dollars\u003c/a> have been spent on Alzheimer's research.\"\u003c/p>\n\u003cp>But aside from scattered interest through the decades, this wasn't the case.\u003c/p>\n\u003cp>In 2017, Norins launched \u003ca href=\"https://alzgerm.org/about/\" target=\"_blank\" rel=\"noopener\">Alzheimer's Germ Quest Inc.\u003c/a>, a public benefit corporation he hopes will drive interest into the germ theory of Alzheimer's, and through which his prize will be distributed. A white paper he penned for the site reads: \"From a two-year review of the scientific literature, I believe it's now clear that just one germ — identity not yet specified, and possibly not yet discovered — causes most AD. I'm calling it the 'Alzheimer's Germ.' \"\u003c/p>\n\u003cp>Norins is quick to cite sources and studies supporting his claim, among them a 2010 study published in the \u003cem>Journal of Neurosurgery\u003c/em> showing that \u003ca href=\"http://thejns.org/doi/pdf/10.3171/2010.1.JNS091740\" target=\"_blank\" rel=\"noopener\">neurosurgeons die from Alzheimer's at a seven-fold higher rate\u003c/a> than they do from other disorders.\u003c/p>\n\u003cp>Another study from that same year, published in The \u003cem>Journal of the American Geriatric Society,\u003c/em> found that people whose \u003ca href=\"https://www.ncbi.nlm.nih.gov/pubmed/20722820/\" target=\"_blank\" rel=\"noopener\">spouses have dementia are at a six-times greater risk\u003c/a> for the condition themselves.\u003c/p>\n\u003cp>Contagion does come to mind. And Norins isn't alone in his thinking.\u003c/p>\n\u003cp>In 2016, 32 researchers from universities around the world signed an editorial in the \u003cem>Journal of Alzheimer's Disease\u003c/em> calling for \"further research on the role of infectious agents in [Alzheimer's] causation.\" Based on much of the same evidence Norins encountered, the authors concluded that clinical trials with antimicrobial drugs in Alzheimer's are now justified.[contextly_sidebar id=\"TlULmPwfIfLNT30W6fAdCGOQeBCymn7e\"]\u003c/p>\n\u003cp>NPR reported on an intriguing \u003ca href=\"https://www.npr.org/sections/health-shots/2018/06/21/621908340/researchers-find-herpes-viruses-in-brains-marked-by-alzheimers-disease\" target=\"_blank\" rel=\"noopener\">study\u003c/a> published in \u003cem>Neuron\u003c/em> in June that suggested that viral infection can influence the progression of Alzheimer's. Led by Mount Sinai genetics professor Joel Dudley, the work was intended to compare the genomes of healthy brain tissue with that affected by dementia.\u003c/p>\n\u003cp>But something kept getting in the way: herpes.\u003c/p>\n\u003cp>Dudley's team noticed an unexpectedly high level of viral DNA from two human herpes viruses, HHV-6 and HHV-7. The viruses are common and cause a rash called roseola in young children (not the sexually transmitted disease caused by other strains).\u003c/p>\n\u003cp>Some viruses have the ability to lie dormant in our neurons for decades by incorporating their genomes into our own. The classic example is chickenpox: A childhood viral infection resolves and lurks silently, returning years later as \u003ca href=\"https://www.cdc.gov/shingles/about/symptoms.html\" target=\"_blank\" rel=\"noopener\">shingles\u003c/a>, an excruciating rash. Like it or not, nearly all of us are chimeras with viral DNA speckling our genomes.\u003c/p>\n\u003cp>But having the herpes viruses alone doesn't mean inevitable brain decline. After all, up to 75 percent of us may \u003ca href=\"https://www.ncbi.nlm.nih.gov/pubmed/11285567\" target=\"_blank\" rel=\"noopener\">harbor HHV-6\u003c/a> .\u003c/p>\n\u003cp>But Dudley also noticed that herpes appeared to interact with human genes known to increase Alzheimer's risk. Perhaps, he says, there is some toxic combination of genetic and infectious influence that results in the disease; a combination that sparks what some feel is the main contributor to the disease, an overactive immune system.\u003c/p>\n\u003cp>The hallmark pathology of Alzheimer's is accumulation of a protein called amyloid in the brain. Many researchers have assumed these aggregates, or plaques, are simply a byproduct of some other process at the core of the disease. Other scientists posit that the protein itself contributes to the condition in some way.\u003c/p>\n\u003cp>The theory that amyloid is the root cause of Alzheimer's is losing steam. But the protein may still contribute to the disease, even if it winds up being deemed infectious.[contextly_sidebar id=\"reNe9dG45Jm18II65oxyuE0ETmculfjN\"]\u003c/p>\n\u003cp>Work by Harvard neuroscientist Rudolph Tanzi suggests it might be a bit of both. Along with colleague Robert Moir, Tanzi has shown that amyloid is lethal to viruses and bacteria in the test tube, and also in mice. He now believes the protein is part of our ancient immune system that like antibodies, ramps up its activity to help fend off unwanted bugs.\u003c/p>\n\u003cp>So does that mean that the microbe is the cause of Alzheimer's, and amyloid a harmless reaction to it? According to Tanzi it's not that simple.\u003c/p>\n\u003cp>Tanzi believes that in many cases of Alzheimer's, microbes are probably the initial seed that sets off a toxic tumble of molecular dominoes. Early in the disease amyloid protein builds up to fight infection, yet too much of the protein begins to impair function of neurons in the brain. The excess amyloid then causes another protein, called tau, to form tangles, which further harm brain cells.\u003c/p>\n\u003cp>But as Tanzi explains, the ultimate neurological insult in Alzheimer's is the body's reaction to this neurotoxic mess. All the excess protein revs up the immune system, causing inflammation — and it's this inflammation that does the most damage to the Alzheimer's-afflicted brain.\u003c/p>\n\u003cp>So what does this say about the future of treatment? Possibly a lot. Tanzi envisions a day when people are screened at, say, 50 years old. \"If their brains are riddled with too much amyloid,\" he says, \"we knock it down a bit with antiviral medications. It's just like how you are prescribed preventative drugs if your cholesterol is too high.\"\u003c/p>\n\u003cp>Tanzi feels that microbes are just one possible seed for the complex pathology behind Alzheimer's. Genetics may also play a role, as certain genes produce a type of amyloid more prone to clumping up. He also feels environmental factors like pollution might contribute.\u003c/p>\n\u003cp>Dr. James Burke, professor of medicine and psychiatry at Duke University's Alzheimer's Disease Research Center, isn't willing to abandon the amyloid theory altogether, but agrees it's time for the field to move on. \"There may be many roads to developing Alzheimer's disease and it would be shortsighted to focus just on amyloid and tau,\" he says. \"A million-dollar prize is attention- getting, but the reward for identifying a treatable target to delay or prevent Alzheimer's disease is invaluable.\"[contextly_sidebar id=\"VDtvU3haNd1M74SuCUvVZuAz4hFEV5iO\"]\u003c/p>\n\u003cp>Any treatment that disrupts the cascade leading to amyloid, tau and inflammation could theoretically benefit an at-risk brain. The vast majority of Alzheimer's treatment trials have failed, including many targeting amyloid. But it could be that the patients included were too far along in their disease to reap any therapeutic benefit.\u003c/p>\n\u003cp>If a microbe is responsible for all or some cases of Alzheimer's, perhaps future treatments or preventive approaches will prevent toxin protein buildup in the first place. Both Tanzi and Norins believe Alzheimer's vaccines against viruses like herpes might one day become common practice.\u003c/p>\n\u003cp>In July of this year, in collaboration with Norins, the Infectious Diseases Society of America announced that they plan to offer two $50,000 grants supporting research into a microbial association with Alzheimer's. According to Norins, this is the first acknowledgement by a leading infectious disease group that Alzheimer's may be microbial in nature – or at least that it's worth exploring.\u003c/p>\n\u003cp>\"The important thing is not the amount of the money, which is a pittance compared with the $2 billion NIH spends on amyloid and tau research,\" says Norins, \"but rather the respectability and more mainstream status the grants confer on investigating of the infectious possibility. Remember when we thought ulcers were caused by stress?\"\u003c/p>\n\u003cp>Ulcers, we now know, are \u003ca href=\"https://www.nobelprize.org/prizes/medicine/2005/press-release/\" target=\"_blank\" rel=\"noopener\">caused by a germ\u003c/a>.\u003c/p>\n\u003cp>[ad floatright]\u003c/p>\n\u003cp>\u003cem>Bret Stetka is a writer based in New York and an editorial director at \u003c/em>\u003ca href=\"http://www.medscape.com/public/bios/bio-bretstetka\">Medscape\u003c/a>.\u003cem> His work has appeared in \u003c/em>Wired, Scientific American\u003cem> and on The Atlantic.com. He graduated from the University of Virginia School of Medicine. He's also on Twitter: \u003c/em>\u003ca href=\"https://twitter.com/BretStetka\" target=\"_blank\" rel=\"noopener\">@BretStetka\u003c/a>.\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2018 NPR. To see more, visit http://www.npr.org/.\u003cimg src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=Infectious+Theory+Of+Alzheimer%27s+Disease+Draws+Fresh+Interest&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n","blocks":[],"excerpt":"Money has poured into Alzheimer's research, but until very recently not much of it went toward investigating infection in causing dementia. A million dollar prize may lead more scientists to try.","status":"publish","parent":0,"modified":1536615990,"stats":{"hasAudio":false,"hasVideo":false,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":38,"wordCount":1587},"headData":{"title":"'Germ Theory' of Alzheimer's May Trigger a Seismic Shift in Treatment | KQED","description":"Money has poured into Alzheimer's research, but until very recently not much of it went toward investigating infection in causing dementia. A million dollar prize may lead more scientists to try.","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":""},"disqusIdentifier":"444402 https://ww2.kqed.org/futureofyou/?p=444402","disqusUrl":"https://ww2.kqed.org/futureofyou/2018/09/10/germ-theory-of-alzheimers-may-trigger-a-seismic-shift-in-treatment/","disqusTitle":"'Germ Theory' of Alzheimer's May Trigger a Seismic Shift in Treatment","source":"Hope/Hype","nprByline":"Bret Stetka, NPR","nprImageAgency":"Ariel Davis for NPR","nprStoryId":"645629133","nprApiLink":"http://api.npr.org/query?id=645629133&apiKey=MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004","nprHtmlLink":"https://www.npr.org/sections/health-shots/2018/09/09/645629133/infectious-theory-of-alzheimers-disease-draws-fresh-interest?ft=nprml&f=645629133","nprRetrievedStory":"1","nprPubDate":"Mon, 10 Sep 2018 11:20:00 -0400","nprStoryDate":"Sun, 09 Sep 2018 07:30:20 -0400","nprLastModifiedDate":"Mon, 10 Sep 2018 11:20:41 -0400","path":"/futureofyou/444402/germ-theory-of-alzheimers-may-trigger-a-seismic-shift-in-treatment","audioTrackLength":null,"parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003cp>Dr. Leslie Norins is willing to hand over $1 million of his own money to anyone who can clarify something: Is Alzheimer's disease, the most common form of dementia worldwide, caused by a germ?\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>By \"germ\" he means microbes like bacteria, viruses, fungi and parasites. In other words, Norins, a physician turned publisher, wants to know if Alzheimer's is infectious.\u003c/p>\n\u003cp>It's an idea that just a few years ago would've seemed to many an easy way to drain your research budget on bunk science. Money has poured into Alzheimer's research for years, but until very recently not much of it went toward investigating infection in causing dementia.\u003c/p>\n\u003cp>But this \"germ theory\" of Alzheimer's, as Norins calls it, has been fermenting in the literature for decades. Even early 20th century Czech physician Oskar Fischer — who, along with his German contemporary Dr. Alois Alzheimer, was integral in first describing the condition — noted a possible connection between the newly identified dementia and tuberculosis.\u003c/p>\n\u003cp>If the germ theory gets traction, even in some Alzheimer's patients, it could trigger a seismic shift in how doctors understand and treat the disease.\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 instance, would we see a day when dementia is prevented with a vaccine, or treated with antibiotics and antiviral medications? Norins thinks it's worth looking into.\u003c/p>\n\u003cp>Norins received his medical degree from Duke in the early 1960s, and after a stint at the Centers for Disease Control and Prevention he fell into a lucrative career in medical publishing. He eventually settled in an admittedly aged community in Naples, Fla., where he took an interest in dementia and began reading up on the condition.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>After scouring the medical literature he noticed a pattern.\u003c/p>\n\u003cp>\"It appeared that many of the reported characteristics of Alzheimer's disease were compatible with an infectious process,\" Norins tells NPR. \"I thought for sure this must have already been investigated, because \u003ca href=\"http://act.alz.org/site/DocServer/2015_Appropriations_Fact_Sheet__FY16_.pdf?docID=3641\" target=\"_blank\" rel=\"noopener\">millions and millions of dollars\u003c/a> have been spent on Alzheimer's research.\"\u003c/p>\n\u003cp>But aside from scattered interest through the decades, this wasn't the case.\u003c/p>\n\u003cp>In 2017, Norins launched \u003ca href=\"https://alzgerm.org/about/\" target=\"_blank\" rel=\"noopener\">Alzheimer's Germ Quest Inc.\u003c/a>, a public benefit corporation he hopes will drive interest into the germ theory of Alzheimer's, and through which his prize will be distributed. A white paper he penned for the site reads: \"From a two-year review of the scientific literature, I believe it's now clear that just one germ — identity not yet specified, and possibly not yet discovered — causes most AD. I'm calling it the 'Alzheimer's Germ.' \"\u003c/p>\n\u003cp>Norins is quick to cite sources and studies supporting his claim, among them a 2010 study published in the \u003cem>Journal of Neurosurgery\u003c/em> showing that \u003ca href=\"http://thejns.org/doi/pdf/10.3171/2010.1.JNS091740\" target=\"_blank\" rel=\"noopener\">neurosurgeons die from Alzheimer's at a seven-fold higher rate\u003c/a> than they do from other disorders.\u003c/p>\n\u003cp>Another study from that same year, published in The \u003cem>Journal of the American Geriatric Society,\u003c/em> found that people whose \u003ca href=\"https://www.ncbi.nlm.nih.gov/pubmed/20722820/\" target=\"_blank\" rel=\"noopener\">spouses have dementia are at a six-times greater risk\u003c/a> for the condition themselves.\u003c/p>\n\u003cp>Contagion does come to mind. And Norins isn't alone in his thinking.\u003c/p>\n\u003cp>In 2016, 32 researchers from universities around the world signed an editorial in the \u003cem>Journal of Alzheimer's Disease\u003c/em> calling for \"further research on the role of infectious agents in [Alzheimer's] causation.\" Based on much of the same evidence Norins encountered, the authors concluded that clinical trials with antimicrobial drugs in Alzheimer's are now justified.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>NPR reported on an intriguing \u003ca href=\"https://www.npr.org/sections/health-shots/2018/06/21/621908340/researchers-find-herpes-viruses-in-brains-marked-by-alzheimers-disease\" target=\"_blank\" rel=\"noopener\">study\u003c/a> published in \u003cem>Neuron\u003c/em> in June that suggested that viral infection can influence the progression of Alzheimer's. Led by Mount Sinai genetics professor Joel Dudley, the work was intended to compare the genomes of healthy brain tissue with that affected by dementia.\u003c/p>\n\u003cp>But something kept getting in the way: herpes.\u003c/p>\n\u003cp>Dudley's team noticed an unexpectedly high level of viral DNA from two human herpes viruses, HHV-6 and HHV-7. The viruses are common and cause a rash called roseola in young children (not the sexually transmitted disease caused by other strains).\u003c/p>\n\u003cp>Some viruses have the ability to lie dormant in our neurons for decades by incorporating their genomes into our own. The classic example is chickenpox: A childhood viral infection resolves and lurks silently, returning years later as \u003ca href=\"https://www.cdc.gov/shingles/about/symptoms.html\" target=\"_blank\" rel=\"noopener\">shingles\u003c/a>, an excruciating rash. Like it or not, nearly all of us are chimeras with viral DNA speckling our genomes.\u003c/p>\n\u003cp>But having the herpes viruses alone doesn't mean inevitable brain decline. After all, up to 75 percent of us may \u003ca href=\"https://www.ncbi.nlm.nih.gov/pubmed/11285567\" target=\"_blank\" rel=\"noopener\">harbor HHV-6\u003c/a> .\u003c/p>\n\u003cp>But Dudley also noticed that herpes appeared to interact with human genes known to increase Alzheimer's risk. Perhaps, he says, there is some toxic combination of genetic and infectious influence that results in the disease; a combination that sparks what some feel is the main contributor to the disease, an overactive immune system.\u003c/p>\n\u003cp>The hallmark pathology of Alzheimer's is accumulation of a protein called amyloid in the brain. Many researchers have assumed these aggregates, or plaques, are simply a byproduct of some other process at the core of the disease. Other scientists posit that the protein itself contributes to the condition in some way.\u003c/p>\n\u003cp>The theory that amyloid is the root cause of Alzheimer's is losing steam. But the protein may still contribute to the disease, even if it winds up being deemed infectious.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>Work by Harvard neuroscientist Rudolph Tanzi suggests it might be a bit of both. Along with colleague Robert Moir, Tanzi has shown that amyloid is lethal to viruses and bacteria in the test tube, and also in mice. He now believes the protein is part of our ancient immune system that like antibodies, ramps up its activity to help fend off unwanted bugs.\u003c/p>\n\u003cp>So does that mean that the microbe is the cause of Alzheimer's, and amyloid a harmless reaction to it? According to Tanzi it's not that simple.\u003c/p>\n\u003cp>Tanzi believes that in many cases of Alzheimer's, microbes are probably the initial seed that sets off a toxic tumble of molecular dominoes. Early in the disease amyloid protein builds up to fight infection, yet too much of the protein begins to impair function of neurons in the brain. The excess amyloid then causes another protein, called tau, to form tangles, which further harm brain cells.\u003c/p>\n\u003cp>But as Tanzi explains, the ultimate neurological insult in Alzheimer's is the body's reaction to this neurotoxic mess. All the excess protein revs up the immune system, causing inflammation — and it's this inflammation that does the most damage to the Alzheimer's-afflicted brain.\u003c/p>\n\u003cp>So what does this say about the future of treatment? Possibly a lot. Tanzi envisions a day when people are screened at, say, 50 years old. \"If their brains are riddled with too much amyloid,\" he says, \"we knock it down a bit with antiviral medications. It's just like how you are prescribed preventative drugs if your cholesterol is too high.\"\u003c/p>\n\u003cp>Tanzi feels that microbes are just one possible seed for the complex pathology behind Alzheimer's. Genetics may also play a role, as certain genes produce a type of amyloid more prone to clumping up. He also feels environmental factors like pollution might contribute.\u003c/p>\n\u003cp>Dr. James Burke, professor of medicine and psychiatry at Duke University's Alzheimer's Disease Research Center, isn't willing to abandon the amyloid theory altogether, but agrees it's time for the field to move on. \"There may be many roads to developing Alzheimer's disease and it would be shortsighted to focus just on amyloid and tau,\" he says. \"A million-dollar prize is attention- getting, but the reward for identifying a treatable target to delay or prevent Alzheimer's disease is invaluable.\"\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>Any treatment that disrupts the cascade leading to amyloid, tau and inflammation could theoretically benefit an at-risk brain. The vast majority of Alzheimer's treatment trials have failed, including many targeting amyloid. But it could be that the patients included were too far along in their disease to reap any therapeutic benefit.\u003c/p>\n\u003cp>If a microbe is responsible for all or some cases of Alzheimer's, perhaps future treatments or preventive approaches will prevent toxin protein buildup in the first place. Both Tanzi and Norins believe Alzheimer's vaccines against viruses like herpes might one day become common practice.\u003c/p>\n\u003cp>In July of this year, in collaboration with Norins, the Infectious Diseases Society of America announced that they plan to offer two $50,000 grants supporting research into a microbial association with Alzheimer's. According to Norins, this is the first acknowledgement by a leading infectious disease group that Alzheimer's may be microbial in nature – or at least that it's worth exploring.\u003c/p>\n\u003cp>\"The important thing is not the amount of the money, which is a pittance compared with the $2 billion NIH spends on amyloid and tau research,\" says Norins, \"but rather the respectability and more mainstream status the grants confer on investigating of the infectious possibility. Remember when we thought ulcers were caused by stress?\"\u003c/p>\n\u003cp>Ulcers, we now know, are \u003ca href=\"https://www.nobelprize.org/prizes/medicine/2005/press-release/\" target=\"_blank\" rel=\"noopener\">caused by a germ\u003c/a>.\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>\u003cem>Bret Stetka is a writer based in New York and an editorial director at \u003c/em>\u003ca href=\"http://www.medscape.com/public/bios/bio-bretstetka\">Medscape\u003c/a>.\u003cem> His work has appeared in \u003c/em>Wired, Scientific American\u003cem> and on The Atlantic.com. He graduated from the University of Virginia School of Medicine. He's also on Twitter: \u003c/em>\u003ca href=\"https://twitter.com/BretStetka\" target=\"_blank\" rel=\"noopener\">@BretStetka\u003c/a>.\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2018 NPR. To see more, visit http://www.npr.org/.\u003cimg src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=Infectious+Theory+Of+Alzheimer%27s+Disease+Draws+Fresh+Interest&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/futureofyou/444402/germ-theory-of-alzheimers-may-trigger-a-seismic-shift-in-treatment","authors":["byline_futureofyou_444402"],"categories":["futureofyou_1062","futureofyou_1","futureofyou_73"],"tags":["futureofyou_999","futureofyou_1023","futureofyou_61","futureofyou_1056"],"collections":["futureofyou_1093","futureofyou_1097"],"featImg":"futureofyou_444403","label":"source_futureofyou_444402"},"futureofyou_444207":{"type":"posts","id":"futureofyou_444207","meta":{"index":"posts_1591205157","site":"futureofyou","id":"444207","score":null,"sort":[1536181218000]},"guestAuthors":[],"slug":"have-the-drug-companies-given-up-on-trying-to-cure-alzheimers-sure-looks-like-it","title":"Looks Like Pharma Has Given Up on Alzheimer's Cure","publishDate":1536181218,"format":"audio","headTitle":"KQED Future of You | KQED Science","labelTerm":{"site":"futureofyou"},"content":"\u003cp>Alzheimer's is currently the sixth leading cause of death in the U.S., according to the Alzheimer's Association. About 5.7 million Americans currently suffer from the disease, with around a half-million new cases diagnosed every year. Fourteen million Americans are projected to have Alzheimer's by 2050.\u003c/p>\n\u003caside class=\"pullquote alignright\">A review of 112 experimental Alzheimer's drugs in clinical trials shows only one aimed at slowing the course of the disease in patients with moderate to severe forms of the disease.\u003c/aside>\n\u003cp>That is an enormous toll taken on patients and families. But unfortunately, the outlook on finding a cure is equally grim, as STAT reporter Sharon Begley recently \u003ca href=\"https://www.statnews.com/2018/08/15/alzheimers-patients-drug-development-outrage/\" target=\"_blank\" rel=\"noopener\">reported\u003c/a>. After more than 20 years of failure to reverse or slow the disease by targeting amyloid plaques in the brain, Begley writes, there are now literally \u003cem>no experimental drugs in late-stage clinical trials\u003c/em> to treat moderate to severe Alzheimer's, the latter of which is characterized by extreme confusion requiring round-the-clock care patient care.\u003c/p>\n\u003cp>Begley spoke about her reporting with KQED's Brian Watt on Friday. The following is a transcript of the interview, edited for length and clarity.\u003c/p>\n\u003cp>\u003cstrong>On the lack of progress in Alzheimer's drug development\u003c/strong>\u003c/p>\n\u003cp>The last drug for Alzheimer's was approved in 2003. So 15 years and we have had nothing.\u003c/p>\n\u003caside class=\"pullquote alignright\">'The drug companies have spent and lost billions of dollars trying to find something that works for Alzheimer's patients. And they're giving up.'\u003c/aside>\n\u003cp>I talked about the situation with patient advocates and neurologists and people in the lab desperately trying to come up with something to help people. One expert used a term that made me just sit up and practically gasp. He called it \"therapeutic nihilism.\" And by that he meant the disease has proved so challenging to scientists that people have almost given up.\u003c/p>\n\u003cp>In studies, drug after drug has failed. The drug companies have spent and lost billions of dollars trying to find something that works for Alzheimer's patients. And they're giving up.\u003c/p>\n\u003cp>\u003cstrong>On the contrast between activism around HIV/AIDS and the lack of advocacy around Alzheimer's \u003c/strong>\u003c/p>\n\u003cp>The amount of attention, drug development, et cetera for HIV/AIDS have been hugely impressive. And that's why I contrasted it with Alzheimer's, wondering: Where is the outrage over the lack of progress?\u003c/p>\n\u003cp>And there you have things like the age of patients. With HIV/AIDS, the tragic toll was, at least initially, on men in their prime. For Alzheimer's, primarily affecting people 65 and older, there's at least some sentiment that they've had a good life, that's the way it goes.\u003c/p>\n\u003cp>\u003cstrong>On the lack of drugs being tested for moderate to severe Alzheimer's\u003c/strong>\u003c/p>\n\u003cp>There's what's called a pipeline analysis done every year by researchers at the Cleveland Clinic. They look at all the experimental compounds being tested in patients, and they ask, \"What kind of patients are they being tested in?\"\u003c/p>\n\u003caside class=\"pullquote alignright\">'There are 5.5 million people and growing that already have the disease. So what we're essentially saying to them is that it's really unfortunate but we have nothing that will help you.'\u003c/aside>\n\u003cp>They broke it down into people who do not have Alzheimer's but have some of the risk factors, and people who have mild, moderate or severe Alzheimer's. What really made me sit up was that the number of drugs being tested to see whether they can stop or even reverse the actual course of the disease in people with moderate or severe Alzheimer's is 1 out of 112.\u003c/p>\n\u003cp>We all hope they can stop Alzheimer's at earlier stages. We all know somebody who has Alzheimer's, and when they first get it if you could look at that person and say, wow, you don't actually have a diagnosis yet, but you're on the cusp, so here's a drug that will help you from getting Alzheimer's ... .\u003c/p>\n\u003cp>But there are 5.5 million people and growing that already have the disease. So what we're essentially saying to them is that it's really unfortunate but we have nothing that will help you. And if there's nothing in the pipeline for people with moderate to severe Alzheimer's, that means there will be nothing for anybody who is diagnosed in 2018, in 2019, and probably for the next 10 years.\u003c/p>\n\u003cp>[ad fullwidth]\u003cbr>\n\u003cstrong>On the response from patient advocates\u003c/strong>\u003c/p>\n\u003cp>I thought I would call them and give them a softball. Let them say, \"This is untenable. We know it's expensive, but these drug companies just really have to step up.\"\u003c/p>\n\u003caside class=\"pullquote alignright\">'I will simply note without comment that the patient advocacy groups get buckets of money from drug developers.'\u003c/aside>\n\u003cp>Instead they told me things like, \"Boy, it's really hard to develop drugs. It's understandable that the drug companies have pulled back.\"\u003c/p>\n\u003cp>I will simply note without comment that the patient advocacy groups get buckets of money from drug developers.\u003c/p>\n\u003cp>The market for preventing the development of Alzheimer's is much greater than for even the people who have it. If you develop something to prevent Alzheimer's that you can give to tens of millions of healthy people, that would be a huge profit boost for your company.\u003c/p>\n\u003cp>So I think it would be naïve of anyone to say that there are no financial considerations here.\u003c/p>\n\u003cp>\u003c/p>\n","blocks":[],"excerpt":"Despite the growing millions of people who suffer from Alzheimer's disease, 20-plus years of failure appears to have caused drug companies to abandon the search for a cure in favor of developing drugs for prevention.","status":"publish","parent":0,"modified":1536249837,"stats":{"hasAudio":false,"hasVideo":false,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":22,"wordCount":915},"headData":{"title":"Looks Like Pharma Has Given Up on Alzheimer's Cure | KQED","description":"Despite the growing millions of people who suffer from Alzheimer's disease, 20-plus years of failure appears to have caused drug companies to abandon the search for a cure in favor of developing drugs for prevention.","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":""},"disqusIdentifier":"444207 https://ww2.kqed.org/futureofyou/?p=444207","disqusUrl":"https://ww2.kqed.org/futureofyou/2018/09/05/have-the-drug-companies-given-up-on-trying-to-cure-alzheimers-sure-looks-like-it/","disqusTitle":"Looks Like Pharma Has Given Up on Alzheimer's Cure","audioUrl":"https://www.kqed.org/.stream/anon/radio/science/2018/09/WattAbandonedAlzheimers.mp3","nprByline":"KQED Future of You","audioTrackLength":217,"path":"/futureofyou/444207/have-the-drug-companies-given-up-on-trying-to-cure-alzheimers-sure-looks-like-it","parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003cp>Alzheimer's is currently the sixth leading cause of death in the U.S., according to the Alzheimer's Association. About 5.7 million Americans currently suffer from the disease, with around a half-million new cases diagnosed every year. Fourteen million Americans are projected to have Alzheimer's by 2050.\u003c/p>\n\u003caside class=\"pullquote alignright\">A review of 112 experimental Alzheimer's drugs in clinical trials shows only one aimed at slowing the course of the disease in patients with moderate to severe forms of the disease.\u003c/aside>\n\u003cp>That is an enormous toll taken on patients and families. But unfortunately, the outlook on finding a cure is equally grim, as STAT reporter Sharon Begley recently \u003ca href=\"https://www.statnews.com/2018/08/15/alzheimers-patients-drug-development-outrage/\" target=\"_blank\" rel=\"noopener\">reported\u003c/a>. After more than 20 years of failure to reverse or slow the disease by targeting amyloid plaques in the brain, Begley writes, there are now literally \u003cem>no experimental drugs in late-stage clinical trials\u003c/em> to treat moderate to severe Alzheimer's, the latter of which is characterized by extreme confusion requiring round-the-clock care patient care.\u003c/p>\n\u003cp>Begley spoke about her reporting with KQED's Brian Watt on Friday. The following is a transcript of the interview, edited for length and clarity.\u003c/p>\n\u003cp>\u003cstrong>On the lack of progress in Alzheimer's drug development\u003c/strong>\u003c/p>\n\u003cp>The last drug for Alzheimer's was approved in 2003. So 15 years and we have had nothing.\u003c/p>\n\u003caside class=\"pullquote alignright\">'The drug companies have spent and lost billions of dollars trying to find something that works for Alzheimer's patients. And they're giving up.'\u003c/aside>\n\u003cp>I talked about the situation with patient advocates and neurologists and people in the lab desperately trying to come up with something to help people. One expert used a term that made me just sit up and practically gasp. He called it \"therapeutic nihilism.\" And by that he meant the disease has proved so challenging to scientists that people have almost given up.\u003c/p>\n\u003cp>In studies, drug after drug has failed. The drug companies have spent and lost billions of dollars trying to find something that works for Alzheimer's patients. And they're giving up.\u003c/p>\n\u003cp>\u003cstrong>On the contrast between activism around HIV/AIDS and the lack of advocacy around Alzheimer's \u003c/strong>\u003c/p>\n\u003cp>The amount of attention, drug development, et cetera for HIV/AIDS have been hugely impressive. And that's why I contrasted it with Alzheimer's, wondering: Where is the outrage over the lack of progress?\u003c/p>\n\u003cp>And there you have things like the age of patients. With HIV/AIDS, the tragic toll was, at least initially, on men in their prime. For Alzheimer's, primarily affecting people 65 and older, there's at least some sentiment that they've had a good life, that's the way it goes.\u003c/p>\n\u003cp>\u003cstrong>On the lack of drugs being tested for moderate to severe Alzheimer's\u003c/strong>\u003c/p>\n\u003cp>There's what's called a pipeline analysis done every year by researchers at the Cleveland Clinic. They look at all the experimental compounds being tested in patients, and they ask, \"What kind of patients are they being tested in?\"\u003c/p>\n\u003caside class=\"pullquote alignright\">'There are 5.5 million people and growing that already have the disease. So what we're essentially saying to them is that it's really unfortunate but we have nothing that will help you.'\u003c/aside>\n\u003cp>They broke it down into people who do not have Alzheimer's but have some of the risk factors, and people who have mild, moderate or severe Alzheimer's. What really made me sit up was that the number of drugs being tested to see whether they can stop or even reverse the actual course of the disease in people with moderate or severe Alzheimer's is 1 out of 112.\u003c/p>\n\u003cp>We all hope they can stop Alzheimer's at earlier stages. We all know somebody who has Alzheimer's, and when they first get it if you could look at that person and say, wow, you don't actually have a diagnosis yet, but you're on the cusp, so here's a drug that will help you from getting Alzheimer's ... .\u003c/p>\n\u003cp>But there are 5.5 million people and growing that already have the disease. So what we're essentially saying to them is that it's really unfortunate but we have nothing that will help you. And if there's nothing in the pipeline for people with moderate to severe Alzheimer's, that means there will be nothing for anybody who is diagnosed in 2018, in 2019, and probably for the next 10 years.\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>\u003cbr>\n\u003cstrong>On the response from patient advocates\u003c/strong>\u003c/p>\n\u003cp>I thought I would call them and give them a softball. Let them say, \"This is untenable. We know it's expensive, but these drug companies just really have to step up.\"\u003c/p>\n\u003caside class=\"pullquote alignright\">'I will simply note without comment that the patient advocacy groups get buckets of money from drug developers.'\u003c/aside>\n\u003cp>Instead they told me things like, \"Boy, it's really hard to develop drugs. It's understandable that the drug companies have pulled back.\"\u003c/p>\n\u003cp>I will simply note without comment that the patient advocacy groups get buckets of money from drug developers.\u003c/p>\n\u003cp>The market for preventing the development of Alzheimer's is much greater than for even the people who have it. If you develop something to prevent Alzheimer's that you can give to tens of millions of healthy people, that would be a huge profit boost for your company.\u003c/p>\n\u003cp>So I think it would be naïve of anyone to say that there are no financial considerations here.\u003c/p>\n\u003cp>\u003c/p>\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/futureofyou/444207/have-the-drug-companies-given-up-on-trying-to-cure-alzheimers-sure-looks-like-it","authors":["byline_futureofyou_444207"],"categories":["futureofyou_1062","futureofyou_1","futureofyou_73","futureofyou_1575"],"tags":["futureofyou_999","futureofyou_1275","futureofyou_80"],"featImg":"futureofyou_444347","label":"futureofyou"},"futureofyou_443668":{"type":"posts","id":"futureofyou_443668","meta":{"index":"posts_1591205157","site":"futureofyou","id":"443668","score":null,"sort":[1533070821000]},"guestAuthors":[],"slug":"alzheimers-study-sparks-new-debate-over-amyloid-hypothesis","title":"Alzheimer’s Study Sparks New Debate Over Amyloid Hypothesis","publishDate":1533070821,"format":"standard","headTitle":"KQED Future of You | KQED Science","labelTerm":{},"content":"\u003cp>In the long-running debate over just what causes Alzheimer’s disease, one side looks to have scored a victory with \u003ca href=\"https://www.statnews.com/2018/07/25/experimental-alzheimers-drug-biogen-eisai/\" target=\"_blank\" rel=\"noopener\">new results with an in-development drug\u003c/a>. But there’s enough variation in the data to ensure that the squabbling factions of Alzheimer’s will have plenty to fight about.[contextly_sidebar id=\"A04l79ZF49Fepp9ayXq47IfI7cWrtD3j\"]\u003c/p>\n\u003cp>At issue is the so-called amyloid hypothesis, a decades-old theory claiming that Alzheimer’s gradual degradation of the brain is caused by the accumulation of sticky plaques. And the new drug is BAN2401, designed by Biogen and Eisai to prevent those amyloid plaques from clustering and attack the clumps that already have.\u003c/p>\n\u003cp>In data presented last week, one group of patients receiving BAN2401 saw their amyloid levels plummet, a result that was tied to a significant reduction in cognitive decline compared with placebo.\u003c/p>\n\u003cp>To the amyloid-inclined, like Dr. Howard Fillit of the Alzheimer’s Drug Discovery Foundation, that marks a clear affirmation of the linkage between plaques and mental fortitude.\u003c/p>\n\u003cp>“I mean if you asked me five or 10 years ago if we’re going to have a drug that can remove the plaques from the brain, I would have thought this was space technology,” Fillit said. “And there was definitely a signal, in my opinion, on clinical outcomes, which is what we’ve all been looking for.”\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>But to skeptics, the trial was laden with confounding details that make it impossible to draw conclusions.\u003c/p>\n\u003cp>“These results are a mess,” wrote Baird biotech analyst Brian Skorney. “Not so much that they indicate an outright failure of the [amyloid] hypothesis, but they don’t really say anything informative at all.”\u003c/p>\n\u003cp>In the trial, every single tested dose had a significant effect on plaques as measured by a brain scan, and the more BAN2401 patients got, the less amyloid they had after 18 months. But looking at cognition, only the highest tested dose was significantly better than placebo at slowing down mental decline. And some of the patients who received lower doses actually declined faster than those who received no treatment at all.[contextly_sidebar id=\"TAyKNwsnIzWapwgWfQcwbB5f1ZW4XVH2\"]\u003c/p>\n\u003cp>If amyloid really is the driving factor behind Alzheimer’s, why didn’t each incremental reduction in plaques lead to a corresponding improvement in cognition?\u003c/p>\n\u003cp>Dr. Al Sandrock, Biogen’s chief scientific officer, said there is likely a threshold of amyloid reduction that must be reached before patients actually benefit. The low doses, despite their effect on plaques, might not have hit that threshold, Sandrock said, thus accounting for their poor performance on cognitive decline.\u003c/p>\n\u003cp>The divergence in the two curves is what gives Dr. Reisa Sperling, who was overall encouraged by the results, “the most pause.” But Sperling, director Center for Alzheimer Research and Treatment at Brigham and Women’s Hospital, noted that some of the study’s arms had small numbers of patients, making it difficult to draw conclusions. She said while there is a biological argument that could underpin the threshold hypothesis, she wanted to see more data from a larger trial with a more traditional design.\u003c/p>\n\u003cp>Even if Sandrock’s theory holds up, what happened to BAN2401 is not a new phenomenon. This year a drug from Merck, meant to shut off the production of plaques by blocking an enzyme called BACE, was successful in reducing amyloid but fared so dismally on cognitive measures that researchers terminated the trial early. A second BACE drug, from Biogen and Eisai, had similar results in miniature, hitting the mark on plaque reduction in a Phase 2 trial but failing to significantly outperform placebo on cognition.\u003c/p>\n\u003cp>The underlying issue, according Dr. Lon Schneider, director of the California Alzheimer’s Disease Center at the University of Southern California, is that “the plaques are not the target — those are biomarkers.”\u003c/p>\n\u003cp>“A target is something that, as a result of hitting it, there will be change downstream in behavior, cognition, and illness course,” Schneider said. “So, yeah we’re knocking down amyloid, but so far we’re not changing behavior much.”\u003c/p>\n\u003cp>Even BAN2401’s saving grace — that its highest dose appeared to both reduce amyloid and improve patient’s clinical results — has come under scrutiny.\u003c/p>\n\u003cp>In the BAN2401 trial, about 70 percent of patients getting placebo had a genetic mutation that triples the risk of Alzheimer’s. But in the high-dose BAN2401 group, just 30 percent of patients had the mutation, called APOE4.[contextly_sidebar id=\"tcdS8fDReoUFY02DP3vnBwSqYDEV9wHe\"]\u003c/p>\n\u003cp>That could explain why BAN2401 seemed to outperform a saline injection in the high-dose group, skeptics say, as past trials suggest that APOE4 carriers have more rapidly progressing Alzheimer’s than patients without the mutation.\u003c/p>\n\u003cp>And it could mean that the drug’s seeming promise is a mirage.\u003c/p>\n\u003cp>Dr. Paul Aisen, who runs the Alzheimer’s Therapeutic Research Institute at the University of Southern California, said the discrepancy “does create a potential bias.” But in trials where patients are confirmed to have amyloid in their brains at the outset, as was the case with BAN2401, “the impact of [APOE4] on progression is modest,” Aisen wrote in an email. “I don’t think this accounts for the apparent slowing of cognitive decline in the high-dose arm.”\u003c/p>\n\u003cp>Sperling agreed that she did not think the arms’ different populations skewed the data, in part because the group that received the second highest dose of the drug had a larger share of APOE4 carriers and saw results that were similar — though not as substantial — as the high dose group.\u003c/p>\n\u003cp>“It’s a similar pattern,” she said. “For me that partially mitigates that concern.”\u003c/p>\n\u003cp>Biogen and Eisai have promised to dig into the data and parse out the effect APOE4 had on whether patients responded to BAN2401, but those results likely won’t be ready for months.\u003c/p>\n\u003cp>In the meantime, companies are still queueing up to take cracks at amyloid.\u003c/p>\n\u003cp>Eli Lilly, which has spent billions on failed Alzheimer’s drugs in recent years, has designed a trial that will test the amyloid hypothesis “in the most definitive way possible,” said Mark Mintun, the company’s vice president of neurodegeneration.\u003c/p>\n\u003cp>The plan is to take a BACE inhibitor and pair it with an injected treatment that targets amyloid already in the brain. That should address the two major concerns with each approach, Mintun said: BACE inhibitors prevent amyloid but don’t address plaques that already exist, while amyloid-targeting therapies don’t stem the flow of new toxic clumps.\u003c/p>\n\u003cp>“I equate it to going down to your basement and finding three feet of water and there’s been a slow drip for four weeks,” Mintun said. “You can turn off the spigot, but it won’t feel like you’ve made much progress, so you’ve got to pump it out, too.”\u003c/p>\n\u003cp>That study is enrolling 375 patients into three groups, planning to study whether the combination can improve cognition compared with placebo over 18 months.\u003c/p>\n\u003cp>\u003cem>Andrew Joseph contributed reporting.\u003c/em>\u003c/p>\n\u003cp>[ad floatright]\u003c/p>\n\u003cp>\u003cem>This story was originally published by \u003ca href=\"https://www.statnews.com/2018/07/30/alzheimers-amyloid-hypothesis/\" target=\"_blank\" rel=\"noopener\">STAT\u003c/a>, an online publication of Boston Globe Media that covers health, medicine, and scientific discovery.\u003c/em>\u003c/p>\n\n","blocks":[],"excerpt":"In data presented recently, one group of patients receiving an experimental drug saw their amyloid levels plummet, a result that was tied to a significant reduction in cognitive decline.","status":"publish","parent":0,"modified":1532989851,"stats":{"hasAudio":false,"hasVideo":false,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":31,"wordCount":1250},"headData":{"title":"Alzheimer’s Study Sparks New Debate Over Amyloid Hypothesis | KQED","description":"In data presented recently, one group of patients receiving an experimental drug saw their amyloid levels plummet, a result that was tied to a significant reduction in cognitive decline.","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":""},"disqusIdentifier":"443668 https://ww2.kqed.org/futureofyou/?p=443668","disqusUrl":"https://ww2.kqed.org/futureofyou/2018/07/31/alzheimers-study-sparks-new-debate-over-amyloid-hypothesis/","disqusTitle":"Alzheimer’s Study Sparks New Debate Over Amyloid Hypothesis","source":"Hope/Hype","nprByline":"Damian Garde\u003cbr />STAT","path":"/futureofyou/443668/alzheimers-study-sparks-new-debate-over-amyloid-hypothesis","audioTrackLength":null,"parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003cp>In the long-running debate over just what causes Alzheimer’s disease, one side looks to have scored a victory with \u003ca href=\"https://www.statnews.com/2018/07/25/experimental-alzheimers-drug-biogen-eisai/\" target=\"_blank\" rel=\"noopener\">new results with an in-development drug\u003c/a>. But there’s enough variation in the data to ensure that the squabbling factions of Alzheimer’s will have plenty to fight about.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>At issue is the so-called amyloid hypothesis, a decades-old theory claiming that Alzheimer’s gradual degradation of the brain is caused by the accumulation of sticky plaques. And the new drug is BAN2401, designed by Biogen and Eisai to prevent those amyloid plaques from clustering and attack the clumps that already have.\u003c/p>\n\u003cp>In data presented last week, one group of patients receiving BAN2401 saw their amyloid levels plummet, a result that was tied to a significant reduction in cognitive decline compared with placebo.\u003c/p>\n\u003cp>To the amyloid-inclined, like Dr. Howard Fillit of the Alzheimer’s Drug Discovery Foundation, that marks a clear affirmation of the linkage between plaques and mental fortitude.\u003c/p>\n\u003cp>“I mean if you asked me five or 10 years ago if we’re going to have a drug that can remove the plaques from the brain, I would have thought this was space technology,” Fillit said. “And there was definitely a signal, in my opinion, on clinical outcomes, which is what we’ve all been looking for.”\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>But to skeptics, the trial was laden with confounding details that make it impossible to draw conclusions.\u003c/p>\n\u003cp>“These results are a mess,” wrote Baird biotech analyst Brian Skorney. “Not so much that they indicate an outright failure of the [amyloid] hypothesis, but they don’t really say anything informative at all.”\u003c/p>\n\u003cp>In the trial, every single tested dose had a significant effect on plaques as measured by a brain scan, and the more BAN2401 patients got, the less amyloid they had after 18 months. But looking at cognition, only the highest tested dose was significantly better than placebo at slowing down mental decline. And some of the patients who received lower doses actually declined faster than those who received no treatment at all.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>If amyloid really is the driving factor behind Alzheimer’s, why didn’t each incremental reduction in plaques lead to a corresponding improvement in cognition?\u003c/p>\n\u003cp>Dr. Al Sandrock, Biogen’s chief scientific officer, said there is likely a threshold of amyloid reduction that must be reached before patients actually benefit. The low doses, despite their effect on plaques, might not have hit that threshold, Sandrock said, thus accounting for their poor performance on cognitive decline.\u003c/p>\n\u003cp>The divergence in the two curves is what gives Dr. Reisa Sperling, who was overall encouraged by the results, “the most pause.” But Sperling, director Center for Alzheimer Research and Treatment at Brigham and Women’s Hospital, noted that some of the study’s arms had small numbers of patients, making it difficult to draw conclusions. She said while there is a biological argument that could underpin the threshold hypothesis, she wanted to see more data from a larger trial with a more traditional design.\u003c/p>\n\u003cp>Even if Sandrock’s theory holds up, what happened to BAN2401 is not a new phenomenon. This year a drug from Merck, meant to shut off the production of plaques by blocking an enzyme called BACE, was successful in reducing amyloid but fared so dismally on cognitive measures that researchers terminated the trial early. A second BACE drug, from Biogen and Eisai, had similar results in miniature, hitting the mark on plaque reduction in a Phase 2 trial but failing to significantly outperform placebo on cognition.\u003c/p>\n\u003cp>The underlying issue, according Dr. Lon Schneider, director of the California Alzheimer’s Disease Center at the University of Southern California, is that “the plaques are not the target — those are biomarkers.”\u003c/p>\n\u003cp>“A target is something that, as a result of hitting it, there will be change downstream in behavior, cognition, and illness course,” Schneider said. “So, yeah we’re knocking down amyloid, but so far we’re not changing behavior much.”\u003c/p>\n\u003cp>Even BAN2401’s saving grace — that its highest dose appeared to both reduce amyloid and improve patient’s clinical results — has come under scrutiny.\u003c/p>\n\u003cp>In the BAN2401 trial, about 70 percent of patients getting placebo had a genetic mutation that triples the risk of Alzheimer’s. But in the high-dose BAN2401 group, just 30 percent of patients had the mutation, called APOE4.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>That could explain why BAN2401 seemed to outperform a saline injection in the high-dose group, skeptics say, as past trials suggest that APOE4 carriers have more rapidly progressing Alzheimer’s than patients without the mutation.\u003c/p>\n\u003cp>And it could mean that the drug’s seeming promise is a mirage.\u003c/p>\n\u003cp>Dr. Paul Aisen, who runs the Alzheimer’s Therapeutic Research Institute at the University of Southern California, said the discrepancy “does create a potential bias.” But in trials where patients are confirmed to have amyloid in their brains at the outset, as was the case with BAN2401, “the impact of [APOE4] on progression is modest,” Aisen wrote in an email. “I don’t think this accounts for the apparent slowing of cognitive decline in the high-dose arm.”\u003c/p>\n\u003cp>Sperling agreed that she did not think the arms’ different populations skewed the data, in part because the group that received the second highest dose of the drug had a larger share of APOE4 carriers and saw results that were similar — though not as substantial — as the high dose group.\u003c/p>\n\u003cp>“It’s a similar pattern,” she said. “For me that partially mitigates that concern.”\u003c/p>\n\u003cp>Biogen and Eisai have promised to dig into the data and parse out the effect APOE4 had on whether patients responded to BAN2401, but those results likely won’t be ready for months.\u003c/p>\n\u003cp>In the meantime, companies are still queueing up to take cracks at amyloid.\u003c/p>\n\u003cp>Eli Lilly, which has spent billions on failed Alzheimer’s drugs in recent years, has designed a trial that will test the amyloid hypothesis “in the most definitive way possible,” said Mark Mintun, the company’s vice president of neurodegeneration.\u003c/p>\n\u003cp>The plan is to take a BACE inhibitor and pair it with an injected treatment that targets amyloid already in the brain. That should address the two major concerns with each approach, Mintun said: BACE inhibitors prevent amyloid but don’t address plaques that already exist, while amyloid-targeting therapies don’t stem the flow of new toxic clumps.\u003c/p>\n\u003cp>“I equate it to going down to your basement and finding three feet of water and there’s been a slow drip for four weeks,” Mintun said. “You can turn off the spigot, but it won’t feel like you’ve made much progress, so you’ve got to pump it out, too.”\u003c/p>\n\u003cp>That study is enrolling 375 patients into three groups, planning to study whether the combination can improve cognition compared with placebo over 18 months.\u003c/p>\n\u003cp>\u003cem>Andrew Joseph contributed reporting.\u003c/em>\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>\u003cem>This story was originally published by \u003ca href=\"https://www.statnews.com/2018/07/30/alzheimers-amyloid-hypothesis/\" target=\"_blank\" rel=\"noopener\">STAT\u003c/a>, 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":"/futureofyou/443668/alzheimers-study-sparks-new-debate-over-amyloid-hypothesis","authors":["byline_futureofyou_443668"],"categories":["futureofyou_1062","futureofyou_1","futureofyou_1064"],"tags":["futureofyou_999","futureofyou_673","futureofyou_1023","futureofyou_141","futureofyou_61"],"collections":["futureofyou_1097"],"featImg":"futureofyou_443671","label":"source_futureofyou_443668"},"futureofyou_443536":{"type":"posts","id":"futureofyou_443536","meta":{"index":"posts_1591205157","site":"futureofyou","id":"443536","score":null,"sort":[1532365245000]},"guestAuthors":[],"slug":"hormone-levels-likely-influence-a-womans-risk-of-alzheimers-but-exactly-how","title":"Hormone Levels Likely Influence A Woman's Risk Of Alzheimer's. But Exactly How?","publishDate":1532365245,"format":"standard","headTitle":"Women’s Health | KQED Future of You | KQED Science","labelTerm":{},"content":"\u003cp>There's new evidence that a woman's levels of female sex hormones, including estrogen and progesterone, can influence her risk of Alzheimer's and other forms of dementia.[contextly_sidebar id=\"rPJOdHYPkIXQXRx2JEsrHPZVgzMtEJk7\"]\u003c/p>\n\u003cp>Women are less likely to develop dementia later in life if they begin to menstruate earlier, go through menopause later, and have more than one child, researchers \u003ca href=\"https://www.alz.org/aaic/pressroom.asp\" target=\"_blank\" rel=\"noopener\">reported\u003c/a> Monday at the \u003ca href=\"https://www.alz.org/aaic/\" target=\"_blank\" rel=\"noopener\">Alzheimer's Association International Conference\u003c/a> in Chicago.\u003c/p>\n\u003cp>And recent studies offer hints that \u003ca href=\"https://medlineplus.gov/hormonereplacementtherapy.html\" target=\"_blank\" rel=\"noopener\">hormone replacement therapy\u003c/a>, which fell out of favor more than a decade ago, might offer a way to protect a woman's brain if it is given at the right time, the researchers said.\u003c/p>\n\u003cp>The findings could help explain why women make up nearly two-thirds of people in the U.S. with Alzheimer's, says \u003ca href=\"http://nationalacademies.org/hmd/Activities/Research/NeuroForum/Member%20Profiles/Maria%20Carrillo.aspx\" target=\"_blank\" rel=\"noopener\">Maria Carrillo\u003c/a>, the association's chief scientific officer.\u003c/p>\n\u003cp>\"It isn't just that women are living longer,\" Carrillo says. \"There is some biological underpinning. And because of the large numbers of women that are affected, it is important to find out [what it is].\"\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>Scientists have long suspected that sex hormones such as estrogen and progesterone play a role in Alzheimer's. And two studies on dementia and what occurs during a women's reproductive years support that idea.[contextly_sidebar id=\"Wwp2fmV71pvuOzg04oa6uZxzPex1NtQ3\"]\u003c/p>\n\u003cp>One of the studies looked at nearly 15,000 women in California. And it found an association between a woman's reproductive history and her risk of memory problems later in life.\u003c/p>\n\u003cp>The risk of dementia for women who had three or more children was 12 percent lower than the risk for women who had one child, according to \u003ca href=\"https://divisionofresearch.kaiserpermanente.org/researchers/gilsanz-paola\" target=\"_blank\" rel=\"noopener\">Paola Gilsanz\u003c/a> of Kaiser Permanente Northern California Division of Research, and \u003ca href=\"https://profiles.ucsf.edu/rachel.whitmer\" target=\"_blank\" rel=\"noopener\">Rachel Whitmer\u003c/a> of the University of California, Davis.\u003c/p>\n\u003cp>Also, women who began to menstruate earlier and went through menopause later were less likely to develop dementia. Menopause at age 45 or younger seemed to increase the risk by 28 percent.\u003c/p>\n\u003cp>Another study of 133 elderly women in the U.K. found that the more months of pregnancy they experienced during their lives, the lower their risk of developing Alzheimer's.\u003c/p>\n\u003cp>The findings all suggest that female sex hormones — which rise at puberty and during pregnancy, then fall at menopause — are somehow affecting a woman's risk of developing Alzheimer's and other forms of dementia. The results also suggest that greater exposure to these hormones, through more pregnancies or more reproductive years, can reduce a woman's risk.\u003c/p>\n\u003cp>But it's still not clear whether the mere presence of female sex hormones is a reason that the frequency of Alzheimer's is greater in women than in men.\u003c/p>\n\u003cp>One possibility is that it's not female sex hormones on their own, but rapid changes in their levels that are a problem, says \u003ca href=\"https://crwg.uic.edu/crwg-home/crwg-staff/pauline-maki-phd/\" target=\"_blank\" rel=\"noopener\">Pauline Maki\u003c/a>, a professor of psychiatry and psychology at the University of Illinois at Chicago, who presented research at the Alzheimer's conference.[contextly_sidebar id=\"YEYwp8N3sM3v9aN2dUZdqE3yWweQzhJS\"]\u003c/p>\n\u003cp>\"Women experience these very dramatic hormonal transitions that in the long run can give rise to Alzheimer's disease,\" she says.\u003c/p>\n\u003cp>One way for women to minimize the dramatic hormonal changes that occur at menopause is to use hormone replacement therapy.\u003c/p>\n\u003cp>That approach fell out of favor more than a decade ago when a \u003ca href=\"https://www.ncbi.nlm.nih.gov/pubmed/12771112\" target=\"_blank\" rel=\"noopener\">large study\u003c/a> found that women who took estrogen plus progestin after menopause were actually more likely to get some form of dementia. They also appeared to have a higher risk of heart disease and breast cancer.\u003c/p>\n\u003cp>But Maki says more recent studies suggest that hormone therapy — especially estrogen alone — really can be helpful if women get it at the right time.\u003c/p>\n\u003cp>\"The effects of hormone therapy depend on the timing of use,\" Maki says. \"Use later in life is detrimental, whereas use early in the menopausal transition could be beneficial.\"\u003c/p>\n\u003cp>An analysis presented at the Alzheimer's conference supports that idea.\u003c/p>\n\u003cp>It found that in two recent studies, women who started taking estrogen after age 65 were more likely to have trouble with thinking and memory. But women who started taking estrogen between 50 and 54 were not.\u003c/p>\n\u003cp>And estrogen may benefit the mental function of younger women because it reduces the hot flashes associated with menopause, Maki says.[contextly_sidebar id=\"v9bruUJ5zucWs4sZPfqccXVqvwa2qouD\"]\u003c/p>\n\u003cp>\"The more hot flashes a woman has, the worse her memory performance,\" Maki says, citing her own research. \"And when we intervene to address those hot flashes, her memory performance bounces back.\"\u003c/p>\n\u003cp>Findings like that are renewing interest in the idea that someday, it may be possible to use hormones around the time of menopause to prevent Alzheimer's and other forms of dementia later on, Maki says.\u003c/p>\n\u003cp>In the meantime, there's evidence that hormonal differences between men and women may affect their brains in ways that affect doctors' ability to accurately diagnose Alzheimer's, Maki says.\u003c/p>\n\u003cp>At the Alzheimer's conference, she presented research showing that women tend to have higher verbal memory skills than men, even when they are in the early stages of Alzheimer's. As a result, women are likely to be diagnosed with the disease later than men.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>It's unclear whether male hormones, such as testosterone, affect a man's risk of Alzheimer's.\u003c/p>\n\u003chr>\n\u003cdiv class=\"fullattribution\">Copyright 2018 NPR. To see more, visit http://www.npr.org/.\u003cimg src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=Hormone+Levels+Likely+Influence+A+Woman%27s+Risk+Of+Alzheimer%27s.+But+Exactly+How%3F&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n","blocks":[],"excerpt":"Scientists are taking a second look at the idea that hormone replacement therapy could reduce a woman's risk of dementia. New research suggests the key may be in giving it at the right time.","status":"publish","parent":0,"modified":1532368619,"stats":{"hasAudio":false,"hasVideo":false,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":28,"wordCount":886},"headData":{"title":"Hormone Levels Likely Influence A Woman's Risk Of Alzheimer's. But Exactly How? | KQED","description":"Scientists are taking a second look at the idea that hormone replacement therapy could reduce a woman's risk of dementia. New research suggests the key may be in giving it at the right time.","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":""},"disqusIdentifier":"443536 https://ww2.kqed.org/futureofyou/?p=443536","disqusUrl":"https://ww2.kqed.org/futureofyou/2018/07/23/hormone-levels-likely-influence-a-womans-risk-of-alzheimers-but-exactly-how/","disqusTitle":"Hormone Levels Likely Influence A Woman's Risk Of Alzheimer's. But Exactly How?","source":"Health","nprImageCredit":"Ronnie Kaufman","nprByline":"Jon Hamilton, NPR","nprImageAgency":"Blend Images/Getty Images","nprStoryId":"630688342","nprApiLink":"http://api.npr.org/query?id=630688342&apiKey=MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004","nprHtmlLink":"https://www.npr.org/sections/health-shots/2018/07/23/630688342/might-sex-hormones-help-protect-women-from-alzheimer-s-after-all-maybe?ft=nprml&f=630688342","nprRetrievedStory":"1","nprPubDate":"Mon, 23 Jul 2018 09:01:00 -0400","nprStoryDate":"Mon, 23 Jul 2018 09:01:17 -0400","nprLastModifiedDate":"Mon, 23 Jul 2018 09:01:17 -0400","path":"/futureofyou/443536/hormone-levels-likely-influence-a-womans-risk-of-alzheimers-but-exactly-how","audioTrackLength":null,"parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003cp>There's new evidence that a woman's levels of female sex hormones, including estrogen and progesterone, can influence her risk of Alzheimer's and other forms of dementia.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>Women are less likely to develop dementia later in life if they begin to menstruate earlier, go through menopause later, and have more than one child, researchers \u003ca href=\"https://www.alz.org/aaic/pressroom.asp\" target=\"_blank\" rel=\"noopener\">reported\u003c/a> Monday at the \u003ca href=\"https://www.alz.org/aaic/\" target=\"_blank\" rel=\"noopener\">Alzheimer's Association International Conference\u003c/a> in Chicago.\u003c/p>\n\u003cp>And recent studies offer hints that \u003ca href=\"https://medlineplus.gov/hormonereplacementtherapy.html\" target=\"_blank\" rel=\"noopener\">hormone replacement therapy\u003c/a>, which fell out of favor more than a decade ago, might offer a way to protect a woman's brain if it is given at the right time, the researchers said.\u003c/p>\n\u003cp>The findings could help explain why women make up nearly two-thirds of people in the U.S. with Alzheimer's, says \u003ca href=\"http://nationalacademies.org/hmd/Activities/Research/NeuroForum/Member%20Profiles/Maria%20Carrillo.aspx\" target=\"_blank\" rel=\"noopener\">Maria Carrillo\u003c/a>, the association's chief scientific officer.\u003c/p>\n\u003cp>\"It isn't just that women are living longer,\" Carrillo says. \"There is some biological underpinning. And because of the large numbers of women that are affected, it is important to find out [what it is].\"\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>Scientists have long suspected that sex hormones such as estrogen and progesterone play a role in Alzheimer's. And two studies on dementia and what occurs during a women's reproductive years support that idea.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>One of the studies looked at nearly 15,000 women in California. And it found an association between a woman's reproductive history and her risk of memory problems later in life.\u003c/p>\n\u003cp>The risk of dementia for women who had three or more children was 12 percent lower than the risk for women who had one child, according to \u003ca href=\"https://divisionofresearch.kaiserpermanente.org/researchers/gilsanz-paola\" target=\"_blank\" rel=\"noopener\">Paola Gilsanz\u003c/a> of Kaiser Permanente Northern California Division of Research, and \u003ca href=\"https://profiles.ucsf.edu/rachel.whitmer\" target=\"_blank\" rel=\"noopener\">Rachel Whitmer\u003c/a> of the University of California, Davis.\u003c/p>\n\u003cp>Also, women who began to menstruate earlier and went through menopause later were less likely to develop dementia. Menopause at age 45 or younger seemed to increase the risk by 28 percent.\u003c/p>\n\u003cp>Another study of 133 elderly women in the U.K. found that the more months of pregnancy they experienced during their lives, the lower their risk of developing Alzheimer's.\u003c/p>\n\u003cp>The findings all suggest that female sex hormones — which rise at puberty and during pregnancy, then fall at menopause — are somehow affecting a woman's risk of developing Alzheimer's and other forms of dementia. The results also suggest that greater exposure to these hormones, through more pregnancies or more reproductive years, can reduce a woman's risk.\u003c/p>\n\u003cp>But it's still not clear whether the mere presence of female sex hormones is a reason that the frequency of Alzheimer's is greater in women than in men.\u003c/p>\n\u003cp>One possibility is that it's not female sex hormones on their own, but rapid changes in their levels that are a problem, says \u003ca href=\"https://crwg.uic.edu/crwg-home/crwg-staff/pauline-maki-phd/\" target=\"_blank\" rel=\"noopener\">Pauline Maki\u003c/a>, a professor of psychiatry and psychology at the University of Illinois at Chicago, who presented research at the Alzheimer's conference.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>\"Women experience these very dramatic hormonal transitions that in the long run can give rise to Alzheimer's disease,\" she says.\u003c/p>\n\u003cp>One way for women to minimize the dramatic hormonal changes that occur at menopause is to use hormone replacement therapy.\u003c/p>\n\u003cp>That approach fell out of favor more than a decade ago when a \u003ca href=\"https://www.ncbi.nlm.nih.gov/pubmed/12771112\" target=\"_blank\" rel=\"noopener\">large study\u003c/a> found that women who took estrogen plus progestin after menopause were actually more likely to get some form of dementia. They also appeared to have a higher risk of heart disease and breast cancer.\u003c/p>\n\u003cp>But Maki says more recent studies suggest that hormone therapy — especially estrogen alone — really can be helpful if women get it at the right time.\u003c/p>\n\u003cp>\"The effects of hormone therapy depend on the timing of use,\" Maki says. \"Use later in life is detrimental, whereas use early in the menopausal transition could be beneficial.\"\u003c/p>\n\u003cp>An analysis presented at the Alzheimer's conference supports that idea.\u003c/p>\n\u003cp>It found that in two recent studies, women who started taking estrogen after age 65 were more likely to have trouble with thinking and memory. But women who started taking estrogen between 50 and 54 were not.\u003c/p>\n\u003cp>And estrogen may benefit the mental function of younger women because it reduces the hot flashes associated with menopause, Maki says.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>\"The more hot flashes a woman has, the worse her memory performance,\" Maki says, citing her own research. \"And when we intervene to address those hot flashes, her memory performance bounces back.\"\u003c/p>\n\u003cp>Findings like that are renewing interest in the idea that someday, it may be possible to use hormones around the time of menopause to prevent Alzheimer's and other forms of dementia later on, Maki says.\u003c/p>\n\u003cp>In the meantime, there's evidence that hormonal differences between men and women may affect their brains in ways that affect doctors' ability to accurately diagnose Alzheimer's, Maki says.\u003c/p>\n\u003cp>At the Alzheimer's conference, she presented research showing that women tend to have higher verbal memory skills than men, even when they are in the early stages of Alzheimer's. As a result, women are likely to be diagnosed with the disease later than men.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>It's unclear whether male hormones, such as testosterone, affect a man's risk of Alzheimer's.\u003c/p>\n\u003chr>\n\u003cdiv class=\"fullattribution\">Copyright 2018 NPR. To see more, visit http://www.npr.org/.\u003cimg src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=Hormone+Levels+Likely+Influence+A+Woman%27s+Risk+Of+Alzheimer%27s.+But+Exactly+How%3F&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/futureofyou/443536/hormone-levels-likely-influence-a-womans-risk-of-alzheimers-but-exactly-how","authors":["byline_futureofyou_443536"],"series":["futureofyou_219"],"categories":["futureofyou_1060","futureofyou_1"],"tags":["futureofyou_999","futureofyou_1023","futureofyou_1008","futureofyou_61","futureofyou_80"],"collections":["futureofyou_1093"],"featImg":"futureofyou_443537","label":"source_futureofyou_443536"},"futureofyou_443236":{"type":"posts","id":"futureofyou_443236","meta":{"index":"posts_1591205157","site":"futureofyou","id":"443236","score":null,"sort":[1531162927000]},"guestAuthors":[],"slug":"family-caregivers-exchange-tips-share-stories-to-ease-alzheimers-losses","title":"Family Caregivers Exchange Tips, Share Stories To Ease Alzheimer's Losses","publishDate":1531162927,"format":"standard","headTitle":"KQED Future of You | KQED Science","labelTerm":{},"content":"\u003cp>Vicki Bartholomew started a support group for wives who are caring for a husband with Alzheimer's disease because she needed that sort of group herself.\u003c/p>\n\u003cp>They meet every month in a conference room at a new memory care facility in Nashville, Tenn., called \u003ca href=\"http://nashvillepublicradio.org/post/nashville-dementia-ward-aims-become-hub-memory-care-research#stream/0\" target=\"_blank\" rel=\"noopener\">Abe's Garden\u003c/a>, where Bartholomew's husband was one of the first residents — a Vietnam veteran and prominent attorney in Nashville.\u003c/p>\n\u003cp>\"My husband's still living, and now I'm in an even more difficult situation — I'm married, but I'm a widow,\" she says.\u003c/p>\n\u003cp>These women draw the shades and open up to each other in ways they can't with their lifelong friends.\u003c/p>\n\u003cp>\"They're still wonderful friends, but they didn't know how to handle this. It was hard for them, and as you all know, your friends don't come around as much as they used to,\" Bartholomew says. \"I was in bad shape. I didn't think I was — I did have health problems, and [now] I know I was depressed.\"\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>As the numbers of Americans afflicted with Alzheimer's disease continue to swell to an estimated 5.7 million, so do the legions of loved ones caring for friends and family members. The toll on Bartholomew's own mental health is one of the reasons the Alzheimer's Foundation of America focuses on the nation's estimated \u003ca href=\"https://www.alz.org/facts/\" target=\"_blank\" rel=\"noopener\">16 million unpaid caregivers\u003c/a>.\u003c/p>\n\u003cp>With no cure on the horizon, the foundation has been highlighting the necessity of better support for those caregivers through a \u003ca href=\"https://alzfdn.org/afa-educating-america-tour/\">national tour\u003c/a>. It stopped in Nashville earlier this spring, was in Tempe, Ariz., in June and heads to Fairfax, Va., in September; the tour includes at least six more cities in the fall.\u003c/p>\n\u003cp>At the live events, Alzheimer's researchers and clinicians offer guidance on a number of topics, including how to ensure safety for patients at home, care planning and even how to \u003ca href=\"https://alzfdn.org/event/afa-educating-america-tour-tempe/\" target=\"_blank\" rel=\"noopener\">entertain someone\u003c/a> with memory loss.\u003c/p>\n\u003cp>The organization promotes in-person and \u003ca href=\"https://alzfdn.org/alzheimers-foundation-americas-national-toll-free-helpline-expanding-seven-days-week/\" target=\"_blank\" rel=\"noopener\">telephone support groups\u003c/a>, since being a caregiver is often a barrier to getting out of the house alone. But even virtual support systems have shown some effectiveness at reducing loneliness, stress and depression \u003ca href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4668714/\" target=\"_blank\" rel=\"noopener\">in a small 2014 study.\u003c/a>\u003c/p>\n\u003cp>\"We have to do everything we can to educate a caregiver, to provide them with the best practices on caring for somebody,\" says \u003ca href=\"https://alzfdn.org/team_member/charles-j-fuschillo-jr/\" target=\"_blank\" rel=\"noopener\">Charles J. Fuschillo Jr.,\u003c/a> the Alzheimer's Foundation of America's CEO.\u003c/p>\n\u003cp>For example, the AFA \u003ca href=\"https://alzfdn.org/caregiving-resources/fact-sheets-information/\" target=\"_blank\" rel=\"noopener\">recommends\u003c/a> that family members:\u003c/p>\n\u003cul>\n\u003cli>Feed Alzheimer's patients one food at a time. \"A busy plate can be confusing,\" the group says.\u003c/li>\n\u003cli>Mark rooms in the house with signs to avoid unnecessary confusion.\u003c/li>\n\u003cli>Remind a person with Alzheimer's to use the toilet; don't wait for them to ask.\u003c/li>\n\u003cli>When traveling, stick with familiar destinations.\u003c/li>\n\u003cli>Watch for a cough while eating; it can signal a swallowing disorder in people with dementia.\u003c/li>\n\u003cli>Schedule overnight stays at a memory-care facility so the caregiver gets some respite.\u003c/li>\n\u003c/ul>\n\u003cp>Just as important, Fuschillo says, \"We want to do everything we can to avoid caregiver burnout.\"\u003c/p>\n\u003cp>The breaking point sneaks up on even the most committed caregiver, say Alzheimer's advocates, especially as the nights grow more sleepless. Alzheimer's patients can tend to pace, or wake up their partner every few minutes. They can even become violent. Or, perhaps worse, they can leave the house.\u003c/p>\n\u003cp>\"And I've had some issues at night that I had to take care of alone,\" says Pam Hawkins, whose husband has Alzheimer's. \"But I'm not ready to have anyone there at night.\"\u003c/p>\n\u003cp>For now, she says, her husband usually sleeps all night. And if there's a problem, her son-in-law is 15 minutes away.\u003c/p>\n\u003cp>She's had to hire caregivers during the day. Knowing how to find and hire the right person is a shared concern by Alzheimer's family members that has inspired an entire\u003ca href=\"https://www.alz.org/national/documents/topicsheet_homehealth.pdf\" target=\"_blank\" rel=\"noopener\"> checklist\u003c/a> for navigating the process. The tips include these: Interview the aide in the home. Over-share information about the patient. Ask what kind of quality control a supervisor will provide.\u003c/p>\n\u003cp>Hawkins is adamant about keeping her husband at home, whatever the cost.\u003c/p>\n\u003cp>\"He's not going anywhere,\" she says. \"He's staying at our home until he moves to heaven. We made that decision a long time ago.\"\u003c/p>\n\u003cp>But many caregivers have no choice.\u003c/p>\n\u003cp>April Simpkins says tending to her husband became all consuming, and she's young enough that she still needs to keep her job; she works at a local university.\u003c/p>\n\u003cp>\"It was not possible for us to keep Joe at home,\" she says.\u003c/p>\n\u003cp>Simpkins found she'd often have to call her husband's siblings to settle him down over the phone. One night, she had to dial 911 when he kept yelling in the hallways of their condo building.\u003c/p>\n\u003cp>And yet she felt some societal pressure that she wasn't doing enough.\u003c/p>\n\u003cp>\"There's a lot of ... glory given to the whole idea of someone being long-suffering and staying at home and giving up their life, basically, to care for their loved one,\" Simpkins says. \"It makes it harder for people who can't do that.\"\u003c/p>\n\u003cp>Everyone around the table nods in agreement. Whatever stage of illness their loved one is experiencing, these caregivers understand the complicated existence that many have dubbed \"the long goodbye.\"\u003c/p>\n\u003cp>Along with sharing the sorrow, they find a way to share in the humor of it all — one woman says her husband wears a laundry-basket's-worth of shirts and pants because he forgets he's already gotten dressed. Even tips on how to reduce the odor from incontinence are offered with a loving laugh.\u003c/p>\n\u003cp>The support group ends with hugs. Some women head for the parking lot. Others buzz through the locked doors to see their husbands.\u003c/p>\n\u003cp>Simpkins sits down for lunch with Joe, who is a former state employee and a youthful-looking 66 years old. She drapes an arm around his slumping shoulders and assists him as he spears a cold strawberry with his fork.\u003c/p>\n\u003cp>\"You know, there are some days,\" she says, interrupted by a random reflection from Joe. \"Yeah, some days are clearer than others.\"\u003c/p>\n\u003cp>Simpkins tries to stop by to see her husband every day. But it's a wicked kind of blessing, she says, that when she misses a visit, Joe no longer notices.\u003c/p>\n\u003cp>[ad floatright]\u003c/p>\n\u003cp>\u003cem>This story is part of NPR's reporting partnership with Nashville Public Radio and Kaiser Health News.\u003c/em>\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2018 Nashville Public Radio. To see more, visit \u003ca href=\"http://www.wpln.org/\" target=\"_blank\" rel=\"noopener\">Nashville Public Radio\u003c/a>.\u003cimg src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=Family+Caregivers+Exchange+Tips%2C+Share+Stories+To+Ease+Alzheimer%27s+Losses&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n","blocks":[],"excerpt":"As the number of people with Alzheimer's climbs, so does the number of loved ones caring for them. The health of 16 million unpaid U.S. caregivers has become a focus for Alzheimer's advocacy groups.","status":"publish","parent":0,"modified":1531169663,"stats":{"hasAudio":false,"hasVideo":false,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":33,"wordCount":1098},"headData":{"title":"Family Caregivers Exchange Tips, Share Stories To Ease Alzheimer's Losses | KQED","description":"As the number of people with Alzheimer's climbs, so does the number of loved ones caring for them. The health of 16 million unpaid U.S. caregivers has become a focus for Alzheimer's advocacy groups.","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":""},"disqusIdentifier":"443236 https://ww2.kqed.org/futureofyou/?p=443236","disqusUrl":"https://ww2.kqed.org/futureofyou/2018/07/09/family-caregivers-exchange-tips-share-stories-to-ease-alzheimers-losses/","disqusTitle":"Family Caregivers Exchange Tips, Share Stories To Ease Alzheimer's Losses","source":"Health","nprImageCredit":"Tang Yau Hoong","nprByline":"Blake Farmer, NPR","nprImageAgency":"Ikon Images/Getty Images","nprStoryId":"621110042","nprApiLink":"http://api.npr.org/query?id=621110042&apiKey=MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004","nprHtmlLink":"https://www.npr.org/sections/health-shots/2018/07/06/621110042/shared-tips-support-help-prevent-burnout-among-alzheimers-family-caregivers?ft=nprml&f=621110042","nprRetrievedStory":"1","nprPubDate":"Fri, 06 Jul 2018 13:18:00 -0400","nprStoryDate":"Fri, 06 Jul 2018 04:59:00 -0400","nprLastModifiedDate":"Fri, 06 Jul 2018 13:18:48 -0400","nprAudio":"https://ondemand.npr.org/anon.npr-mp3/npr/me/2018/07/20180706_me_family_caregivers_exchange_tips_share_stories_to_ease_alzheimers_losses.mp3?orgId=577&topicId=1128&d=229&p=3&story=621110042&ft=nprml&f=621110042","nprAudioM3u":"http://api.npr.org/m3u/1626442145-cdcb9f.m3u?orgId=577&topicId=1128&d=229&p=3&story=621110042&ft=nprml&f=621110042","path":"/futureofyou/443236/family-caregivers-exchange-tips-share-stories-to-ease-alzheimers-losses","audioUrl":"https://ondemand.npr.org/anon.npr-mp3/npr/me/2018/07/20180706_me_family_caregivers_exchange_tips_share_stories_to_ease_alzheimers_losses.mp3?orgId=577&topicId=1128&d=229&p=3&story=621110042&ft=nprml&f=621110042","audioTrackLength":null,"parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003cp>Vicki Bartholomew started a support group for wives who are caring for a husband with Alzheimer's disease because she needed that sort of group herself.\u003c/p>\n\u003cp>They meet every month in a conference room at a new memory care facility in Nashville, Tenn., called \u003ca href=\"http://nashvillepublicradio.org/post/nashville-dementia-ward-aims-become-hub-memory-care-research#stream/0\" target=\"_blank\" rel=\"noopener\">Abe's Garden\u003c/a>, where Bartholomew's husband was one of the first residents — a Vietnam veteran and prominent attorney in Nashville.\u003c/p>\n\u003cp>\"My husband's still living, and now I'm in an even more difficult situation — I'm married, but I'm a widow,\" she says.\u003c/p>\n\u003cp>These women draw the shades and open up to each other in ways they can't with their lifelong friends.\u003c/p>\n\u003cp>\"They're still wonderful friends, but they didn't know how to handle this. It was hard for them, and as you all know, your friends don't come around as much as they used to,\" Bartholomew says. \"I was in bad shape. I didn't think I was — I did have health problems, and [now] I know I was depressed.\"\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>As the numbers of Americans afflicted with Alzheimer's disease continue to swell to an estimated 5.7 million, so do the legions of loved ones caring for friends and family members. The toll on Bartholomew's own mental health is one of the reasons the Alzheimer's Foundation of America focuses on the nation's estimated \u003ca href=\"https://www.alz.org/facts/\" target=\"_blank\" rel=\"noopener\">16 million unpaid caregivers\u003c/a>.\u003c/p>\n\u003cp>With no cure on the horizon, the foundation has been highlighting the necessity of better support for those caregivers through a \u003ca href=\"https://alzfdn.org/afa-educating-america-tour/\">national tour\u003c/a>. It stopped in Nashville earlier this spring, was in Tempe, Ariz., in June and heads to Fairfax, Va., in September; the tour includes at least six more cities in the fall.\u003c/p>\n\u003cp>At the live events, Alzheimer's researchers and clinicians offer guidance on a number of topics, including how to ensure safety for patients at home, care planning and even how to \u003ca href=\"https://alzfdn.org/event/afa-educating-america-tour-tempe/\" target=\"_blank\" rel=\"noopener\">entertain someone\u003c/a> with memory loss.\u003c/p>\n\u003cp>The organization promotes in-person and \u003ca href=\"https://alzfdn.org/alzheimers-foundation-americas-national-toll-free-helpline-expanding-seven-days-week/\" target=\"_blank\" rel=\"noopener\">telephone support groups\u003c/a>, since being a caregiver is often a barrier to getting out of the house alone. But even virtual support systems have shown some effectiveness at reducing loneliness, stress and depression \u003ca href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4668714/\" target=\"_blank\" rel=\"noopener\">in a small 2014 study.\u003c/a>\u003c/p>\n\u003cp>\"We have to do everything we can to educate a caregiver, to provide them with the best practices on caring for somebody,\" says \u003ca href=\"https://alzfdn.org/team_member/charles-j-fuschillo-jr/\" target=\"_blank\" rel=\"noopener\">Charles J. Fuschillo Jr.,\u003c/a> the Alzheimer's Foundation of America's CEO.\u003c/p>\n\u003cp>For example, the AFA \u003ca href=\"https://alzfdn.org/caregiving-resources/fact-sheets-information/\" target=\"_blank\" rel=\"noopener\">recommends\u003c/a> that family members:\u003c/p>\n\u003cul>\n\u003cli>Feed Alzheimer's patients one food at a time. \"A busy plate can be confusing,\" the group says.\u003c/li>\n\u003cli>Mark rooms in the house with signs to avoid unnecessary confusion.\u003c/li>\n\u003cli>Remind a person with Alzheimer's to use the toilet; don't wait for them to ask.\u003c/li>\n\u003cli>When traveling, stick with familiar destinations.\u003c/li>\n\u003cli>Watch for a cough while eating; it can signal a swallowing disorder in people with dementia.\u003c/li>\n\u003cli>Schedule overnight stays at a memory-care facility so the caregiver gets some respite.\u003c/li>\n\u003c/ul>\n\u003cp>Just as important, Fuschillo says, \"We want to do everything we can to avoid caregiver burnout.\"\u003c/p>\n\u003cp>The breaking point sneaks up on even the most committed caregiver, say Alzheimer's advocates, especially as the nights grow more sleepless. Alzheimer's patients can tend to pace, or wake up their partner every few minutes. They can even become violent. Or, perhaps worse, they can leave the house.\u003c/p>\n\u003cp>\"And I've had some issues at night that I had to take care of alone,\" says Pam Hawkins, whose husband has Alzheimer's. \"But I'm not ready to have anyone there at night.\"\u003c/p>\n\u003cp>For now, she says, her husband usually sleeps all night. And if there's a problem, her son-in-law is 15 minutes away.\u003c/p>\n\u003cp>She's had to hire caregivers during the day. Knowing how to find and hire the right person is a shared concern by Alzheimer's family members that has inspired an entire\u003ca href=\"https://www.alz.org/national/documents/topicsheet_homehealth.pdf\" target=\"_blank\" rel=\"noopener\"> checklist\u003c/a> for navigating the process. The tips include these: Interview the aide in the home. Over-share information about the patient. Ask what kind of quality control a supervisor will provide.\u003c/p>\n\u003cp>Hawkins is adamant about keeping her husband at home, whatever the cost.\u003c/p>\n\u003cp>\"He's not going anywhere,\" she says. \"He's staying at our home until he moves to heaven. We made that decision a long time ago.\"\u003c/p>\n\u003cp>But many caregivers have no choice.\u003c/p>\n\u003cp>April Simpkins says tending to her husband became all consuming, and she's young enough that she still needs to keep her job; she works at a local university.\u003c/p>\n\u003cp>\"It was not possible for us to keep Joe at home,\" she says.\u003c/p>\n\u003cp>Simpkins found she'd often have to call her husband's siblings to settle him down over the phone. One night, she had to dial 911 when he kept yelling in the hallways of their condo building.\u003c/p>\n\u003cp>And yet she felt some societal pressure that she wasn't doing enough.\u003c/p>\n\u003cp>\"There's a lot of ... glory given to the whole idea of someone being long-suffering and staying at home and giving up their life, basically, to care for their loved one,\" Simpkins says. \"It makes it harder for people who can't do that.\"\u003c/p>\n\u003cp>Everyone around the table nods in agreement. Whatever stage of illness their loved one is experiencing, these caregivers understand the complicated existence that many have dubbed \"the long goodbye.\"\u003c/p>\n\u003cp>Along with sharing the sorrow, they find a way to share in the humor of it all — one woman says her husband wears a laundry-basket's-worth of shirts and pants because he forgets he's already gotten dressed. Even tips on how to reduce the odor from incontinence are offered with a loving laugh.\u003c/p>\n\u003cp>The support group ends with hugs. Some women head for the parking lot. Others buzz through the locked doors to see their husbands.\u003c/p>\n\u003cp>Simpkins sits down for lunch with Joe, who is a former state employee and a youthful-looking 66 years old. She drapes an arm around his slumping shoulders and assists him as he spears a cold strawberry with his fork.\u003c/p>\n\u003cp>\"You know, there are some days,\" she says, interrupted by a random reflection from Joe. \"Yeah, some days are clearer than others.\"\u003c/p>\n\u003cp>Simpkins tries to stop by to see her husband every day. But it's a wicked kind of blessing, she says, that when she misses a visit, Joe no longer notices.\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>\u003cem>This story is part of NPR's reporting partnership with Nashville Public Radio and Kaiser Health News.\u003c/em>\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2018 Nashville Public Radio. To see more, visit \u003ca href=\"http://www.wpln.org/\" target=\"_blank\" rel=\"noopener\">Nashville Public Radio\u003c/a>.\u003cimg src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=Family+Caregivers+Exchange+Tips%2C+Share+Stories+To+Ease+Alzheimer%27s+Losses&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/futureofyou/443236/family-caregivers-exchange-tips-share-stories-to-ease-alzheimers-losses","authors":["byline_futureofyou_443236"],"categories":["futureofyou_1060","futureofyou_1","futureofyou_73"],"tags":["futureofyou_999","futureofyou_56","futureofyou_1023","futureofyou_1008","futureofyou_61"],"collections":["futureofyou_1093"],"featImg":"futureofyou_443237","label":"source_futureofyou_443236"},"futureofyou_442958":{"type":"posts","id":"futureofyou_442958","meta":{"index":"posts_1591205157","site":"futureofyou","id":"442958","score":null,"sort":[1529606096000]},"guestAuthors":[],"slug":"researchers-find-herpes-viruses-in-alzheimers-brains","title":"Researchers Find Herpes Viruses In Alzheimer's Brains","publishDate":1529606096,"format":"standard","headTitle":"KQED Future of You | KQED Science","labelTerm":{},"content":"\u003cp>Two common herpes viruses appear to play a role in Alzheimer's disease.[contextly_sidebar id=\"xGMrgC5mfby5S92heGXjVDaxhvly8p6M\"]\u003c/p>\n\u003cp>The viruses, best known for causing a distinctive skin rash in young children, are abundant in brain tissue from people with Alzheimer's, a team of scientists \u003ca href=\"http://www.cell.com/neuron/fulltext/S0896-6273(18)30421-5\">reports\u003c/a> Thursday in \u003cem>Neuron.\u003c/em> The team also found evidence that the viruses can interact with brain cells in ways that could accelerate the disease.\u003c/p>\n\u003cp>\"Our hypothesis is that they put gas on the flame,\" says \u003ca href=\"https://www.mountsinai.org/profiles/joel-dudley\">Joel Dudley\u003c/a>, an author of the study and an associate professor of genetics and genomic sciences at the Icahn School of Medicine at Mt. Sinai in New York City.\u003c/p>\n\u003cp>The finding adds credence to a decades-old idea that an infection can cause Alzheimer's disease. It also suggests that it may be possible to prevent or \u003ca href=\"https://www.nia.nih.gov/alzheimers/clinical-trials/valacyclovir-mild-alzheimers-disease\">slow Alzheimer's using antiviral drugs\u003c/a>, or drugs that modulate how immune cells in the brain respond to an infection.\u003c/p>\n\u003cp>But the study doesn't prove that herpes viruses are involved in Alzheimer's, says \u003ca href=\"https://www.nia.nih.gov/about/staff/hodes-richard\">Dr. Richard Hodes\u003c/a>, director of the National Institute on Aging, which helped fund the research.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>\"The data are very provocative, but fall short of showing a direct causal role,\" he says. \"And if viral infections are playing a part, they are not the sole actor.\"\u003c/p>\n\u003cp>Even so, the study offers strong evidence that viral infections can influence the course of Alzheimer's, Hodes says.\u003c/p>\n\u003cp>Like a lot of scientific discoveries, this one was an accident. \"Viruses were the last thing we were looking for,\" Dudley says.\u003c/p>\n\u003cp>He and a team of researchers were using genetic data to look for differences between healthy brain tissue and brain tissue from people who died with Alzheimer's.[contextly_sidebar id=\"8UKShQkLN6fHi6cnpzNKDWdZydXn4g8E\"]\u003c/p>\n\u003cp>The goal was to identify new targets for drugs. Instead, the team kept finding hints that that brain tissue from Alzheimer's patients contained higher levels of viruses.\u003c/p>\n\u003cp>\"When we started analyzing the differences, it just sort of came screaming out at us from the data,\" Dudley says.\u003c/p>\n\u003cp>The team found that levels of two human herpes viruses, HHV-6 and HHV-7, were up to twice as high in brain tissue from people with Alzheimer's. They confirmed the finding by analyzing data from a consortium of brain banks.\u003c/p>\n\u003cp>These herpes viruses are extremely common, and can cause a skin rash called \u003ca href=\"http://kidshealth.org/en/parents/roseola.html\">roseola\u003c/a> in young children. But the viruses also can get into the brain, where they may remain inactive for decades.\u003c/p>\n\u003cp>Once the researchers knew the viruses were associated with Alzheimer's they started trying to figure out how a virus could affect the course of a brain disease. That meant identifying interactions between the virus genes and other genes in brain cells.\u003c/p>\n\u003cp>\"We mapped out the social network, if you will, of which genes the viruses are friends with and who they're talking to inside the brain,\" Dudley says. In essence, he says, they wanted to know: \"If the viruses are tweeting, who's tweeting back?\"\u003c/p>\n\u003cp>And what they found was that the herpes virus genes were interacting with genes known to increase a person's risk for Alzheimer's.\u003c/p>\n\u003cp>They also found that these Alzheimer's risk genes seem to make a person's brain more vulnerable to infection with the two herpes viruses.\u003c/p>\n\u003cp>But just having herpes virus present in the brain isn't enough to cause Alzheimer's, Dudley says. Something needs to activate the viruses, which causes them to begin replicating.[contextly_sidebar id=\"gGYh4qorVVvYdrsEtJY48IAc6q49hNUX\"]\u003c/p>\n\u003cp>It's not clear what causes the activation, Dudley says, though he suspects some sort of change in the internal functions of brain cells.\u003c/p>\n\u003cp>Once the viruses do become active, they appear to influence things like the accumulation of the plaques and tangles in the brain associated with Alzheimer's. \"They are sort of throwing a wrench in the works,\" he says.\u003c/p>\n\u003cp>The herpes viruses also seem to trigger an immune response in certain brain cells, Hodes says. These cells are part of an ancient immune system that has \u003ca href=\"https://www.npr.org/sections/health-shots/2018/02/18/580475245/scientists-explore-ties-between-alzheimers-and-brains-ancient-immune-system\">previously been implicated\u003c/a> in Alzheimer's.\u003c/p>\n\u003cp>Most previous efforts to prevent or treat Alzheimer's have involved trying to reduce the plaques and tangles associated with the disease. Those efforts have failed to improve brain function even when they accomplished their immediate goal.\u003c/p>\n\u003cp>Those \"distressing and disappointing failures\" suggest it's time for some new approaches, Hodes says. And the new study suggests at least two.\u003c/p>\n\u003cp>One is to give antiviral drugs to people with high levels of herpes virus in their brains. The Institute on Aging is already funding a study to test this approach in people in the early stages of Alzheimer's, Hodes says.\u003c/p>\n\u003cp>Another approach is to prevent the brain's immune cells from reacting to the virus in ways that accelerate Alzheimer's, Hodes says. That's tricky, he says, because simply disabling the brain's immune cells could be harmful.\u003c/p>\n\u003cp>Even so, Hodes is optimistic.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\"The more we learn about the disease process and the more targets we can address,\" he says, \"the greater the probability we are going to slow or prevent the progression of Alzheimer's disease.\"\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2018 NPR. To see more, visit http://www.npr.org/.\u003cimg src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=Researchers+Find+Herpes+Viruses+In+Brains+Marked+By+Alzheimer%27s+Disease&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n","blocks":[],"excerpt":"Two herpes viruses that cause skin rashes in toddlers may accelerate Alzheimer's disease when they infect brain cells. The finding suggests antiviral drugs might help protect the brain.","status":"publish","parent":0,"modified":1529606195,"stats":{"hasAudio":false,"hasVideo":false,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":29,"wordCount":866},"headData":{"title":"Researchers Find Herpes Viruses In Alzheimer's Brains | KQED","description":"Two herpes viruses that cause skin rashes in toddlers may accelerate Alzheimer's disease when they infect brain cells. The finding suggests antiviral drugs might help protect the brain.","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":""},"disqusIdentifier":"442958 https://ww2.kqed.org/futureofyou/?p=442958","disqusUrl":"https://ww2.kqed.org/futureofyou/2018/06/21/researchers-find-herpes-viruses-in-alzheimers-brains/","disqusTitle":"Researchers Find Herpes Viruses In Alzheimer's Brains","source":"Health","nprByline":"Jon Hamilton, NPR","nprStoryId":"621908340","nprApiLink":"http://api.npr.org/query?id=621908340&apiKey=MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004","nprHtmlLink":"https://www.npr.org/sections/health-shots/2018/06/21/621908340/researchers-find-herpes-viruses-in-brains-marked-by-alzheimers-disease?ft=nprml&f=621908340","nprRetrievedStory":"1","nprPubDate":"Thu, 21 Jun 2018 11:31:00 -0400","nprStoryDate":"Thu, 21 Jun 2018 11:16:00 -0400","nprLastModifiedDate":"Thu, 21 Jun 2018 11:31:51 -0400","path":"/futureofyou/442958/researchers-find-herpes-viruses-in-alzheimers-brains","audioTrackLength":null,"parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003cp>Two common herpes viruses appear to play a role in Alzheimer's disease.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>The viruses, best known for causing a distinctive skin rash in young children, are abundant in brain tissue from people with Alzheimer's, a team of scientists \u003ca href=\"http://www.cell.com/neuron/fulltext/S0896-6273(18)30421-5\">reports\u003c/a> Thursday in \u003cem>Neuron.\u003c/em> The team also found evidence that the viruses can interact with brain cells in ways that could accelerate the disease.\u003c/p>\n\u003cp>\"Our hypothesis is that they put gas on the flame,\" says \u003ca href=\"https://www.mountsinai.org/profiles/joel-dudley\">Joel Dudley\u003c/a>, an author of the study and an associate professor of genetics and genomic sciences at the Icahn School of Medicine at Mt. Sinai in New York City.\u003c/p>\n\u003cp>The finding adds credence to a decades-old idea that an infection can cause Alzheimer's disease. It also suggests that it may be possible to prevent or \u003ca href=\"https://www.nia.nih.gov/alzheimers/clinical-trials/valacyclovir-mild-alzheimers-disease\">slow Alzheimer's using antiviral drugs\u003c/a>, or drugs that modulate how immune cells in the brain respond to an infection.\u003c/p>\n\u003cp>But the study doesn't prove that herpes viruses are involved in Alzheimer's, says \u003ca href=\"https://www.nia.nih.gov/about/staff/hodes-richard\">Dr. Richard Hodes\u003c/a>, director of the National Institute on Aging, which helped fund the research.\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>\"The data are very provocative, but fall short of showing a direct causal role,\" he says. \"And if viral infections are playing a part, they are not the sole actor.\"\u003c/p>\n\u003cp>Even so, the study offers strong evidence that viral infections can influence the course of Alzheimer's, Hodes says.\u003c/p>\n\u003cp>Like a lot of scientific discoveries, this one was an accident. \"Viruses were the last thing we were looking for,\" Dudley says.\u003c/p>\n\u003cp>He and a team of researchers were using genetic data to look for differences between healthy brain tissue and brain tissue from people who died with Alzheimer's.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>The goal was to identify new targets for drugs. Instead, the team kept finding hints that that brain tissue from Alzheimer's patients contained higher levels of viruses.\u003c/p>\n\u003cp>\"When we started analyzing the differences, it just sort of came screaming out at us from the data,\" Dudley says.\u003c/p>\n\u003cp>The team found that levels of two human herpes viruses, HHV-6 and HHV-7, were up to twice as high in brain tissue from people with Alzheimer's. They confirmed the finding by analyzing data from a consortium of brain banks.\u003c/p>\n\u003cp>These herpes viruses are extremely common, and can cause a skin rash called \u003ca href=\"http://kidshealth.org/en/parents/roseola.html\">roseola\u003c/a> in young children. But the viruses also can get into the brain, where they may remain inactive for decades.\u003c/p>\n\u003cp>Once the researchers knew the viruses were associated with Alzheimer's they started trying to figure out how a virus could affect the course of a brain disease. That meant identifying interactions between the virus genes and other genes in brain cells.\u003c/p>\n\u003cp>\"We mapped out the social network, if you will, of which genes the viruses are friends with and who they're talking to inside the brain,\" Dudley says. In essence, he says, they wanted to know: \"If the viruses are tweeting, who's tweeting back?\"\u003c/p>\n\u003cp>And what they found was that the herpes virus genes were interacting with genes known to increase a person's risk for Alzheimer's.\u003c/p>\n\u003cp>They also found that these Alzheimer's risk genes seem to make a person's brain more vulnerable to infection with the two herpes viruses.\u003c/p>\n\u003cp>But just having herpes virus present in the brain isn't enough to cause Alzheimer's, Dudley says. Something needs to activate the viruses, which causes them to begin replicating.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>It's not clear what causes the activation, Dudley says, though he suspects some sort of change in the internal functions of brain cells.\u003c/p>\n\u003cp>Once the viruses do become active, they appear to influence things like the accumulation of the plaques and tangles in the brain associated with Alzheimer's. \"They are sort of throwing a wrench in the works,\" he says.\u003c/p>\n\u003cp>The herpes viruses also seem to trigger an immune response in certain brain cells, Hodes says. These cells are part of an ancient immune system that has \u003ca href=\"https://www.npr.org/sections/health-shots/2018/02/18/580475245/scientists-explore-ties-between-alzheimers-and-brains-ancient-immune-system\">previously been implicated\u003c/a> in Alzheimer's.\u003c/p>\n\u003cp>Most previous efforts to prevent or treat Alzheimer's have involved trying to reduce the plaques and tangles associated with the disease. Those efforts have failed to improve brain function even when they accomplished their immediate goal.\u003c/p>\n\u003cp>Those \"distressing and disappointing failures\" suggest it's time for some new approaches, Hodes says. And the new study suggests at least two.\u003c/p>\n\u003cp>One is to give antiviral drugs to people with high levels of herpes virus in their brains. The Institute on Aging is already funding a study to test this approach in people in the early stages of Alzheimer's, Hodes says.\u003c/p>\n\u003cp>Another approach is to prevent the brain's immune cells from reacting to the virus in ways that accelerate Alzheimer's, Hodes says. That's tricky, he says, because simply disabling the brain's immune cells could be harmful.\u003c/p>\n\u003cp>Even so, Hodes is optimistic.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\"The more we learn about the disease process and the more targets we can address,\" he says, \"the greater the probability we are going to slow or prevent the progression of Alzheimer's disease.\"\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2018 NPR. To see more, visit http://www.npr.org/.\u003cimg src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=Researchers+Find+Herpes+Viruses+In+Brains+Marked+By+Alzheimer%27s+Disease&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/futureofyou/442958/researchers-find-herpes-viruses-in-alzheimers-brains","authors":["byline_futureofyou_442958"],"categories":["futureofyou_1","futureofyou_73","futureofyou_1064"],"tags":["futureofyou_999","futureofyou_673","futureofyou_952","futureofyou_1056","futureofyou_652"],"collections":["futureofyou_1094"],"featImg":"futureofyou_442960","label":"source_futureofyou_442958"},"futureofyou_440728":{"type":"posts","id":"futureofyou_440728","meta":{"index":"posts_1591205157","site":"futureofyou","id":"440728","score":null,"sort":[1523386836000]},"guestAuthors":[],"slug":"scientists-push-plan-to-change-how-researchers-define-alzheimers","title":"Scientists Push Plan To Change How Researchers Define Alzheimer's","publishDate":1523386836,"format":"standard","headTitle":"KQED Future of You | KQED Science","labelTerm":{},"content":"\u003cp>An international coalition of brain researchers is suggesting a new way of looking at Alzheimer's.\u003c/p>\n\u003cp>Instead of defining the disease through symptoms like memory problems or fuzzy thinking, the scientists want to focus on biological changes in the brain associated with Alzheimer's. These include the plaques and tangles that build up in the brains of people with the disease.\u003c/p>\n\u003cp>But they say the new approach is intended only for research studies, and isn't yet ready for use by most doctors who treat Alzheimer's patients.[contextly_sidebar id=\"Zc2PdHyXHi6M2lDV49kQiFVNaKeIPoB0\"]\u003c/p>\n\u003cp>If the new approach is widely adopted, it would help researchers study patients whose brain function is still normal, but are likely to develop dementia caused by Alzheimer's.\u003c/p>\n\u003cp>\"There is a stage of the disease where there are no symptoms and we need to have some sort of a marker,\" says \u003ca href=\"https://www.nia.nih.gov/research/blog/2016/09/meet-director-division-neuroscience\">Eliezer Masliah\u003c/a>, who directs the Division of Neuroscience at the National Institute on Aging.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>The new approach would be a dramatic departure from the traditional way of looking at Alzheimer's, says \u003ca href=\"http://www.mayo.edu/research/faculty/jack-clifford-r-jr-m-d/bio-00026247\" target=\"_blank\" rel=\"noopener\">Clifford Jack\u003c/a>, an Alzheimer's researcher at Mayo Clinic Rochester.\u003c/p>\n\u003cp>In the past, \"a person displayed a certain set of signs and symptoms and it was expected that they had Alzheimer's pathology,\" says Jack, who is the first author of the central paper describing the proposed new \"research framework.\"[contextly_sidebar id=\"cR0O5c7lGyXeCBcMlKvsHUcXDud9KX3K\"]\u003c/p>\n\u003cp>But researchers began to see the flaws in that approach when they took a close look at the brains of people receiving experimental drugs for the disease, Jack says. \"About 30 percent of people who met all the appropriate clinical criteria did not have Alzheimer's disease.\"\u003c/p>\n\u003cp>Their memory or thinking problems were being caused by something else.\u003c/p>\n\u003cp>So researchers have been looking for more reliable ways of determining whether someone really has Alzheimer's. And they've focused on the two best-known brain changes associated with the disease.\u003c/p>\n\u003cp>\"What we're seeing now is that Alzheimer's disease is defined by the presence of plaques and tangles in your brain,\" Jack says. And in this way of thinking, he says, \"symptoms become the result of the disease, not the definition of the disease.\"\u003c/p>\n\u003cp>Once it was virtually impossible to detect plaques and tangles in a living person. But over time, scientists have developed a number of ways to spot the abnormalities using special brain scans or tests of spinal fluid.[contextly_sidebar id=\"YZk4pmpKdzGmEy59QhebIBpZRwnapuqb\"]\u003c/p>\n\u003cp>These tests for what are known as biomarkers of Alzheimer's are allowing scientists to do experiments that would have been impossible relying on symptoms alone. \"One could, let's say, start preventive treatment five years before the onset of the symptoms,\" Masliah says.\u003c/p>\n\u003cp>The new approach has detractors, who argue that it's not yet a reliable replacement for clinical symptoms in research. And proponents have responded to these complaints by including symptom measures in their proposal, and acknowledging that biomarkers are still in an early stage of development.\u003c/p>\n\u003cp>Proponents have also stressed that the biomarker approach is not yet the right tool for most doctors who treat Alzheimer's patients.\u003c/p>\n\u003cp>\"It's a research framework meant to be tested, a tool for researchers, not for the doctor's office,\" says \u003ca href=\"https://www.alz.org/research/funding/advisory_council_alzheimers_association.asp\" target=\"_blank\" rel=\"noopener\">Maria Carrillo\u003c/a>, chief scientific officer of the Alzheimer's Association.\u003c/p>\n\u003cp>But Carrillo hopes that when drugs to prevent Alzheimer's finally arrive, biomarker tests can show who should get them.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>The proposal, and several commentaries supporting it, appears Tuesday in the April 2018 issue of \u003ca href=\"http://www.alzheimersanddementia.com/\" target=\"_blank\" rel=\"noopener\">\u003cem>Alzheimer's & Dementia: The journal of the Alzheimer's Association\u003c/em>\u003c/a>\u003cem>.\u003c/em>\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2018 NPR. To see more, visit http://www.npr.org/.\u003cimg src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=Scientists+Push+Plan+To+Change+How+Researchers+Define+Alzheimer%27s+&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n","blocks":[],"excerpt":"The new approach would be a dramatic departure from the traditional way of looking at Alzheimer's.","status":"publish","parent":0,"modified":1523383386,"stats":{"hasAudio":false,"hasVideo":false,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":20,"wordCount":604},"headData":{"title":"Scientists Push Plan To Change How Researchers Define Alzheimer's | KQED","description":"The new approach would be a dramatic departure from the traditional way of looking at Alzheimer's.","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":""},"disqusIdentifier":"440728 https://ww2.kqed.org/futureofyou/?p=440728","disqusUrl":"https://ww2.kqed.org/futureofyou/2018/04/10/scientists-push-plan-to-change-how-researchers-define-alzheimers/","disqusTitle":"Scientists Push Plan To Change How Researchers Define Alzheimer's","source":"Health","nprImageCredit":"Cecil Fox","nprByline":"Jon Hamilton\u003cbr />NPR Shots","nprImageAgency":"Science Source","nprStoryId":"600944750","nprApiLink":"http://api.npr.org/query?id=600944750&apiKey=MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004","nprHtmlLink":"https://www.npr.org/sections/health-shots/2018/04/10/600944750/scientists-push-plan-to-change-how-researchers-define-alzheimers?ft=nprml&f=600944750","nprRetrievedStory":"1","nprPubDate":"Tue, 10 Apr 2018 11:34:00 -0400","nprStoryDate":"Tue, 10 Apr 2018 05:04:00 -0400","nprLastModifiedDate":"Tue, 10 Apr 2018 05:50:56 -0400","nprAudio":"https://ondemand.npr.org/anon.npr-mp3/npr/me/2018/04/20180410_me_scientists_push_plan_to_change_how_researchers_define_alzheimers_.mp3?orgId=1&topicId=1128&d=174&p=3&story=600944750&ft=nprml&f=600944750","nprAudioM3u":"http://api.npr.org/m3u/1601072306-f70dc6.m3u?orgId=1&topicId=1128&d=174&p=3&story=600944750&ft=nprml&f=600944750","path":"/futureofyou/440728/scientists-push-plan-to-change-how-researchers-define-alzheimers","audioUrl":"https://ondemand.npr.org/anon.npr-mp3/npr/me/2018/04/20180410_me_scientists_push_plan_to_change_how_researchers_define_alzheimers_.mp3?orgId=1&topicId=1128&d=174&p=3&story=600944750&ft=nprml&f=600944750","audioTrackLength":null,"parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003cp>An international coalition of brain researchers is suggesting a new way of looking at Alzheimer's.\u003c/p>\n\u003cp>Instead of defining the disease through symptoms like memory problems or fuzzy thinking, the scientists want to focus on biological changes in the brain associated with Alzheimer's. These include the plaques and tangles that build up in the brains of people with the disease.\u003c/p>\n\u003cp>But they say the new approach is intended only for research studies, and isn't yet ready for use by most doctors who treat Alzheimer's patients.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>If the new approach is widely adopted, it would help researchers study patients whose brain function is still normal, but are likely to develop dementia caused by Alzheimer's.\u003c/p>\n\u003cp>\"There is a stage of the disease where there are no symptoms and we need to have some sort of a marker,\" says \u003ca href=\"https://www.nia.nih.gov/research/blog/2016/09/meet-director-division-neuroscience\">Eliezer Masliah\u003c/a>, who directs the Division of Neuroscience at the National Institute on Aging.\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>The new approach would be a dramatic departure from the traditional way of looking at Alzheimer's, says \u003ca href=\"http://www.mayo.edu/research/faculty/jack-clifford-r-jr-m-d/bio-00026247\" target=\"_blank\" rel=\"noopener\">Clifford Jack\u003c/a>, an Alzheimer's researcher at Mayo Clinic Rochester.\u003c/p>\n\u003cp>In the past, \"a person displayed a certain set of signs and symptoms and it was expected that they had Alzheimer's pathology,\" says Jack, who is the first author of the central paper describing the proposed new \"research framework.\"\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>But researchers began to see the flaws in that approach when they took a close look at the brains of people receiving experimental drugs for the disease, Jack says. \"About 30 percent of people who met all the appropriate clinical criteria did not have Alzheimer's disease.\"\u003c/p>\n\u003cp>Their memory or thinking problems were being caused by something else.\u003c/p>\n\u003cp>So researchers have been looking for more reliable ways of determining whether someone really has Alzheimer's. And they've focused on the two best-known brain changes associated with the disease.\u003c/p>\n\u003cp>\"What we're seeing now is that Alzheimer's disease is defined by the presence of plaques and tangles in your brain,\" Jack says. And in this way of thinking, he says, \"symptoms become the result of the disease, not the definition of the disease.\"\u003c/p>\n\u003cp>Once it was virtually impossible to detect plaques and tangles in a living person. But over time, scientists have developed a number of ways to spot the abnormalities using special brain scans or tests of spinal fluid.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>These tests for what are known as biomarkers of Alzheimer's are allowing scientists to do experiments that would have been impossible relying on symptoms alone. \"One could, let's say, start preventive treatment five years before the onset of the symptoms,\" Masliah says.\u003c/p>\n\u003cp>The new approach has detractors, who argue that it's not yet a reliable replacement for clinical symptoms in research. And proponents have responded to these complaints by including symptom measures in their proposal, and acknowledging that biomarkers are still in an early stage of development.\u003c/p>\n\u003cp>Proponents have also stressed that the biomarker approach is not yet the right tool for most doctors who treat Alzheimer's patients.\u003c/p>\n\u003cp>\"It's a research framework meant to be tested, a tool for researchers, not for the doctor's office,\" says \u003ca href=\"https://www.alz.org/research/funding/advisory_council_alzheimers_association.asp\" target=\"_blank\" rel=\"noopener\">Maria Carrillo\u003c/a>, chief scientific officer of the Alzheimer's Association.\u003c/p>\n\u003cp>But Carrillo hopes that when drugs to prevent Alzheimer's finally arrive, biomarker tests can show who should get them.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>The proposal, and several commentaries supporting it, appears Tuesday in the April 2018 issue of \u003ca href=\"http://www.alzheimersanddementia.com/\" target=\"_blank\" rel=\"noopener\">\u003cem>Alzheimer's & Dementia: The journal of the Alzheimer's Association\u003c/em>\u003c/a>\u003cem>.\u003c/em>\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2018 NPR. To see more, visit http://www.npr.org/.\u003cimg src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=Scientists+Push+Plan+To+Change+How+Researchers+Define+Alzheimer%27s+&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/futureofyou/440728/scientists-push-plan-to-change-how-researchers-define-alzheimers","authors":["byline_futureofyou_440728"],"categories":["futureofyou_452","futureofyou_1"],"tags":["futureofyou_999","futureofyou_56","futureofyou_1023","futureofyou_141","futureofyou_61","futureofyou_1056"],"featImg":"futureofyou_440729","label":"source_futureofyou_440728"},"futureofyou_439938":{"type":"posts","id":"futureofyou_439938","meta":{"index":"posts_1591205157","site":"futureofyou","id":"439938","score":null,"sort":[1520029180000]},"guestAuthors":[],"slug":"scientists-sip-beer-discover-link-between-alzheimers-and-brains-ancient-immune-system","title":"Scientists Sip Beer, Discover Link Between Alzheimer's And Brain's Ancient Immune System","publishDate":1520029180,"format":"standard","headTitle":"KQED Future of You | KQED Science","labelTerm":{"site":"futureofyou"},"content":"\u003cp>Beer has fueled a lot of bad ideas. But on a Friday afternoon in 2007, it helped two Alzheimer's researchers come up with a really a good one.\u003c/p>\n\u003cp>Neuroscientists \u003ca href=\"http://www.massgeneral.org/neurology/researcher_profiles/moir_robert.aspx\">Robert Moir\u003c/a> and \u003ca href=\"http://www.massgeneral.org/neurology/researcher_profiles/tanzi_rudolph.aspx\">Rudolph Tanzi\u003c/a> were sipping Coronas in separate offices during \"attitude adjustment hour\" at Massachusetts General Hospital, Harvard's largest teaching hospital. And, by chance, each scientist found himself wondering about an apparent link between Alzheimer's disease and the immune system.\u003c/p>\n\u003cp>Moir had been surfing through random scientific papers online — something he does for an hour or so on most Fridays. \"I cruise wherever my fancy takes me,\" he says.[contextly_sidebar id=\"7M1TEDtx5VpvYNAuLZ4fq7p1cSKlsEay\"]\u003c/p>\n\u003cp>And on this day, he cruised to research on molecules known as antimicrobial peptides. They're part of the ancient immune system that's found in all forms of life and plays an important role in protecting the human brain.\u003c/p>\n\u003cp>One way antimicrobial peptides protect us is by engulfing and neutralizing a germ or some other foreign invader. That gives newer parts of the immune system time to get mobilized.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>These peptides are \"extremely important,\" Moir says. \"They're not like legacies from an immune system we don't use anymore. If you don't have them, you're going to die in a couple of hours.\"\u003c/p>\n\u003caside class=\"pullquote alignright\">'What if those sticky plaques were actually an effort to protect the brain.'\u003c/aside>\n\u003cp>As Moir surfed through paper after paper, he realized that one of these ancient molecules, known as LL-37, looked a lot like a molecule closely associated with Alzheimer's. That molecule is called amyloid-beta and it forms the sticky plaques that tend to build up in the brains of people with dementia[contextly_sidebar id=\"IYHDaMptIPqJzYR9l5XweOSqbSXwwBlK\"]\u003c/p>\n\u003cp>LL-37 and Amyloid-beta \"looked just like peas in a pod,\" Moir says.\u003c/p>\n\u003cp>That was really surprising. Even more surprising, on that same Friday afternoon, Moir's colleague Tanzi had also noticed a connection between Alzheimer's and the ancient immune system, which scientists refer to as innate immunity.\u003c/p>\n\u003cp>Tanzi had been spending the same hour that Friday afternoon reviewing a list of genes he'd found that were somehow related to Alzheimer's. \"I was enjoying my first or second Corona,\" he says, \"and I noticed that many of the genes coming up were involved with innate immunity.\"\u003c/p>\n\u003cp>\"I was like, well, what does that mean?\" Tanzi says. \"So I wandered into [Moir's] office, carrying my Corona in hand, and I said, 'What do you know about innate immunity in the brain?' \"\u003c/p>\n\u003cp>The two researchers decided to team up to figure out precisely how innate immunity figures into Alzheimer's. They later sketched out their research plan while sipping Bordeaux on the deck of Tanzi's house along the coast.\u003c/p>\n\u003cp>\"We spent a lot of evenings out there making a dent in his very nice cellar,\" Moir says.\u003c/p>\n\u003cp>\u003cstrong>The Brain's Immune System\u003c/strong>\u003cbr>\nThe two scientists began to discuss a wild idea. What if amyloid-beta was an integral part of the ancient immune system? What if those sticky plaques were actually an effort to protect the brain by encapsulating foreign invaders?\u003c/p>\n\u003cp>Their idea was that the brain was producing amyloid for much the same reason an oyster forms a pearl — for self-defense. \"Maybe amyloid plaques are a brain pearl,\" Moir says, \"a way for our body to trap and permanently sequester these invading pathogens.\"\u003c/p>\n\u003cp>That was a pretty radical idea. For decades, most scientists thought amyloid-beta was no more than a toxic waste product. \"In all those scenarios it's bad, bad, bad, bad, bad,\" Moir says.\u003c/p>\n\u003cp>But Moir and Tanzi suspected amyloid-beta was usually good — unless the brain started making too much. Then it could kill brain cells and lead to dementia.\u003c/p>\n\u003cp>This hypothesis was not immediately embraced by other scientists, Tanzi says.\u003c/p>\n\u003caside class=\"pullquote alignright\">'It may be possible to interrupt the process before it causes Alzheimer's.'\u003c/aside>\n\u003cp>\"I had folks emailing me, ex-mentors — Nobel laureates — saying, 'Rudy have you lost your mind?' Luckily neither Rob nor I have a really good track record of listening to people.\"\u003c/p>\n\u003cp>So. Tanzi and Moir set out to prove that amyloid really is part of the immune system. And they were lucky enough to have a funder, the \u003ca href=\"https://curealz.org/\">Cure Alzheimer's Fund\u003c/a>, that was willing to take a chance on their idea.\u003c/p>\n\u003cp>The effort took years. But in 2010, Moir, Tanzi, and their team \u003ca href=\"http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0009505\">demonstrated\u003c/a> that amyloid is really good at killing viruses and bacteria in a test tube. And, in 2016, they \u003ca href=\"http://stm.sciencemag.org/content/8/340/340ra72\">showed\u003c/a> it did the same thing in worms and mice.\u003c/p>\n\u003cp>\"It was very clear that amyloid protected against infection,\" Tanzi says. \"If a mouse had meningitis or encephalitis, [and] if that mouse was making amyloid it lived longer.\" In contrast, mice that did not produce amyloid died quickly from the infection.\u003c/p>\n\u003cp>\u003cimg class=\" wp-image-93427 alignleft\" src=\"https://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2016/01/iStock_000060595932_Large-800x600.jpg\" alt=\"\" width=\"401\" height=\"301\" srcset=\"https://ww2.kqed.org/app/uploads/sites/13/2016/01/iStock_000060595932_Large-800x600.jpg 800w, https://ww2.kqed.org/app/uploads/sites/13/2016/01/iStock_000060595932_Large-400x300.jpg 400w, https://ww2.kqed.org/app/uploads/sites/13/2016/01/iStock_000060595932_Large-768x576.jpg 768w, https://ww2.kqed.org/app/uploads/sites/13/2016/01/iStock_000060595932_Large-1180x885.jpg 1180w, https://ww2.kqed.org/app/uploads/sites/13/2016/01/iStock_000060595932_Large-1920x1440.jpg 1920w, https://ww2.kqed.org/app/uploads/sites/13/2016/01/iStock_000060595932_Large-960x720.jpg 960w\" sizes=\"(max-width: 401px) 100vw, 401px\">Today, Tanzi and Moir's wild idea is no longer considered so wild. Lots of scientists are now \u003ca href=\"https://www.nature.com/articles/ng.3916\">studying\u003c/a> the ancient immune system's connection to Alzheimer's.\u003c/p>\n\u003cp>And Tanzi says it's become clear that Alzheimer's involves a lot more than just plaques and tangles in the brain.\u003c/p>\n\u003cp>\"Even though we really concentrate on these plaques and tangles in Alzheimer's disease, it looks like it's the brain's immune system — the very primitive immune system of the brain — that's gone awry,\" Tanzi says, \"and the plaques and tangles are a part of that system.\"\u003c/p>\n\u003cp>The question now is: What's causing the glitch in the ancient immune system?\u003c/p>\n\u003cp>One possibility is that it's overreacting to viruses and bacteria that get into the brain. Or, the system could be getting confused and attacking healthy cells — a lot like what happens in diseases like lupus or multiple sclerosis.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>If either idea holds up, it may be possible to interrupt the process before it causes Alzheimer's, Moir says. \"That's a pretty good outcome from a couple of Coronas 10 years ago.\"\u003c/p>\n\u003cdiv class=\"fullattribution\">\u003cem>Copyright 2018 NPR. To see more, visit \u003ca href=\"http://www.npr.org/\" target=\"_blank\" rel=\"noopener\">http://www.npr.org/\u003c/a>.\u003cimg src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=Scientists+Explore+Ties+Between+Alzheimer%27s+And+Brain%27s+Ancient+Immune+System&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/em>\u003c/div>\n\n","blocks":[],"excerpt":"Harvard researchers explain why they think Alzheimer's disease may be traced to an immunity glitch.","status":"publish","parent":0,"modified":1520097160,"stats":{"hasAudio":false,"hasVideo":false,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":30,"wordCount":1008},"headData":{"title":"Scientists Sip Beer, Discover Link Between Alzheimer's And Brain's Ancient Immune System | KQED","description":"Harvard researchers explain why they think Alzheimer's disease may be traced to an immunity glitch.","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":""},"disqusIdentifier":"439938 https://ww2.kqed.org/futureofyou/?p=439938","disqusUrl":"https://ww2.kqed.org/futureofyou/2018/03/02/scientists-sip-beer-discover-link-between-alzheimers-and-brains-ancient-immune-system/","disqusTitle":"Scientists Sip Beer, Discover Link Between Alzheimer's And Brain's Ancient Immune System","nprImageCredit":"Martin M. Rotker","nprByline":"Jon Hamilton\u003cbr />NPR Shots","nprImageAgency":"Science Source","nprStoryId":"580475245","nprApiLink":"http://api.npr.org/query?id=580475245&apiKey=MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004","nprHtmlLink":"https://www.npr.org/sections/health-shots/2018/02/18/580475245/scientists-explore-ties-between-alzheimers-and-brains-ancient-immune-system?ft=nprml&f=580475245","nprRetrievedStory":"1","nprPubDate":"Tue, 20 Feb 2018 17:31:00 -0500","nprStoryDate":"Sun, 18 Feb 2018 05:00:00 -0500","nprLastModifiedDate":"Tue, 20 Feb 2018 17:31:55 -0500","path":"/futureofyou/439938/scientists-sip-beer-discover-link-between-alzheimers-and-brains-ancient-immune-system","audioTrackLength":null,"parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003cp>Beer has fueled a lot of bad ideas. But on a Friday afternoon in 2007, it helped two Alzheimer's researchers come up with a really a good one.\u003c/p>\n\u003cp>Neuroscientists \u003ca href=\"http://www.massgeneral.org/neurology/researcher_profiles/moir_robert.aspx\">Robert Moir\u003c/a> and \u003ca href=\"http://www.massgeneral.org/neurology/researcher_profiles/tanzi_rudolph.aspx\">Rudolph Tanzi\u003c/a> were sipping Coronas in separate offices during \"attitude adjustment hour\" at Massachusetts General Hospital, Harvard's largest teaching hospital. And, by chance, each scientist found himself wondering about an apparent link between Alzheimer's disease and the immune system.\u003c/p>\n\u003cp>Moir had been surfing through random scientific papers online — something he does for an hour or so on most Fridays. \"I cruise wherever my fancy takes me,\" he says.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>And on this day, he cruised to research on molecules known as antimicrobial peptides. They're part of the ancient immune system that's found in all forms of life and plays an important role in protecting the human brain.\u003c/p>\n\u003cp>One way antimicrobial peptides protect us is by engulfing and neutralizing a germ or some other foreign invader. That gives newer parts of the immune system time to get mobilized.\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>These peptides are \"extremely important,\" Moir says. \"They're not like legacies from an immune system we don't use anymore. If you don't have them, you're going to die in a couple of hours.\"\u003c/p>\n\u003caside class=\"pullquote alignright\">'What if those sticky plaques were actually an effort to protect the brain.'\u003c/aside>\n\u003cp>As Moir surfed through paper after paper, he realized that one of these ancient molecules, known as LL-37, looked a lot like a molecule closely associated with Alzheimer's. That molecule is called amyloid-beta and it forms the sticky plaques that tend to build up in the brains of people with dementia\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>LL-37 and Amyloid-beta \"looked just like peas in a pod,\" Moir says.\u003c/p>\n\u003cp>That was really surprising. Even more surprising, on that same Friday afternoon, Moir's colleague Tanzi had also noticed a connection between Alzheimer's and the ancient immune system, which scientists refer to as innate immunity.\u003c/p>\n\u003cp>Tanzi had been spending the same hour that Friday afternoon reviewing a list of genes he'd found that were somehow related to Alzheimer's. \"I was enjoying my first or second Corona,\" he says, \"and I noticed that many of the genes coming up were involved with innate immunity.\"\u003c/p>\n\u003cp>\"I was like, well, what does that mean?\" Tanzi says. \"So I wandered into [Moir's] office, carrying my Corona in hand, and I said, 'What do you know about innate immunity in the brain?' \"\u003c/p>\n\u003cp>The two researchers decided to team up to figure out precisely how innate immunity figures into Alzheimer's. They later sketched out their research plan while sipping Bordeaux on the deck of Tanzi's house along the coast.\u003c/p>\n\u003cp>\"We spent a lot of evenings out there making a dent in his very nice cellar,\" Moir says.\u003c/p>\n\u003cp>\u003cstrong>The Brain's Immune System\u003c/strong>\u003cbr>\nThe two scientists began to discuss a wild idea. What if amyloid-beta was an integral part of the ancient immune system? What if those sticky plaques were actually an effort to protect the brain by encapsulating foreign invaders?\u003c/p>\n\u003cp>Their idea was that the brain was producing amyloid for much the same reason an oyster forms a pearl — for self-defense. \"Maybe amyloid plaques are a brain pearl,\" Moir says, \"a way for our body to trap and permanently sequester these invading pathogens.\"\u003c/p>\n\u003cp>That was a pretty radical idea. For decades, most scientists thought amyloid-beta was no more than a toxic waste product. \"In all those scenarios it's bad, bad, bad, bad, bad,\" Moir says.\u003c/p>\n\u003cp>But Moir and Tanzi suspected amyloid-beta was usually good — unless the brain started making too much. Then it could kill brain cells and lead to dementia.\u003c/p>\n\u003cp>This hypothesis was not immediately embraced by other scientists, Tanzi says.\u003c/p>\n\u003caside class=\"pullquote alignright\">'It may be possible to interrupt the process before it causes Alzheimer's.'\u003c/aside>\n\u003cp>\"I had folks emailing me, ex-mentors — Nobel laureates — saying, 'Rudy have you lost your mind?' Luckily neither Rob nor I have a really good track record of listening to people.\"\u003c/p>\n\u003cp>So. Tanzi and Moir set out to prove that amyloid really is part of the immune system. And they were lucky enough to have a funder, the \u003ca href=\"https://curealz.org/\">Cure Alzheimer's Fund\u003c/a>, that was willing to take a chance on their idea.\u003c/p>\n\u003cp>The effort took years. But in 2010, Moir, Tanzi, and their team \u003ca href=\"http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0009505\">demonstrated\u003c/a> that amyloid is really good at killing viruses and bacteria in a test tube. And, in 2016, they \u003ca href=\"http://stm.sciencemag.org/content/8/340/340ra72\">showed\u003c/a> it did the same thing in worms and mice.\u003c/p>\n\u003cp>\"It was very clear that amyloid protected against infection,\" Tanzi says. \"If a mouse had meningitis or encephalitis, [and] if that mouse was making amyloid it lived longer.\" In contrast, mice that did not produce amyloid died quickly from the infection.\u003c/p>\n\u003cp>\u003cimg class=\" wp-image-93427 alignleft\" src=\"https://ww2.kqed.org/futureofyou/wp-content/uploads/sites/13/2016/01/iStock_000060595932_Large-800x600.jpg\" alt=\"\" width=\"401\" height=\"301\" srcset=\"https://ww2.kqed.org/app/uploads/sites/13/2016/01/iStock_000060595932_Large-800x600.jpg 800w, https://ww2.kqed.org/app/uploads/sites/13/2016/01/iStock_000060595932_Large-400x300.jpg 400w, https://ww2.kqed.org/app/uploads/sites/13/2016/01/iStock_000060595932_Large-768x576.jpg 768w, https://ww2.kqed.org/app/uploads/sites/13/2016/01/iStock_000060595932_Large-1180x885.jpg 1180w, https://ww2.kqed.org/app/uploads/sites/13/2016/01/iStock_000060595932_Large-1920x1440.jpg 1920w, https://ww2.kqed.org/app/uploads/sites/13/2016/01/iStock_000060595932_Large-960x720.jpg 960w\" sizes=\"(max-width: 401px) 100vw, 401px\">Today, Tanzi and Moir's wild idea is no longer considered so wild. Lots of scientists are now \u003ca href=\"https://www.nature.com/articles/ng.3916\">studying\u003c/a> the ancient immune system's connection to Alzheimer's.\u003c/p>\n\u003cp>And Tanzi says it's become clear that Alzheimer's involves a lot more than just plaques and tangles in the brain.\u003c/p>\n\u003cp>\"Even though we really concentrate on these plaques and tangles in Alzheimer's disease, it looks like it's the brain's immune system — the very primitive immune system of the brain — that's gone awry,\" Tanzi says, \"and the plaques and tangles are a part of that system.\"\u003c/p>\n\u003cp>The question now is: What's causing the glitch in the ancient immune system?\u003c/p>\n\u003cp>One possibility is that it's overreacting to viruses and bacteria that get into the brain. Or, the system could be getting confused and attacking healthy cells — a lot like what happens in diseases like lupus or multiple sclerosis.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>If either idea holds up, it may be possible to interrupt the process before it causes Alzheimer's, Moir says. \"That's a pretty good outcome from a couple of Coronas 10 years ago.\"\u003c/p>\n\u003cdiv class=\"fullattribution\">\u003cem>Copyright 2018 NPR. To see more, visit \u003ca href=\"http://www.npr.org/\" target=\"_blank\" rel=\"noopener\">http://www.npr.org/\u003c/a>.\u003cimg src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=Scientists+Explore+Ties+Between+Alzheimer%27s+And+Brain%27s+Ancient+Immune+System&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/em>\u003c/div>\n\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/futureofyou/439938/scientists-sip-beer-discover-link-between-alzheimers-and-brains-ancient-immune-system","authors":["byline_futureofyou_439938"],"categories":["futureofyou_1","futureofyou_73"],"tags":["futureofyou_532","futureofyou_999","futureofyou_56","futureofyou_141","futureofyou_426","futureofyou_61","futureofyou_327"],"featImg":"futureofyou_439939","label":"futureofyou"},"futureofyou_439750":{"type":"posts","id":"futureofyou_439750","meta":{"index":"posts_1591205157","site":"futureofyou","id":"439750","score":null,"sort":[1519426064000]},"guestAuthors":[],"slug":"superagers-maintain-memory-into-80s-and-90s","title":"‘Superagers’ Maintain Memory Into 80s and 90s","publishDate":1519426064,"format":"standard","headTitle":"KQED Future of You | KQED Science","labelTerm":{"term":1093,"site":"futureofyou"},"content":"\u003cp>It's pretty extraordinary for people in their 80s and 90s to keep the same sharp memory as someone several decades younger, and now scientists are peeking into the brains of these \"superagers\" to uncover their secret.\u003c/p>\n\u003cp>The work is the flip side of the disappointing hunt for new drugs to fight or prevent Alzheimer's disease.\u003c/p>\n\u003cp>Instead, \"why don't we figure out what it is we might need to do to maximize our memory?\" said neuroscientist Emily Rogalski, who leads the SuperAging study at Northwestern University in Chicago.\u003c/p>\n\u003cp>Parts of the brain shrink with age, one of the reasons why most [contextly_sidebar id=\"G3H8QC9o82TylnWZAr296D2zVHqEWAob\"]people experience a gradual slowing of at least some types of memory late in life, even if they avoid diseases like Alzheimer's.\u003c/p>\n\u003cp>But it turns out that superagers' brains aren't shrinking nearly as fast as their peers'. And autopsies of the first superagers to die during the study show they harbor a lot more of a special kind of nerve cell in a deep brain region that's important for attention, Rogalski told a recent meeting of the American Association for the Advancement of Science.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>These elite elders are \"more than just an oddity or a rarity,\" said neuroscientist Molly Wagster of the National Institute on Aging, which helps fund the research. \"There's the potential for learning an enormous amount and applying it to the rest of us, and even to those who may be on a trajectory for some type of neurodegenerative disease.\"\u003c/p>\n\u003cp>What does it take to be a superager? A youthful brain in the body of someone 80 or older. Rogalski's team has given a battery of tests to more than 1,000 people who thought they'd qualify, and only about 5 percent pass. The key \u003ca href=\"https://ww2.kqed.org/futureofyou/2018/02/07/a-tiny-pulse-of-electricity-to-the-brain-can-boost-memory/\" target=\"_blank\" rel=\"noopener\">memory challenge\u003c/a>: Listen to 15 unrelated words, and a half-hour later recall at least nine. That's the norm for 50-year-olds, but the average 80-year-old recalls five. Some superagers remember them all.[contextly_sidebar id=\"CmEYEjCmwB2h2qN7hBJIIlooU2YvQ8dj\"]\u003c/p>\n\u003cp>\"It doesn't mean you're any smarter,\" stressed superager William \"Bill\" Gurolnick, who turns 87 next month and joined the study two years ago.\u003c/p>\n\u003cp>Nor can he credit protective genes: Gurolnick's father developed Alzheimer's in his 50s. He thinks his own \u003ca href=\"https://ww2.kqed.org/perspectives/2018/02/12/the-memory-of-stuff/\" target=\"_blank\" rel=\"noopener\">stellar memory\u003c/a> is bolstered by keeping busy. He bikes, and plays tennis and water volleyball. He stays social through regular lunches and meetings with a men's group he co-founded.\u003c/p>\n\u003cp>\"Absolutely that's a critical factor about keeping your wits about you,\" exclaimed Gurolnick, fresh off his monthly gin game.\u003c/p>\n\u003cp>\u003cstrong>Brain Scans\u003c/strong>\u003c/p>\n\u003cp>Rogalski's superagers tend to be extroverts and report strong social networks, but otherwise they come from all walks of life, making it hard to find a common trait \u003ca href=\"https://ww2.kqed.org/forum/2017/04/11/emotions-are-a-construct-of-the-brain-says-psychologist-lisa-feldman-barrett/\" target=\"_blank\" rel=\"noopener\">for brain health\u003c/a>. Some went to college, some didn't. Some have high IQs, some are average. She's studied people who've experienced enormous trauma, including a Holocaust survivor; fitness buffs and smokers; teetotalers and those who tout a nightly martini.\u003c/p>\n\u003cp>But deep in their brains is where she's finding compelling hints that somehow, superagers are more resilient against the ravages of time.\u003c/p>\n\u003cp>Early on, brain scans showed that a superager's cortex — an outer brain layer critical for memory and other key functions — is much thicker than normal for their age. It looks more like the cortex of healthy 50- and 60-year-olds.\u003c/p>\n\u003cp>It's not clear if they were born that way. But Rogalski's team found another possible explanation: A superager's cortex doesn't shrink as fast. Over 18 months, average 80-somethings experienced more than twice the rate of loss.\u003c/p>\n\u003cp>Another clue: Deeper in the brain, that attention region is larger in superagers, too. And inside, autopsies showed that brain region was packed with unusual large, spindly neurons — a special and little understood type called von Economo neurons thought to play a role in social processing and awareness.\u003c/p>\n\u003cp>The superagers had four to five times more of those neurons than the typical octogenarian, Rogalski said — more even than the average young adult.[contextly_sidebar id=\"AJFvjFXNb2dpYXWnAkrRzU9vWHQngSNl\"]\u003c/p>\n\u003cp>The Northwestern study isn't the only attempt at unraveling long-lasting memory. At the University of California, Irvine, Dr. Claudia Kawas studies the oldest-old, people 90 and above. Some have Alzheimer's. Some have maintained excellent memory and some are in between.\u003c/p>\n\u003cp>About 40 percent of the oldest-old who showed no symptoms of dementia in life nonetheless have full-fledged signs of Alzheimer's disease\u003ca href=\"https://ww2.kqed.org/stateofhealth/2017/08/09/lag-in-brain-donation-hampers-understanding-of-dementia-in-blacks/\" target=\"_blank\" rel=\"noopener\"> in their brains\u003c/a> at death, Kawas told the AAAS meeting.\u003c/p>\n\u003cp>Rogalski also found varying amounts of amyloid and tau, hallmark Alzheimer's proteins, in the brains of some superagers.\u003c/p>\n\u003cp>Now scientists are exploring how these people deflect damage. Maybe superagers have different pathways\u003ca href=\"https://ww2.kqed.org/futureofyou/2017/01/06/obesity-can-lead-to-memory-loss/\" target=\"_blank\" rel=\"noopener\"> to brain health.\u003c/a>\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\"They are living long and living well,\" Rogalski said. \"Are there modifiable things we can think about today, in our everyday lives\" to do the same?\u003c/p>\n\n","blocks":[],"excerpt":"Scientists are peeking into the brains of \"superagers\" to uncover their secrets to sharp memory.","status":"publish","parent":0,"modified":1519426064,"stats":{"hasAudio":false,"hasVideo":false,"hasChartOrMap":false,"iframeSrcs":[],"hasGoogleForm":false,"hasGallery":false,"hasHearkenModule":false,"hasPolis":false,"paragraphCount":24,"wordCount":835},"headData":{"title":"‘Superagers’ Maintain Memory Into 80s and 90s | KQED","description":"Scientists are peeking into the brains of "superagers" to uncover their secrets to sharp memory.","ogTitle":"","ogDescription":"","ogImgId":"","twTitle":"","twDescription":"","twImgId":""},"disqusIdentifier":"439750 https://ww2.kqed.org/futureofyou/?p=439750","disqusUrl":"https://ww2.kqed.org/futureofyou/2018/02/23/superagers-maintain-memory-into-80s-and-90s/","disqusTitle":"‘Superagers’ Maintain Memory Into 80s and 90s","nprByline":"Lauran Neergaard\u003cbr />The Associated Press","path":"/futureofyou/439750/superagers-maintain-memory-into-80s-and-90s","audioTrackLength":null,"parsedContent":[{"type":"contentString","content":"\u003cdiv class=\"post-body\">\u003cp>\u003cp>It's pretty extraordinary for people in their 80s and 90s to keep the same sharp memory as someone several decades younger, and now scientists are peeking into the brains of these \"superagers\" to uncover their secret.\u003c/p>\n\u003cp>The work is the flip side of the disappointing hunt for new drugs to fight or prevent Alzheimer's disease.\u003c/p>\n\u003cp>Instead, \"why don't we figure out what it is we might need to do to maximize our memory?\" said neuroscientist Emily Rogalski, who leads the SuperAging study at Northwestern University in Chicago.\u003c/p>\n\u003cp>Parts of the brain shrink with age, one of the reasons why most \u003c/p>\u003cp>\u003c/p>\u003cp>people experience a gradual slowing of at least some types of memory late in life, even if they avoid diseases like Alzheimer's.\u003c/p>\n\u003cp>But it turns out that superagers' brains aren't shrinking nearly as fast as their peers'. And autopsies of the first superagers to die during the study show they harbor a lot more of a special kind of nerve cell in a deep brain region that's important for attention, Rogalski told a recent meeting of the American Association for the Advancement of Science.\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>These elite elders are \"more than just an oddity or a rarity,\" said neuroscientist Molly Wagster of the National Institute on Aging, which helps fund the research. \"There's the potential for learning an enormous amount and applying it to the rest of us, and even to those who may be on a trajectory for some type of neurodegenerative disease.\"\u003c/p>\n\u003cp>What does it take to be a superager? A youthful brain in the body of someone 80 or older. Rogalski's team has given a battery of tests to more than 1,000 people who thought they'd qualify, and only about 5 percent pass. The key \u003ca href=\"https://ww2.kqed.org/futureofyou/2018/02/07/a-tiny-pulse-of-electricity-to-the-brain-can-boost-memory/\" target=\"_blank\" rel=\"noopener\">memory challenge\u003c/a>: Listen to 15 unrelated words, and a half-hour later recall at least nine. That's the norm for 50-year-olds, but the average 80-year-old recalls five. Some superagers remember them all.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>\"It doesn't mean you're any smarter,\" stressed superager William \"Bill\" Gurolnick, who turns 87 next month and joined the study two years ago.\u003c/p>\n\u003cp>Nor can he credit protective genes: Gurolnick's father developed Alzheimer's in his 50s. He thinks his own \u003ca href=\"https://ww2.kqed.org/perspectives/2018/02/12/the-memory-of-stuff/\" target=\"_blank\" rel=\"noopener\">stellar memory\u003c/a> is bolstered by keeping busy. He bikes, and plays tennis and water volleyball. He stays social through regular lunches and meetings with a men's group he co-founded.\u003c/p>\n\u003cp>\"Absolutely that's a critical factor about keeping your wits about you,\" exclaimed Gurolnick, fresh off his monthly gin game.\u003c/p>\n\u003cp>\u003cstrong>Brain Scans\u003c/strong>\u003c/p>\n\u003cp>Rogalski's superagers tend to be extroverts and report strong social networks, but otherwise they come from all walks of life, making it hard to find a common trait \u003ca href=\"https://ww2.kqed.org/forum/2017/04/11/emotions-are-a-construct-of-the-brain-says-psychologist-lisa-feldman-barrett/\" target=\"_blank\" rel=\"noopener\">for brain health\u003c/a>. Some went to college, some didn't. Some have high IQs, some are average. She's studied people who've experienced enormous trauma, including a Holocaust survivor; fitness buffs and smokers; teetotalers and those who tout a nightly martini.\u003c/p>\n\u003cp>But deep in their brains is where she's finding compelling hints that somehow, superagers are more resilient against the ravages of time.\u003c/p>\n\u003cp>Early on, brain scans showed that a superager's cortex — an outer brain layer critical for memory and other key functions — is much thicker than normal for their age. It looks more like the cortex of healthy 50- and 60-year-olds.\u003c/p>\n\u003cp>It's not clear if they were born that way. But Rogalski's team found another possible explanation: A superager's cortex doesn't shrink as fast. Over 18 months, average 80-somethings experienced more than twice the rate of loss.\u003c/p>\n\u003cp>Another clue: Deeper in the brain, that attention region is larger in superagers, too. And inside, autopsies showed that brain region was packed with unusual large, spindly neurons — a special and little understood type called von Economo neurons thought to play a role in social processing and awareness.\u003c/p>\n\u003cp>The superagers had four to five times more of those neurons than the typical octogenarian, Rogalski said — more even than the average young adult.\u003c/p>\u003cp>\u003c/p>\u003cp>\u003c/p>\n\u003cp>The Northwestern study isn't the only attempt at unraveling long-lasting memory. At the University of California, Irvine, Dr. Claudia Kawas studies the oldest-old, people 90 and above. Some have Alzheimer's. Some have maintained excellent memory and some are in between.\u003c/p>\n\u003cp>About 40 percent of the oldest-old who showed no symptoms of dementia in life nonetheless have full-fledged signs of Alzheimer's disease\u003ca href=\"https://ww2.kqed.org/stateofhealth/2017/08/09/lag-in-brain-donation-hampers-understanding-of-dementia-in-blacks/\" target=\"_blank\" rel=\"noopener\"> in their brains\u003c/a> at death, Kawas told the AAAS meeting.\u003c/p>\n\u003cp>Rogalski also found varying amounts of amyloid and tau, hallmark Alzheimer's proteins, in the brains of some superagers.\u003c/p>\n\u003cp>Now scientists are exploring how these people deflect damage. Maybe superagers have different pathways\u003ca href=\"https://ww2.kqed.org/futureofyou/2017/01/06/obesity-can-lead-to-memory-loss/\" target=\"_blank\" rel=\"noopener\"> to brain health.\u003c/a>\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>\"They are living long and living well,\" Rogalski said. \"Are there modifiable things we can think about today, in our everyday lives\" to do the same?\u003c/p>\n\n\u003c/div>\u003c/p>","attributes":{"named":{},"numeric":[]}}],"link":"/futureofyou/439750/superagers-maintain-memory-into-80s-and-90s","authors":["byline_futureofyou_439750"],"categories":["futureofyou_1060","futureofyou_1"],"tags":["futureofyou_999","futureofyou_56","futureofyou_1008","futureofyou_61","futureofyou_1047"],"collections":["futureofyou_1093"],"featImg":"futureofyou_439764","label":"futureofyou_1093"}},"programsReducer":{"possible":{"id":"possible","title":"Possible","info":"Possible is hosted by entrepreneur Reid Hoffman and writer Aria Finger. 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Hosted by journalists of color, the show tackles the subject of race head-on, exploring how it impacts every part of society — from politics and pop culture to history, sports and more.\u003cbr />\u003cbr />\u003cem>Life Kit\u003c/em>, which will be in the second part of the hour, guides you through spaces and feelings no one prepares you for — from finances to mental health, from workplace microaggressions to imposter syndrome, from relationships to parenting. The show features experts with real world experience and shares their knowledge. 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