Links for Keyword: Alzheimers

Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.


Links 1 - 20 of 1289

By Simon Makin Something in elderly blood is bad for brains. Plasma from old mice or humans worsens cognition and biological indicators of brain health, when infused into young mice. Conversely, plasma from young mice (or humans) rejuvenates old brains. Much of this research has come from neurobiologist Tony Wyss-Coray’s group at Stanford University, which is pursuing what constituents of blood might be responsible. One previous study identified a protein, which declines with age, that has powerful beneficial effects. That protein can cross from the blood into the brain, but Wyss-Coray wondered how certain molecules contained in blood typically “talk” to the brain. Must they interact with brain cells directly, or can they communicate indirectly, through the gateway to the brain, the blood-brain barrier? To investigate, Wyss-Coray’s team tried a new approach in their latest study, published May 13 in Nature Medicine. “We reasoned that the most obvious way plasma would interact with the brain is through blood vessels,” Wyss-Coray says. “So, we looked at proteins that change with age and had something to do with the vasculature.” One protein that becomes more abundant with age, VCAM1, stood out, and the team showed that it appears to play a pivotal role in the effects of aged blood on the brain. Biological and cognitive measures alike indicated that blocking VCAM1 not only prevents old plasma from damaging young mouse brains but can even reverse deficits in old mice. The work has important implications for age-related cognitive decline and brain diseases. “Cognitive dysfunction in aging is one of our biggest biomedical challenges, and we have no effective medical therapies. None,” says neuroscientist Dena Dubal, of the University of California, San Francisco, who was not involved in the study. “It’s such an important line of investigation; it has tremendous implications.” © 2019 Scientific American

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 26237 - Posted: 05.15.2019

Jon Hamilton Scientists are setting a new course in their quest to treat Alzheimer's disease. The shift comes out of necessity. A series of expensive failures with experimental drugs aimed at a toxic protein called amyloid-beta have led to a change in approach. The most recent disappointment came in March, when drugmaker Biogen and its partner Eisai announced they were halting two large clinical trials of an amyloid drug called aducanumab. "It was like being punched in the stomach," says Phil Gutis, 57, an Alzheimer's patient in one of the trials. "Participating in this trial, it gave me hope for the future." Gutis, who once was a reporter for The New York Times and worked as an advocate at the American Civil Liberties Union, had hoped the experimental drug would preserve some of his remaining memories. "I'm just being erased," he says. The day before the aducanumab trial ended, Gutis had been leafing through pictures of his dog, Abe, a Jack Russell terrier who died last year. He was trying to remember the companion who'd shared his life for 12 years. © 2019 npr

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 26208 - Posted: 05.04.2019

By James Gallagher Health and science correspondent, BBC News Dementia is the greatest health challenge of our time, the charity Alzheimer's Research UK has warned. Dementia was first described by the German doctor Alois Alzheimer in 1906 after he performed an autopsy on a woman with profound memory loss. What he found was a dramatically shrunken brain and abnormalities in and around nerve cells. At the time dementia was rare and was then barely studied for decades. But today somebody is diagnosed with it every three seconds, it is the biggest killer in some wealthier countries and is completely untreatable. So what is this disease? Why is it becoming more common? And is there any hope? Is dementia the same as Alzheimer's? No - dementia is a symptom found in many diseases of the brain. Memory loss is the most common feature of dementia, particularly the struggle to remember recent events. Other symptoms can include changes to behaviour, mood and personality, becoming lost in familiar places or being unable to find the right word in a conversation. It can reach the point where people don't know they need to eat or drink. Alzheimer's disease is by far the most common of the diseases that cause dementia. Others include vascular dementia, dementia with Lewy bodies, fronto-temporal dementia, Parkinson's disease dementia, amyotrophic lateral sclerosis and the newly discovered Late. © 2019 BBC

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 26207 - Posted: 05.04.2019

Laura Sanders A newly described dementia strikes people in their last decades of life. The disease, aptly named LATE, comes with symptoms that resemble Alzheimer’s disease, but is thought to be caused by something completely different. An international team of scientists and clinicians describe the disease and officially christen it LATE, which stands for the more technical description, “limbic-predominant age-related TDP-43 encephalopathy,” online April 30 in Brain. Study coauthor Peter Nelson, a neuropathologist at the University of Kentucky in Lexington, helped organize a meeting last year that addressed a growing realization among doctors and scientists: “There’s this disease, and it doesn’t have a name,” he says. Estimates vary, but it’s possible that about a quarter of people age 85 and older have LATE, Nelson says. “This is a disease that really attacks the very latest portion of the human aging spectrum,” he says. LATE comes with memory trouble and dementia — symptoms that mirror Alzheimer’s, Nelson says. But instead of the plaques and tangles that mark the brains of people with Alzheimer’s disease, LATE is characterized by a lesser-known protein called TDP-43. In LATE, that protein accumulates and spreads through parts of the brain that are key to thinking and memory, including the amygdala and hippocampus. In Brain, Nelson and his colleagues describe the signs of LATE in the brain in a series of stages, from less severe to most severe. But the trouble is that these signs, which include the spread of TDP-43 and occasionally signs of damage to the hippocampus, can be found only after a person has died. There are currently no surefire clinical tests that identify LATE in a living person. |© Society for Science & the Public 2000 - 2019.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 26192 - Posted: 05.01.2019

By Lisa Sanders, M.D. “I don’t know where I am,” said a terrified voice on the phone. It was the woman’s husband, and he was scared. “I’m lost,” he said in a panicked tone. It’s O.K., she told him, sounding as calm and reassuring as she could. Her husband, a former high school English teacher in his 60s, left his mother-in-law’s that morning to return to their home several hours away in Pinon Hills, just north of San Bernardino, Calif. It was a route he drove often enough to know well. But after making his way through towns that seemed familiar, he lost his sense of how to get home. With her voice on the speakerphone, she guided him. His voice shook, and she knew he was crying. She wanted to cry, too, but forced herself to be the strength he needed. She still loved her husband, but he’d changed so much. Where was the man she married over 30 years ago? Twenty years earlier, he found out he had multiple sclerosis. It started with numbness in his arms and hands. Sometimes his vision would darken on the periphery, as if he were in a tunnel. And then, after a couple of hours or so, he’d be fine. He was referred to a local neurologist, who did some testing. An M.R.I. of his brain showed patchy white clouds among the normal gray swirls of brain. That finding was suggestive of multiple sclerosis. In M.S., the immune system goes awry and attacks the fatty sleeves that surround the nerves in the brain and spine; that’s what causes the characteristic M.R.I. findings. But it wasn’t a perfect fit. The fluid taken from his spine did not show the proteins that are usually seen in M.S. Moreover, while M.S. is characterized by episodes of unusual neurological symptoms that come and go, they usually last days or weeks rather than hours. Still, there are different forms of the disorder, and they can vary widely in symptom intensity and rate of progression. And there are few diseases that result in the M.R.I. findings and intermittent symptoms that this man had. Subsequent neurologists confirmed the diagnosis of M.S. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 26191 - Posted: 05.01.2019

Nicola Davis Olfactory tests could help doctors spot older adults who are at greater risk of developing dementia, researchers say. The sense of smell is known to deteriorate with age. However, researchers have previously found it might also hint at health problems: older adults who struggle to identify odours have a greater chance of dying in the near future regardless of how old they are. Other studies have found older adults who have difficulties in identifying and remembering smells are more likely to have characteristics linked to a greater risk of developing Alzheimer’s disease even if there is no current sign of cognitive decline. Get Society Weekly: our newsletter for public service professionals Read more It is thought the sense of smell is one of the first faculties affected by certain neurodegenerative diseases. Now experts say they have probed further, and those diseases alone do not explain why a poor sense of smell might bode ill. “My suspicion is [the] process of smell in older adults probably has much broader potential health implications than what we already know about,” said Prof Honglei Chen, a co-author of the research from Michigan State University. He suggested it could be linked to conditions of the immune system and even psychiatric disorders. © 2019 Guardian News & Media Limited

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 9: Hearing, Vestibular Perception, Taste, and Smell
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 26184 - Posted: 04.30.2019

By Gina Kolata Allan Gallup, a retired lawyer and businessman, grew increasingly forgetful in his last few years. Eventually, he could no longer remember how to use a computer or the television. Although he needed a catheter, he kept forgetting and pulling it out. It was Alzheimer’s disease, the doctors said. So after Mr. Gallup died in 2017 at age 87, his brain was sent to Washington University in St. Louis to be examined as part of a national study of the disease. But it wasn’t just Alzheimer’s disease, the researchers found. Although Mr. Gallup’s brain had all the hallmarks — plaques made of one abnormal protein and tangled strings of another — the tissue also contained clumps of proteins called Lewy bodies, as well as signs of silent strokes. Each of these, too, is a cause of dementia. Mr. Gallup’s brain was typical for an elderly patient with dementia. Although almost all of these patients are given a diagnosis of Alzheimer’s disease, nearly every one of them has a mixture of brain abnormalities. For researchers trying to find treatments, these so-called mixed pathologies have become a huge scientific problem. Researchers can’t tell which of these conditions is the culprit in memory loss in a particular patient, or whether all of them together are to blame. Another real possibility, noted Roderick A. Corriveau, who directs dementia research programs at the National Institute of Neurological Disorders and Stroke, is that these abnormalities are themselves the effects of a yet-to-be-discovered cause of dementia. These questions strike at the very definition of Alzheimer’s disease. And if you can’t define the condition, how can you find a treatment? © 2019 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 13: Memory, Learning, and Development
Link ID: 26125 - Posted: 04.09.2019

By Jane E. Brody Attention all consumers seeking to protect brain health: You can save hundreds of dollars a year and enhance the health of your brain and body by ignoring the myriad unproven claims for anti-dementia supplements and instead focusing on a lifestyle long linked to better mental and physical well-being. How many of these purported brain boosters have you already tried — Ginkgo biloba, coenzyme Q10, huperzine A, caprylic acid and coconut oil, coral calcium, among others? The Alzheimer’s Association says that, with the possible exception of omega-3 fatty acids, all that were properly tested thus far have been found wanting. I admit it’s very appealing to think you can maintain your cognitive powers by swallowing a few pills a day instead of adopting a brain-healthy diet, getting regular exercise and adequate sleep, among other health-preserving measures like not smoking. But you’d only be fooling yourself and wasting precious dollars that could be better spent on nutritious foods and a good pair of walking shoes. “No known dietary supplement prevents cognitive decline or dementia,” Dr. Joanna Hellmuth stated emphatically in JAMA in January. “Yet,” she added, “supplements advertised as such are widely available and appear to gain legitimacy when sold by major U.S. retailers.” Dr. Hellmuth, a neurologist at the University of California, San Francisco, Memory and Aging Center, reminds consumers that supplement manufacturers do not have to test their products for effectiveness or safety. Lacking sound scientific backing, most are promoted by testimonials that appeal to people worried about developing dementia. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 26101 - Posted: 04.01.2019

By Simon Makin Neurodegenerative diseases all involve the accumulation of toxic versions of naturally produced proteins in the brain. Multiple proteins are often abnormal in a patient, and the same aberrant protein can be involved in several different conditions. One common culprit is tau, which is abnormal in various conditions: chronic traumatic encephalopathy, a neurodegenerative disorder caused by repeated head trauma; a group of conditions known collectively as frontotemporal dementia; and, most famously, Alzheimer’s disease (AD). Normally, tau stabilizes structures inside neural connections, called microtubules, which facilitate chemical communication between cells. In disease states, tau is chemically altered, becoming misshapen and breaking away from microtubules. These toxic versions accumulate into structures called “neurofibrillary tangles,” which disrupt cells’ ability to communicate and may trigger other forms of damage, such as inflammation. Tau is involved in AD, but abnormalities in a different protein, amyloid-beta, are thought to be the initial trigger for a chain of biological events (including tau pathology) that underlies neurodegeneration. This is why most AD drugs developed to date have targeted amyloid, although tau has received increasing attention as multiple drugs intended to remove amyloid have failed. A new study, published Wednesday in Science Translational Medicine, suggests that an existing drug, lonafarnib, could be repurposed to treat neurodegenerative diseases that involve tau. A team of researchers, led by neuroscientist Kenneth Kosik of the University of California, Santa Barbara, found the drug had beneficial effects on tau-related pathology in mice, if administered early over an extended period. They also found evidence suggesting it works via a previously unknown biological mechanism. “This opens up a previously completely unsuspected pathway for tau degradation,” says Kosik, a longtime tau researcher. “We don’t have all the molecular details, but as a place to look, this is full of new opportunities.” © 2019 Scientific American

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 26093 - Posted: 03.29.2019

By Jennifer Couzin-Franke Earlier this week, the Lieber Institute for Brain Development, a nonprofit housed at Johns Hopkins University School of Medicine in Baltimore, Maryland, announced a new neuroscience research initiative that aims to tackle a gaping hole in medicine: the interplay between brain diseases and their genomic drivers among African-Americans. The goal is to better understand how brain diseases play out in this population, which has been profoundly underrepresented in neuroscience research. To build trust among African-Americans in Baltimore and eventually beyond, the venture includes a partnership with the African-American Clergy Medical Research Initiative, a group of clergy leaders in the city. African-American scientists at Lieber are already involved, but project leaders hope to engage those at other institutions as the work expands. The effort builds on Lieber’s rapidly growing brain bank, which now stands at about 3000 brains, with more than 400 new brains collected each year, all donated by next of kin. Many are from young and middle-aged people who die suddenly of suicide, drug overdose, or other causes. Although most of the brains are from people of European ancestry, more than 700 are from African-Americans. Despite growing recognition that African-Americans are underrepresented in medical research—and face discrimination and other hardships that can heighten health risks—study of brain diseases in this population have lagged behind, says Daniel Weinberger, the institute’s director. ScienceInsider spoke with Weinberger, a psychiatrist and schizophrenia researcher who came to the Lieber Institute in 2011 from the National Institute of Mental Health. The conversation has been edited for brevity and clarity. © 2019 American Association for the Advancement of Science

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 26069 - Posted: 03.23.2019

By Kelly Servick “Futile”—that’s the devastating label now attached to two highly anticipated clinical trials of a drug that targets β-amyloid, the neuron-killing protein fragment littering the brains of people with Alzheimer’s disease. Biogen in Cambridge, Massachusetts, and Eisai in Tokyo, the pharmaceutical partners developing the drug, called aducanumab, today announced their decision to halt a pair of ongoing phase III trials after seeing the results of a “futility analysis,” in which an independent committee found that the drug was unlikely to slow cognitive decline as intended. This latest blow to the β-amyloid approach has left researchers asking: Do any of the remaining antiamyloid drug trials have a better chance, or is it time to declare the whole approach, well, futile? “Amyloid definitely has something to do with Alzheimer’s—there’s far too much evidence to dismiss,” organic chemist Derek Lowe wrote today on his drug industry blog In the Pipeline. (The blog is hosted by Science Translational Medicine, which, like ScienceInsider, is published by AAAS.) “But the situation is clearly more complicated than people have hoped, because otherwise, all the attempts to address amyloid … would have yielded some tiny bit of clinical benefit.” There were reasons to think that aducanumab might succeed where antiamyloid drugs from Merck & Co., Eli Lilly and Company, and others had failed. The drug is an antibody designed to bind to and eliminate sticky β-amyloid plaques that build up around neurons, block their communication, and, ultimately, kill them. And it was clear from a smaller clinical trial that this drug was very effective at clearing plaques—“that’s one of the reasons we were sanguine about this trial,” says neurologist Dennis Selkoe of Brigham and Women’s Hospital in Boston, who treats patients who were enrolled in one of the trials. Studies also suggest aducanumab can attack the most noxious form of amyloid—so-called oligomers—that other drugs may have left untouched. © 2019 American Association for the Advancement of Science

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 26061 - Posted: 03.22.2019

Jon Hamilton In the U.S., older people with dementia are usually told they have Alzheimer's disease. But a range of other brain diseases can also impair thinking, and memory and judgment, according to scientists attending a summit on dementias held Thursday and Friday at the National Institutes of Health. These include strokes, a form of Parkinson's disease, and a disease that damages brain areas that regulate emotion and behavior. "There's a host of things that can cause loss of cognitive function," says Dr. Julie Schneider, a professor at the Rush Alzheimer's Disease Center in Chicago and scientific chair of the NIH summit. And many patients have more than one disease affecting the brain, she says. Most of these diseases can't be stopped, Schneider says. But it's important that families get the right diagnosis in order to get the best care and plan for the future. The emphasis on non-Alzheimer's dementias reflects a change in doctors' understanding of what happens to aging brains. When Schneider was training to be a doctor in the 1980s and '90s, dementia was simple. "We were taught that almost all dementia is Alzheimer's disease," she says. But since then, studies have shown that 20 percent to 40 percent of the nation's 5.8 million dementia patients have some other disease. © 2019 npr

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 26044 - Posted: 03.18.2019

By Pam Belluck Could people’s eyes and ears help fix the damage Alzheimer’s disease does to the brain? Just by looking at flashing light and listening to flickering sound? A new study led by a prominent M.I.T. neuroscientist offers tantalizing promise. It found that when mice engineered to exhibit Alzheimer’s-like qualities were exposed to strobe lights and clicking sounds, important brain functions improved and toxic levels of Alzheimer’s-related proteins diminished. What’s more, the rapid-fire soundtrack appeared to make mice better at cognitive and memory skills, like navigating mazes and recognizing objects. Of course, mice are not people. And many drugs that have helped Alzheimer’s-engineered mice haven’t done much for people with Alzheimer’s, which affects 44 million people worldwide, including 5.5 million Americans. Also, because the technique didn’t have long-lasting effects — results faded about a week after the sensory stimulation was stopped — any therapy developed from the research might have to be repeated regularly. Still, seeing that a noninvasive daily dose of light and sound could have such significant effects in mice give some experts reason for optimism. “It’s exciting, I think,” said Dr. Lennart Mucke, director of the Gladstone Institute of Neurological Disease, who was not involved in the study. “Reading the paper made me quite enthusiastic about seeing this move forward into some well-crafted clinical trials.” The experiments were led by Li-Huei Tsai, director of MIT’s Picower Institute for Learning and Memory. She and her colleagues showed that light and sound delivered to mice at a certain frequency — 40 hertz or 40 flashes or clicks per second — appears to synchronize the rhythm of the brain’s gamma waves, which is disrupted in patients with Alzheimer’s. Gamma waves are among several types of electrical brain waves believed to be involved in concentration, sleep, perception and movement. The experiment setup where flickering light and sound were delivered to Alzheimer’s-engineered mice in the tubs.CreditPicower Institute for Learning and Memory, M.I.T. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 13: Memory, Learning, and Development
Link ID: 26040 - Posted: 03.15.2019

Eating mushrooms more than twice a week could prevent memory and language problems occurring in the over-60s, research from Singapore suggests. A unique antioxidant present in mushrooms could have a protective effect on the brain, the study found. The more mushrooms people ate, the better they performed in tests of thinking and processing. But researchers said it was not possible to prove a direct link between the fungi and brain function. The National University of Singapore study's findings were based on 663 Chinese adults, aged over 60, whose diet and lifestyle were tracked from 2011 to 2017. Over the six-year study the researchers found that eating more than two portions of mushrooms a week lowered the chances of mild cognitive impairment by 50%, compared with those who ate fewer than one portion. Mild cognitive impairment (MCI) can make people forgetful, affect their memory and cause problems with language, attention and locating objects in spaces - but the changes can be subtle. It is not serious enough to be defined as dementia. The participants in the study were asked how often they ate six different types of mushrooms: oyster, shiitake, white button, dried, golden and tinned. Mushroom eaters performed better in brain tests and were found to have faster processing speed - and this was particularly noticeable in those who ate more than two portions a week, or more than 300g (10.5oz). "This correlation is surprising and encouraging," said assistant professor Lei Feng, the lead study author, from the university's department of psychological medicine. Image copyright Getty Images "It seems that a commonly available single ingredient could have a dramatic effect on cognitive decline. © 2019 BBC

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 13: Memory, Learning, and Development
Link ID: 26034 - Posted: 03.15.2019

GPs are urging women not to be alarmed by research linking long-term hormone replacement therapy (HRT) use with a small increased risk of Alzheimer's. They say HRT is an effective and safe treatment for most women with menopause symptoms and the risk is "extremely low". The BMJ research looked at data on 170,000 women in Finland over 14 years. It found a 9%-17% increased risk for Alzheimer's, particularly in women taking HRT for more than 10 years. This equates to between nine and 18 extra cases of the disease per year in every 10,000 women aged between 70 and 80, the researchers said. But the study was observational and, as a result, it cannot be said for certain that other factors had not affected the results. Other studies have found that HRT actually improves brain function. The Royal College of GPs said the research does not prove that HRT causes Alzheimer's disease, and women currently taking it should continue to do so. Prof Helen Stokes-Lampard, chairwoman of the College, said: "Hormone replacement therapy can be of greatest benefit to many women who are suffering from some of the unpleasant side-effects of the menopause, such as hot flushes and night sweats - and there is a large body of evidence that shows it is an effective and safe treatment for most women. "We would urge patients not to be alarmed by this research - as the researchers state, any risk is extremely low - and if they are currently taking HRT, to continue doing so as prescribed by their doctor. " However, she said there were risks with any medication and it was important that women were aware of them. "To minimise any risk, best practice for most women is to prescribe the lowest possible dose of hormones for the shortest possible time in order to achieve satisfactory relief of symptoms," Prof Stokes-Lampard said. © 2019 BBC

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 8: Hormones and Sex
Link ID: 26015 - Posted: 03.07.2019

By Karen Weintraub For decades researchers have focused their attacks against Alzheimer’s on two proteins, amyloid beta and tau. Their buildup in the brain often serves as a defining indicator of the disease. Get rid of the amyloid and tau, and patients should do better, the thinking goes. But drug trial after drug trial has failed to improve patients’ memory, agitation and anxiety. One trial of a drug that removes amyloid even seemed to make some patients worse. The failures suggest researchers were missing something. A series of observations and recently published research findings have hinted at a somewhat different path for progression of Alzheimer’s, offering new ways to attack a disease that robs memories and devastates the lives of 5.7 million Americans and their families. One clue hinting at the need to look further afield was a close inspection of the 1918 worldwide flu pandemic, which left survivors with a higher chance of later developing Alzheimer’s or Parkinson’s. A second inkling came from the discovery that the amyloid of Alzheimer’s and the alpha-synuclein protein that characterizes Parkinson’s are antimicrobials, which help the immune system fight off invaders. The third piece of evidence was the finding in recent years, as more genes involved in Alzheimer’s have been identified, that traces nearly all of them to the immune system. Finally, neuroscientists have paid attention to cells that had been seen as ancillary—“helper” or “nursemaid” cells. They have come to recognize these brain cells, called microglia and astrocytes, play a central role in brain function—and one intimately related to the immune system. © 2019 Scientific American

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 11: Emotions, Aggression, and Stress
Link ID: 26007 - Posted: 03.05.2019

By Paula Span Donna Kaye Hill realized that her 80-year-old mother was faltering cognitively when her phone suddenly stopped working. When Ms. Hill called the phone company, “they told me she hadn’t paid her bill in three months.” Finding other alarming evidence of memory gaps, she took her mother, Katie, to a memory clinic. A geriatrician there diagnosed dementia and recommended two prescription drugs and a dietary supplement, a form of vitamin E. Katie Hill dutifully took vitamin E capsules, along with a host of other medications, until she died four years later. As she declined, her daughter didn’t think the vitamin, or the two prescription medications, was making much difference. “But if it doesn’t hurt, if there’s a chance it helps even a tiny bit, why not?” she reasoned. Ms. Hill, 62, a retired public employee in Danville, Va., takes fish oil capsules daily herself, hoping they’ll help ward off the disease that killed her mother. The elder Ms. Hill was unusual only in that a doctor had recommended the supplement; most older Americans are taking them without medical guidance. The Food and Drug Administration estimates that 80 percent of older adults rely on dietary supplements, many purporting to prevent or treat Alzheimer’s and other forms of dementia. Last month, the F.D.A. cracked down on this burgeoning market, sending warning letters or advisories to 17 companies selling about 60 supplements with names like Cogni-Flex and Mind Ignite. The warnings pointed out that the companies had touted these products as working like Alzheimer’s drugs, “but naturally and without side effects.” Or as “clinically shown to help diseases of the brain, such as Alzheimer’s.” The pills, oils and capsules were said to treat other diseases, too, from stroke to erectile dysfunction. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 26002 - Posted: 03.02.2019

Analysis of genetic data from more than 94,000 individuals has revealed five new risk genes for Alzheimer’s disease, and confirmed 20 known others. An international team of researchers also reports for the first time that mutations in genes specific to tau, a hallmark protein of Alzheimer’s disease, may play an earlier role in the development of the disease than originally thought. These new findings support developing evidence that groups of genes associated with specific biological processes, such as cell trafficking, lipid transport, inflammation and the immune response, are “genetic hubs” that are an important part of the disease process. The study, which was funded in part by the National Institute on Aging (NIA) and other components of the National Institutes of Health, follows results from 2013. It will be published online February 28, 2019 in the journal Nature Genetics . “This continuing collaborative research into the genetic underpinnings of Alzheimer’s is allowing us to dig deeper into the complexities of this devastating disease,” said Richard J. Hodes, M.D., director of the NIA. “The size of this study provides additional clarity on the genes to prioritize as we continue to better understand and target ways to treat and prevent Alzheimer’s.” The researchers, members of the International Genomic Alzheimer’s Project (IGAP), analyzed both rare and common gene variants in 94,437 individuals with late onset Alzheimer’s disease, the most common form of dementia in older adults. IGAP is made up of four consortia in the United States and Europe that have been working together since 2011 on genome-wide association studies (GWAS) involving thousands of DNA samples and shared datasets. GWAS are aimed at detecting variations in the genome that are associated with Alzheimer’s. Understanding genetic variants is helping researchers define the molecular mechanisms that influence disease onset and progression.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 26001 - Posted: 03.02.2019

By Pallab Ghosh Science correspondent, BBC News, Washington DC New results suggest ageing brains can potentially be rejuvenated, at least in mice, according to researchers. Very early-stage experiments indicate that drugs can be developed to stop or even reverse mental decline. The results were presented at the 2019 meeting of the American Association for the Advancement of Science. The US and Canadian researchers took two new approaches to trying to prevent the loss of memory and cognitive decline that can come with old age. One team, from the University of California, Berkeley, showed MRI scans which indicated that mental decline may be caused by molecules leaking into the brain. Blood vessels in the brain are different from those in other parts of the body. They protect the organ by allowing only nutrients, oxygen and some drugs to flow through into the brain, but block larger, potentially damaging molecules. This is known as the blood-brain barrier. The scans revealed that this barrier becomes increasingly leaky as we get older. For example, 30-40% of people in their 40s have some disruption to their blood-brain barrier, compared with 60% of 60-year-olds. The scans also showed that the brain was inflamed in the leaky areas. Prof Daniela Kaufer, who leads the Berkeley group, said that young mice altered to have leaky blood-brain barriers showed many signs of aging. She discovered a chemical that stops the damage to the barrier from causing inflammation to the brain. Prof Kaufer told BBC News that not only did the chemical stop the genetically altered young mice from showing signs of aging, it reversed the signs of aging in older mice. © 2019 BBC

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 13: Memory, Learning, and Development
Link ID: 25966 - Posted: 02.15.2019

Ian Sample Science editor An experimental drug that bolsters ailing brain cells has raised hopes of a treatment for memory loss, poor decision making and other mental impairments that often strike in old age. The drug could be taken as a daily pill by over-55s if clinical trials, which are expected to start within two years, show that the medicine is safe and effective at preventing memory lapses. Tests in the lab showed that old animals had far better memory skills half an hour after receiving the drug. After two months on the treatment, brain cells which had shrunk in the animals had grown back, scientists found. Etienne Sibille, at the Centre for Addiction and Mental Health in Toronto, said the treatment was aimed not only at the “normal” cognitive decline that leads to senior moments, but at memory loss and mental impairments that commonly afflict people with depression, schizophrenia and Alzheimer’s disease. If the drug did well in human trials, Sibille said it was possible that “anybody over the age of 55-60 who may be at risk of cognitive problems later on could benefit from this treatment”. “Our findings have direct implications for poor cognition in normal ageing,” he said, with the drug potentially improving learning, memory, decision making and essential life planning. “But we see this deficiency across disorders from depression to schizophrenia and Alzheimer’s.” © 2019 Guardian News & Media Limited

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 13: Memory, Learning, and Development
Link ID: 25964 - Posted: 02.14.2019