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By David H. Freedman Two levels below ground, under a small, drab building at the University of Bonn, is a wall of cages containing mice that, according to standard tests, are extraordinarily average. They learn and remember how to run mazes no better nor worse than other mice. It takes them a typical amount of time to figure out how to extricate themselves from a tank of water with hidden exit steps. There’s nothing out of line about how they interact with other mice, nor their willingness to explore open spaces. And yet these mice are the center of attention at the lab of Andreas Zimmer. That’s because their boringly average minds may well hold the key to beating Alzheimer’s and elderly dementia. Many of the mice are 18 months old, roughly equivalent to a 70-year-old human. Mice normally start to show mental decline at around a year old, and by 18 months, struggle with mazes and other mental tasks, as well as with socializing. But not these rodent seniors. “You can’t tell the difference between them and two-month-old mice,” says Zimmer. Even more surprising is what Zimmer has done to get these elderly mice remembering and behaving like younger ones. It’s not special genes, a particular training regimen, nor an unusual diet. They don’t get any approved memory drug, nor a new investigational procedure. Basically, Zimmer keeps them very slightly stoned. A longtime U.S. National Institutes of Health (NIH) researcher who is now one of Germany’s most respected neuroscientists, Zimmer has been on a long journey to answer a question that few researchers had thought to ask: Is it possible that weed, long seen as the stuff of slackers, might actually contain the secret to sharpening the aging brain? © 2020 Kalmbach Media Co.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 27094 - Posted: 03.05.2020

By Jane Wakefield Technology reporter An ambitious project to develop a wearable device to detect early signs of Alzheimer's disease has been launched. The Early Detection of Neurodegenerative diseases (Edon) is being spearheaded by charity Alzheimer's Research UK. It will initially analyse data from continuing studies into the disease, using artificial intelligence. And this data will be used to design a prototype device within three years. Wearables collect a variety of data including gait, heart rate and sleep patterns and the hope is by analysing this data, researchers can begin to map signs of the disease years before symptoms develop. The global initiative has already won funding from tech founder turned philanthropist Bill Gates. But it also forms part of the UK government's wider ambition to use artificial intelligence and data to help better understand and prevent chronic diseases. Initially, EDoN will work with the UK's national institute for data science and artificial intelligence, The Alan Turing Institute, to trawl through data from continuing studies into Alzheimer's disease. Prof Chris Holmes, health programme director at the institute, said: "Artificial intelligence has the potential to transform the learning opportunities from large-scale data studies such as Edon by integrating information from multiple sources. "We will use AI to deliver new insights into the early signals of disease by combining digital data measurements with traditional sources such as brain imaging and memory tests." There are currently 850,000 people living with dementia in the UK, according to Alzheimer's Research UK. © 2020 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: 27064 - Posted: 02.24.2020

By Judith Graham, Kaiser Health News Do I know I’m at risk for developing dementia? You bet. My father died of Alzheimer’s disease at age 72; my sister was felled by frontotemporal dementia at 58. And that’s not all: Two maternal uncles had Alzheimer’s, and my maternal grandfather may have had vascular dementia. (In his generation, it was called senility.) So what happens when I misplace a pair of eyeglasses or can’t remember the name of a movie I saw a week ago? “Now comes my turn with dementia,” I think. Then I talk myself down from that emotional cliff. Am I alone in this? Hardly. Many people, like me, who’ve watched this cruel illness destroy a family member, dread the prospect that they, too, might become demented. The lack of a cure or effective treatments only adds to the anxiety. It seems a common refrain, the news that another treatment to stop Alzheimer’s has failed. How do we cope as we face our fears and peer into our future? Andrea Kline, whose mother, as well as her aunt and uncle, had Alzheimer’s disease, just turned 71 and lives in Boynton Beach, Fla. She’s a retired registered nurse who teaches yoga to seniors at community centers and assisted-living facilities. “I worry about dementia incessantly: Every little thing that goes wrong, I’m convinced it’s the beginning,” she told me. Because Ms. Kline has had multiple family members with Alzheimer’s, she’s more likely to have a genetic vulnerability than someone with a single occurrence in their family. But that doesn’t mean this condition lies in her future. A risk is just that: It’s not a guarantee. The age of onset is also important. People with close relatives struck by dementia early — before age 65 — are more likely to be susceptible genetically. Ms. Kline was the primary caregiver for her mother, Charlotte Kline, who received an Alzheimer’s diagnosis in 1999 and passed away in 2007 at age 80. “I try to eat very healthy. I exercise. I have an advance directive, and I’ve discussed what I want” in the way of care “with my son,” she said. © 2020 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: 27056 - Posted: 02.20.2020

By Gina Kolata The study aimed to show that Alzheimer’s disease could be stopped if treatment began before symptoms emerged. The participants were the best candidates that scientists could find: still healthy, but with a rare genetic mutation that guaranteed they would develop dementia. For five years, on average, the volunteers received monthly infusions or injections of one of two experimental drugs, along with annual blood tests, brain scans, spinal taps and cognitive tests. Now, the verdict is in: The drugs did nothing to slow or stop cognitive decline in these subjects, dashing the hopes of scientists. Dr. Randall Bateman, a neurologist at Washington University in St. Louis and principal investigator of the study, said he was “shocked” when he first saw the data: “It was really crushing.” The results are a deep disappointment, scientists said — but not a knockout punch. The drugs did not work, but the problems may be fixable: perhaps the doses were too low, or they should have been given to patients much younger. Few experts want to give up on the hypothesis that amyloid plaques in the brain are intimately involved in Alzheimer’s disease. The data from this international study, called DIAN-TU, are still being analyzed and are to be presented on April 2 at scientific conferences in Vienna in April and in Amsterdam in July. The trial was sponsored by Washington University in St. Louis, two drug companies that supplied the drugs — Eli Lilly and Roche, with a subsidiary, Genentech — the National Institutes of Health and philanthropies, including the Alzheimer’s Association. © 2020 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: 27038 - Posted: 02.13.2020

Sarah O’Meara Xiaoming Zhou is a neurobiologist at East China Normal University in Shanghai. Here he speaks to Nature about his research into age-related hearing loss, and explains why he hopes that brain training could help to lessen declines in sensory perception generally, and so ward off neurodegenerative diseases. What is your current research focus? We want to better understand the neural basis for why a person’s hearing function declines as they grow older. For example, we have performed research to see whether we can reverse age-related changes to the auditory systems of rodents. We gave the animals a set of tasks, such as learning to discriminate between sounds of different frequencies or intensities. These exercises caused the rodents’ hearing to improve, and also promoted changes to the hippocampus, a part of the brain structure closely associated with learning and memory. The relationship with the hippocampus suggests that new kinds of brain training might help to attenuate our declines in perception and other brain functions, such as learning and memory, as we grow older — and so have the potential to stave off neurodegenerative diseases. How is ageing-related science developing in China? As has happened in the rest of the world, a rapidly ageing population has brought significant concern to policymakers. However, as far as I know, only a few neuroscience laboratories in China are specifically focused on learning more about the underlying mechanisms that cause changes in brain function as we age. This is despite the fact that such research could have a considerable impact on the welfare of older people in the future. © 2020 Springer Nature Limited

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: 27023 - Posted: 02.07.2020

By Nicholas Bakalar Flavonols, a large class of compounds found in most fruits and vegetables, may be associated with a reduced risk for Alzheimer’s disease. Flavonols are known to have antioxidant and anti-inflammatory effects, and animal studies have suggested they may improve memory and learning. A study in Neurology involved 921 men and women, average age 81 and free of dementia, who reported their diet using well-validated food questionnaires. During an average follow-up of six years, 220 developed Alzheimer’s disease. People with the highest levels of flavonol intake tended to have higher levels of education and were more physically active. But after controlling for these factors plus age, sex, the Apo E4 gene (which increases the risk for dementia) and late-life cognitive activity, the scientists found that compared with those in the lowest one-fifth for flavonol intake, those in the highest one-fifth had a 48 percent reduced risk for Alzheimer’s disease. The study covered four types of flavonols: kaempferol, quercetin, isorhamnetin and myricetin. All except quercetin showed a strong association with Alzheimer’s risk reduction. These flavonols are available as supplements, but the lead author, Dr. Thomas M. Holland, a professor of medicine at Rush Medical College in Chicago, said that foods are a better source. “You get a broader intake of vitamins, minerals and bioactives in food than in the supplements,” he said. © 2020 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: 27015 - Posted: 02.04.2020

By Laura Sanders A cruel twist of genetic fate brought Alzheimer’s disease to a sprawling Colombian family. But thanks to a second twist, one member of the clan, a woman, managed to evade the symptoms for decades. Her escape may hold the key to halting, or even preventing, Alzheimer’s. The inherited version of Alzheimer’s disease erodes people’s memories early, starting around age 40. In this family and others, a mutation in a gene called presenilin 1 eventually leaves its carriers profoundly confused and unable to care for themselves. Locals around the Colombian city of Medellín have a name for the condition: la bobera, or “the foolishness.” The woman in the afflicted family who somehow fended off the disease carried the same mutation that usually guarantees dementia. And her brain was filled with plaques formed by a sticky protein called amyloid. Many scientists view that accumulation as one of the earliest signs of the disease. Yet she stayed sharp until her 70s. Researchers were stumped, until they discovered that the woman also carried another, extremely rare genetic mutation that seemed to be protecting her from the effects of the first one. This second mutation, in a different Alzheimer’s-related gene called APOE, seemed to slow the disease down by decades, says Joseph Arboleda-Velasquez, a cell biologist at Harvard Medical School. “There was this idea of inevitability,” he says. But the woman’s circumstances bring “a different perspective” — one in which amyloid buildup no longer guarantees problems. Arboleda-Velasquez and colleagues reported the details of the woman’s exceptional case November 4 in Nature Medicine, omitting the woman’s name and precise age to protect her privacy. © Society for Science & the Public 2000–2020

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: 26999 - Posted: 01.27.2020

Katarina Zimmer Around 30 years ago, researchers in the UK discovered DNA strands of herpes simplex virus 1 in postmortem brain samples of Alzheimer’s patients at much higher levels than in healthy brains, hinting that viral infection could be somehow involved in the disease. Since then, a string of studies has bolstered the association between Alzheimer’s disease and HSV1, as well as other pathogens, particularly the herpesviruses HHV6A and HHV6B, yet proving causality has remained elusive. Now, in an extensive screen of hundreds of diseased brains from three separate cohorts, a collaboration of US-based researchers reports no evidence for increased RNA or DNA levels of HHV6A or HHV6B in tissue from people with Alzheimer’s disease relative to that from healthy individuals, contradicting the results of some previous results. The scientists also failed to find an association between transcripts of other viruses that have been linked to Alzheimer’s, such as Epstein-Barr virus and cytomegalovirus, and Alzheimer’s, they report today (January 23) in Neuron. “I’m very surprised,” Ruth Itzhaki, an Alzheimer’s disease researcher currently at the University of Oxford who was among those who first associated HSV1, and later HHV6, with the disease, writes to The Scientist in an email. “If their findings are correct, absence of HHV6 would make any involvement in Alzheimer’s disease unlikely,” although not impossible, she notes. Several groups have reported the presence of HHV6 viruses in the brains of Alzheimer’s patients, most notably in a 2018 Neuron study. In that investigation, researchers had found higher levels of HHV6A in patients than in healthy controls, largely based on RNA and DNA sequencing data. © 1986–2020 The Scientist

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: 26989 - Posted: 01.24.2020

Edward Bullmore Unlikely as it may seem, #inflammation has become a hashtag. It seems to be everywhere suddenly, up to all sorts of tricks. Rather than simply being on our side, fighting infections and healing wounds, it turns out to have a dark side as well: the role it plays in causing us harm. It’s now clear that inflammation is part of the problem in many, if not all, diseases of the body. And targeting immune or inflammatory causes of disease has led to a series of breakthroughs, from new treatments for rheumatoid arthritis and other auto-immune diseases in the 1990s, through to the advent of immunotherapy for some cancers in the 2010s. Even more pervasively, low-grade inflammation, detectable only by blood tests, is increasingly considered to be part of the reason why common life experiences such as poverty, stress, obesity or ageing are bad for public health. Advertisement The brain is rapidly emerging as one of the new frontiers for inflammation. Doctors like myself, who went to medical school in the 20th century, were taught to think that there was an impermeable barrier between the brain and the immune system. In the 21st century, however, it has become clear that they are deeply interconnected and talk to each other all the time. Medical minds are now opening up to the idea that inflammation could be as widely and deeply implicated in brain and mind disorders as it is in bodily disorders. Advances in treatment of multiple sclerosis have shown the way. Many of the new medicines for MS were designed and proven to protect patients from brain damage caused by their own immune systems. The reasonably well-informed hope – and I emphasise those words at this stage – is that targeting brain inflammation could lead to breakthroughs in prevention and treatment of depression, dementia and psychosis on a par with the proven impact of immunological medicines for arthritis, cancer and MS. Indeed, a drug originally licensed for multiple sclerosis is already being tried as a possible immune treatment for schizophrenia. © 2020 Guardian News & Media Limited

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 26975 - Posted: 01.21.2020

By Karen Weintraub Alzheimer's disease has long been characterized by the buildup of two distinct proteins in the brain: first beta-amyloid, which accumulates in clumps, or plaques, and then tau, which forms toxic tangles that lead to cell death. But how beta-amyloid leads to the devastation of tau has never been precisely clear. Now a new study at the University of Alabama at Birmingham appears to describe that missing mechanism. The study details a cascade of events. Buildup of beta-amyloid activates a receptor that responds to a brain chemical called norepinephrine, which is commonly known for mobilizing the brain and body for action. Activation of this receptor by both beta-amyloid and norepinephrine boosts the activity of an enzyme that activates tau and increases the vulnerability of brain cells to it, according to the study, published in Science Translational Medicine. Essentially, beta-amyloid hijacks the norepinephrine pathway to trigger a toxic buildup of tau, says Qin Wang, the study’s senior author and a professor of neuropharmacology in the department of cell, developmental and integrative biology at the University of Alabama at Birmingham. “We really show that this norepinephrine is a missing piece of this whole Alzheimer’s disease puzzle,” she says. This cascade explains why so many previous Alzheimer’s treatments have failed, Wang says. Most of the drugs developed in recent decades have targeted the elimination of beta-amyloid. But the new research suggests that norepinephrine amplifies the damage wrought by that protein. © 2020 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: 26967 - Posted: 01.17.2020

There are differences in the way English and Italian speakers are affected by dementia-related language problems, a small study suggests. While English speakers had trouble pronouncing words, Italian speakers came out with shorter, simpler sentences. The findings could help ensure accurate diagnoses for people from different cultures, the researchers said. Diagnostic criteria are often based on English-speaking patients. In the University of California study of 20 English-speaking patients and 18 Italian-speaking patients, all had primary progressive aphasia - a neuro-degenerative disease which affects areas of the brain linked to language. It is a feature of Alzheimer's disease and other dementia disorders. Brain scans and tests showed similar levels of cognitive function in people in both language groups. But when the researchers asked participants to complete a number of linguistic tests, they picked up obvious differences between the two groups in the challenges they faced. 'Easier to pronounce' "We think this is specifically because the consonant clusters that are so common in English pose a challenge for a degenerating speech-planning system," said study author Maria Luisa Gorno-Tempini, professor of neurology and psychiatry. "In contrast, Italian is easier to pronounce, but has much more complex grammar, and this is how Italian speakers with [primary progressive aphasia] tend to run into trouble." As a result, the English speakers tended to speak less while the Italian speakers had fewer pronunciation problems, but simplified what they did say. English is a Germanic language while Italian is a Romance language, derived from Latin along with French, Spanish and Portuguese. The researchers, writing in Neurology, are concerned that many non-native English speakers may not be getting the right diagnosis "because their symptoms don't match what is described in clinical manuals based on studies of native English speakers". The San Francisco research team says it now wants to repeat the research in larger groups of patients, and look for differences between speakers of other languages, such as Chinese and Arabic. © 2020 BBC

Related chapters from BN8e: Chapter 19: Language and Lateralization; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 15: Brain Asymmetry, Spatial Cognition, and Language; Chapter 13: Memory, Learning, and Development
Link ID: 26954 - Posted: 01.13.2020

Jerold Chun, M.D., Ph.D. Alzheimer’s disease (AD) is the most common cause of dementia, currently affecting an estimated 5.8 million Americans. It has been over a century since AD was first described, but it is still not sufficiently well understood to enable development of drugs to treat it. As lifespan continues to rise and for myriad other reasons, the number of AD cases per state in the US is predicted to increase 12 to 43 percent over the next five years. The lack of disease-modifying treatments may reflect a feature of AD pathology that was first noted in its initial description: the vast heterogeneity of the hallmark “senile plaques” that are found in all AD brains. When Alois Alzheimer and Oskar Fischer described the first cases of AD, they noted plaque accumulations of a protein called amyloid that builds up in between brain cells and interrupts cell-to-cell communication; amyloid plaques vary in size, shape, abundance, and location within the brain. “Among the plaques in the cerebral cortex many were of an extraordinary size, such as I have never seen,” Alois Alzheimer stated. “Some evidently arose from the fusion of smaller ones since they contained several central cores, but others had one exceptionally big central core and uncommonly large halo.” Disease heterogeneity extends to behavior and includes varying age of onset, symptoms, and disease progression. Some variability may be explained by genetic heterogeneity, since more than 33 AD risk factor genes have been identified via a technique called “genome wide association studies” (GWAS), which broadly samples DNA from cells outside of the brain to identify mutations that are present in every cell of the body. None of these genes, however, are considered to cause AD. © 2020 The Dana Foundation

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: 26931 - Posted: 01.04.2020

Nicola Davis and Hannah Devlin Tangles of a protein found inside the brain cells of people with Alzheimer’s disease can be used to predict future brain shrinkage, research suggests. In healthy people, a protein called tau is important in supporting the internal structure of brain cells. However, in those with Alzheimer’s, chemical changes take place that cause the protein to form tangles that disrupt the cells. Such tangles have previously been linked to a loss of brain cells. Now scientists have used imaging techniques to track the extent of tau tangles in the brains of those with early signs of Alzheimer’s, revealing that levels of the protein predict not only how much brain shrinkage will subsequently occur, but where. “Our study supports the notion that tau pathology accumulates upstream of brain tissue loss and clinical symptoms,” said Prof Gil Rabinovici, a co-author of the research from the University of California, San Francisco. A number of drugs targeting tau tangles are currently in clinical trials, including some that aim to interfere with the production of tau in the brain or its spread between cells. Dr Renaud La Joie, another author of the research, said the findings suggested the imaging technique could prove valuable both in choosing which patients to enrol to test such drugs and in monitoring whether the drugs work. Dr Laura Phipps, of Alzheimer’s Research UK, said: “The ability to track tau in the brain will be critical for testing treatments designed to prevent the protein causing damage, and the scans used in this study could be an important tool for future clinical trials.” Writing in the journal Science Translational Medicine, La Joie and colleagues report how they used an imaging technique called PET to study the brains of 32 people aged between 49 and 83 who were in the early stages of showing Alzheimer’s symptoms. © 2020 Guardian News & Media Limited

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 26928 - Posted: 01.02.2020

By Gretchen Reynolds What’s good for your muscles can also be good for your mind. A Single Workout Can Alter the Brain A single, moderate workout may immediately change how our brains function and how well we recognize common names and similar information, according to a promising new study of exercise, memory and aging. The study adds to growing evidence that exercise can have rapid effects on brain function and also that these effects could accumulate and lead to long-term improvements in how our brains operate and we remember. Until recently, scientists thought that by adulthood, human brains were relatively fixed in their structure and function, especially compared to malleable tissues, like muscle, that continually grow and shrivel in direct response to how we live our lives. But multiple, newer experiments have shown that adult brains, in fact, can be quite plastic, rewiring and reshaping themselves in various ways, depending on our lifestyles. A hormone that is released during exercise may improve brain health and lessen the damage and memory loss that occur during dementia, a new study finds. The study, which was published this month in Nature Medicine, involved mice, but its findings could help to explain how, at a molecular level, exercise protects our brains and possibly preserves memory and thinking skills, even in people whose pasts are fading. Considerable scientific evidence already demonstrates that exercise remodels brains and affects thinking. Researchers have shown in rats and mice that running ramps up the creation of new brain cells in the hippocampus, a portion of the brain devoted to memory formation and storage. Exercise also can improve the health and function of the synapses between neurons there, allowing brain cells to better communicate. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 13: Memory, Learning, and Development
Link ID: 26925 - Posted: 12.30.2019

By Gina Kolata Not long ago, the only way to know if someone had Alzheimer’s disease was to examine the brain in an autopsy. That is changing — and fast — with brain scans and spinal taps that can detect beta amyloid, the telltale Alzheimer’s protein. There is a blood test on the horizon that can detect beta amyloid, and researchers are experimenting with scans to look for another protein, called tau, also characteristic of Alzheimer’s. As this sort of diagnostic testing becomes widespread, more people who fear their memories are slipping will face a difficult question: Would I really want to know if I were getting Alzheimer’s disease? “This is a new era, and we are just at the precipice,” said Dr. Gil Rabinovici, a neurologist at the University of California, San Francisco. A positive test could help you get your affairs in order and plan your future. And a drug company, Biogen, claims to have the first treatment that may slow the course of the disease if begun early enough. Health insurers are prohibited by law — for now, at least — from denying coverage if you have Alzheimer’s. But there is nothing that prevents long-term-care and life insurers from denying you. Will your friends stay with you? How about your spouse? What would it be like to live with the knowledge that you will eventually be unable to recognize your family, or even to speak? For some who have been given diagnostic tests, those questions are all too real. When Dr. Daniel Gibbs, 68, a neurologist in Portland, Ore., noticed his memory starting to slip, he wanted to know if it was Alzheimer’s. He had seen its damage all too often in his patients. © 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: 26909 - Posted: 12.21.2019

By Gina Kolata Robert D. Moir, a Harvard scientist whose radical theories of the brain plaques in Alzheimer’s defied conventional views of the disease, but whose research ultimately led to important proposals for how to treat it, died on Friday at a hospice in Milton, Mass. He was 58. His wife, Julie Alperen, said the cause was glioblastoma, a type of brain cancer. Dr. Moir, who grew up on a farm in Donnybrook, a small town in Western Australia, had a track record for confounding expectations. He did not learn to read or write until he was nearly 12; Ms. Alperen said he told her that the teacher at his one-room schoolhouse was “a demented nun.” Yet, she said, he also knew from age 7 that he wanted to be a scientist. He succeeded in becoming a researcher who was modest and careful, said his Ph.D. adviser, Dr. Colin Masters, a neuropathologist at the University of Melbourne. So Dr. Masters was surprised when Dr. Moir began publishing papers proposing an iconoclastic rethinking of the pathology of Alzheimer’s disease. Dr. Moir’s hypothesis “was and is a really novel and controversial idea that he alone developed,” Dr. Masters said. “I never expected this to come from this quiet achiever.” Dr. Moir’s theory involved the protein beta amyloid, which forms plaques in the brains of Alzheimer’s patients. Conventional wisdom held that beta amyloid accumulation was a central part of the disease, and that clearing the brain of beta amyloid would be a good thing for patients. Dr. Moir proposed instead that beta amyloid is there for a reason: It is the way the brain defends itself against infections. Beta amyloid, he said, forms a sticky web that can trap microbes. The problem is that sometimes the brain goes overboard producing it, and when that happens the brain is damaged. © 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: 26908 - Posted: 12.21.2019

By Andrea Petersen Anne Firmender, 74, was working with her psychologist to come up with a list of her positive attributes. “I cook for others,” said Ms. Firmender. “It’s giving,” encouraged the psychologist, Dimitris Kiosses. “Good kids,” continued Ms. Firmender, who has four grown children and four grandchildren. “And great mother,” added Dr. Kiosses. Ms. Firmender smiled. Dr. Kiosses typed up the list and handed a printout to Ms. Firmender to take home. “When you’re feeling down and hard on yourself, you can remind yourself of your strengths,” he told her. Ms. Firmender, who has a history of mental health problems, was in therapy for depression. But she also has mild cognitive impairment and can have trouble remembering what day it is. So Dr. Kiosses was treating her with a novel approach called Problem Adaptation Therapy, or PATH. The therapy, developed at Weill Cornell Medicine in New York City and White Plains, N.Y., focuses on solving tangible problems that fuel feelings of sadness and hopelessness. It incorporates tools, like checklists, calendars, signs and videos, to make it accessible for people with memory issues. A caregiver is often involved. The approach is one of several new psychotherapies to treat anxiety and depression in people with cognitive impairments, including early to moderate dementia. Another, the Peaceful Mind program, developed by researchers at Baylor College of Medicine and elsewhere for patients with anxiety and dementia, simplifies traditional cognitive behavioral therapy and focuses on scheduling pleasurable activities and skills, like deep breathing. Therapy sessions are short and take place in patients’ homes. A program designed by researchers at University College London gives cards to patients to take home to remind them of key strategies. One that says “Stop and Think” prompts them to pause when they have panicky and unhelpful thoughts to help keep those thoughts from spiraling and creating more anxiety. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 26884 - Posted: 12.09.2019

By Laura Sanders Call it a comeback — maybe. After being shelved earlier this year for lackluster preliminary results, a drug designed to slow Alzheimer’s progression is showing new signs of life. A more in-depth look at the data from two clinical trials suggests that patients on the biggest doses of the drug, called aducanumab, may indeed benefit, the company reported December 5. People who took the highest amounts of the drug declined about 30 percent less, as measured by a commonly used Alzheimer’s scale, than people who took a placebo, Samantha Haeberlein of the biotechnology company Biogen reported at the Clinical Trials on Alzheimer’s Disease meeting in San Diego. With these encouraging results in hand, Biogen, based in Cambridge, Mass., plans to seek drug approval from the U.S. Food and Drug Administration in early 2020. The results are “exhilarating, not just to the scientific community but our patients as well,” Sharon Cohen, a behavioral neurologist at the Toronto Memory Program, said during a panel discussion at the meeting. Cohen participated in the clinical trials and has received funding from Biogen. The presentation marks “an important moment for the Alzheimer’s field,” says Rebecca Edelmayer, director of scientific engagement for the Alzheimer’s Association in Chicago. Alzheimer’s disease slowly kills cells in the brain, gradually erasing people’s abilities to remember, navigate and think clearly. Current Alzheimer’s medicines can hold off symptoms temporarily, but don’t fight the underlying brain destruction. A treatment that could actually slow or even stop the damage would have a “huge impact for patients and their caregivers,” she says. © 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: 26879 - Posted: 12.06.2019

By Kelly Servick When Samantha Budd Haeberlein, Biogen’s head of clinical development, took the stage in San Diego, California, before a room full of Alzheimer’s disease researchers and physicians this morning, she knew she had some explaining to do. In October, the pharmaceutical company, based in Cambridge, Massachusetts, unexpectedly revived an experimental Alzheimer’s drug that it had declared a failure 7 months earlier. Ever since, scientists and industry analysts have been hungry for more detail about two large clinical trials meant to prove that Biogen’s drug, an antibody called aducanumab, slows down cognitive decline in the early stages of disease. At the Clinical Trials on Alzheimer’s Disease congress today, Budd Haeberlein tried to clarify what has emboldened the company to apply to the U.S. Food and Drug Administration (FDA) for market approval for aducanumab early next year. After analyzing more patient data than were available at the time of a discouraging preliminary analysis, she explained, the company found evidence that the higher of two tested doses led to 22% less cognitive decline after 78 weeks than a placebo in one trial. However, the other trial failed to show any benefit, leaving some researchers with a grim outlook on the drug. “I surely don’t think that it should be given market approval on the basis of these data,” says Robert Howard, a psychiatrist at University College London who has run clinical trials of potential Alzheimer’s treatments. More positive results from a subset of patients that weren’t preselected at the trial’s launch are not convincing, he says. “[Biogen has] broken all the rules, really, about how you analyze data and report it.” © 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: 26878 - Posted: 12.06.2019

Richard Harris Scientists know that if they transfuse blood from a young mouse to an old one, then they can stave off or even reverse some signs of aging. But they don't know what in the blood is responsible for this remarkable effect. Researchers now report that they've identified hundreds of proteins in human blood that wax and wane in surprising ways as we age. The findings could provide important clues about which substances in the blood can slow aging. The scientists studied nearly 3,000 proteins in blood plasma that was drawn from more than 4,000 people with a span of ages from 18 to 95. The project focused on proteins that change in both men and women. "When we went into this, we assumed you aged gradually, so we would see these changes taking place relatively steadily as individuals get older," said Tony Wyss-Coray, a professor of neurology at Stanford University. Instead, Wyss-Coray and his colleagues report in Nature Medicine on Thursday that these proteins change in three distinct waves, the first of which happens "very surprisingly" during our 30s, peaking around age 34. "Then we found a second wave around 60, and then we found a third one, the most prominent one, really around 80 years of age," Wyss-Coray said. (An earlier version of their paper is freely available on the bioRxiv preprint server.) This observation raises a host of questions about the biology of aging. What age-related transition is occurring in our 30s? And what do the changes in the blood actually mean? "Most of the proteins in the blood are actually from other tissue sources," he said. "So we can start to ask where ... these proteins come from and if they change with age," he said. For example, in proteins traced back to the liver, "that would tell us that the liver is aging." © 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: 26876 - Posted: 12.06.2019