Links for Keyword: Alzheimers

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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

Shawna Williams In September of this year, pharmaceutical companies Biogen and Eisai announced that they were halting Phase 3 clinical trials of a drug, elenbecestat, aimed at thwarting amyloid-β buildup in Alzheimer’s disease. Although the drug had seemed so promising that the companies elected to test it in two Phase 3 trials simultaneously, preliminary analyses determined that elenbecestat’s risks outweighed its benefits, and the drug shouldn’t be moved to market. The cancellation “amounts to a further step in the unwinding of Biogen’s expensive, painful, and ultimately fruitless investment in Alzheimer’s disease (AD) drug development,” analyst Geoffrey Porges told Reuters at the time. Biogen’s misfortune is just the latest in a slew of late-stage Alzheimer’s drug failures. Six months earlier, the company had halted another set of parallel Phase 3 trials due to lack of efficacy of a different drug candidate, aducanumab (though after further data analysis, Biogen announced that it will seek approval for aducanumab after all). And between 2013 and 2018, Pfizer, Eli Lilly, Merck, and Johnson & Johnson all terminated Phase 3 or Phase 2/3 trials due to poor early results. Yet some Alzheimer’s researchers say they think they’ve spotted a silver lining in this cloud of bad news—a hint in the data from these studies about how future work might meet with more success. In some of these trials, Alzheimer’s patients who were at earlier stages of the disease did better than those with more advanced cognitive decline, says Colin Masters, a neuroscientist at Florey Institute of Neuroscience and Mental Health in Australia who was not involved in the trials. This indicates that the key to finding an effective treatment might be to catch subjects before their condition advances too far, he adds. © 1986–2019 The Scientist

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: 26868 - Posted: 12.04.2019

By Claudia Wallis For more than 25 years one idea has dominated scientific thinking about Alzheimer's disease: the amyloid cascade hypothesis. It holds that the disorder, which afflicts about one in 10 Americans age 65 or older, is caused by a buildup in the brain of abnormal amyloid-beta protein, which eventually destroys neurons and synapses, producing the tragic symptoms of dementia. There's plenty of evidence for this. First, the presence of sticky clumps or “plaques” containing amyloid is a classic hallmark of the disease (along with tangles of a protein called tau). It was what Alois Alzheimer saw in the autopsied brain of patient zero in 1906. Second, families with inherited defects in amyloid precursor protein (APP) or in genes encoding proteins that process APP are plagued by early-onset Alzheimer's. Third, mice genetically engineered to churn out excess amyloid tend to develop memory problems and do better when the amyloid pileup is stopped. This evidence and more has led grant makers and drug companies to pour billions of dollars into amyloid-targeting therapies. More than a dozen have been tested, and one by one they have flopped. One of the biggest heartbreaks came last March, when a promising antibody to amyloid, called aducanumab, performed no better than placebo in patients with very early Alzheimer's. Meanwhile researchers pursuing nonamyloid approaches were often left out in the cold, struggling to get grants and to have their work published. Science journalist Sharon Begley spent more than a year reporting on the lost opportunities in an article for the Web site Stat entitled “The Maddening Saga of How an Alzheimer's ‘Cabal’ Thwarted Progress toward a Cure for Decades.” Begley notes that the amyloid crowd was “neither organized nor nefarious,” but its outsized influence stifled other avenues of investigation. © 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: 26867 - Posted: 12.04.2019

Emily Makowski China’s approval of the drug oligomannate earlier this month for treating mild to moderate Alzheimer’s disease has been met with surprise and skepticism from some members of the scientific community, who claim that the preclinical data raise questions about the underlying mechanism of the drug. One microbiome researcher has pointed out inconsistencies between the researchers’ data and their proposed mechanism for how oligomannate could treat Alzheimer’s. “The field is seeing this [research] with a large dose of skepticism,” Malú Tansey, a neuroimmunologist at the University of Florida College of Medicine, tells The Scientist. On November 2, Shanghai Green Valley Pharmaceuticals announced that oligomannate, an oligosaccharide mixture derived from brown algae, had been approved by the National Medical Product Administration (NMPA), China’s equivalent of the US Food and Drug Administration. The announcement followed the completion of a Phase 3 clinical trial in China that found the drug appeared to slow cognitive decline in Alzheimer’s patients. In addition, researchers led by Meiyu Geng at the Shanghai Institute of Materia Medica published a paper in Cell Research in September on oligomannate’s ability to remodel the gut microbiome in mice and reduce neuroinflammation. There is an emerging link between the gut microbiome and Alzheimer’s disease in humans. In the study, the researchers gave oligomannate to mice that are genetically engineered to show physical and behavioral symptoms similar to Alzheimer’s disease. The team collected mouse feces to study the microorganisms present in gut microbiota, drew blood to analyze the presence of immune cells, and also examined the levels of cytokines, which are inflammatory compounds, in the brain. © 1986–2019 The Scientist

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: 26821 - Posted: 11.16.2019

By Gary Stix Socrates famously railed against the evils of writing. The sage warned that it would “introduce forgetfulness into the soul of those who learn it: they will not practice using their memory because they will put their trust in writing.” He got a few things wrong. For one, people nurture Socrates’ memory because of all of the books written about him. But he also was off the mark in his musings about a forgetfulness of the soul. If anything, it appears that just the opposite holds: a study of hundreds of illiterate people living at the northern end of an island considered to be a world media capital roundly contradicts the father of Western philosophy. Evaluations of the elderly in the environs of Manhattan’s Washington Heights (the neighborhood immortalized by a Lin-Manuel Miranda musical) reveal that the very act of reading or writing—largely apart from any formal education—may help protect against the forgetfulness of dementia. “The people who were illiterate in the study developed dementia at an earlier age than people who were literate in the study,” says Jennifer J. Manly, senior author of the paper, which appeared on November 13in Neurology. Earlier studies trying to parse this topic had not been able to disentangle the role of reading and writing from schooling to determine whether literacy, by itself, could be a pivotal factor safeguarding people against dementia later in life. The researchers conducting the new study, who are mostly at Columbia University’s Vagelos College of Physicians and Surgeons, recruited 983 people with four years or less of schooling who were part of the renowned Washington Heights–Inwood Columbia Community Aging Project. Of that group, 238 were illiterate, which was determined by asking the participants point-blank, “Did you ever learn to read or write?”—followed by reading tests administered to a subsample. Even without much time in school, study subjects sometimes learned from other family members. © 2019 Scientific American

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: 26819 - Posted: 11.14.2019

By Sara Manning Peskin, M.D. At 66, Bob Karger was losing language. It was not the tip-of-the-tongue feeling that melts when you recall a sought-after word. He had lost the connection between sounds and meaning — the way ba-na-na recalls a soft, yellow fruit or ea-gle calls to mind a large bird of prey. In a recent conversation, he had thought acorns grew on pine trees. Mr. Karger did not know how to use items around the house, either. When he picked up a can opener, he would not realize it could remove the top from a tin. If he held a hammer, he might grasp it by the head, turning it around in his palm, not knowing he could swing it into a nail. His world was filled with incomprehensible items. His wife, Sandy Karger, noticed other changes. When she told her husband about a family member who died, Mr. Karger laughed instead of comforting her. He tipped excessively, slipping $20 bills to strangers, because they reminded him of close friends. He fixated on obese people. “Look at that person, they’re really fat,” he would say loudly, in public. Overcome by impatience, he would push people ahead of him in line at the store. “Can’t you hurry up?” he’d yell. “Do you really need to buy that?” In other ways, Mr. Karger’s mind was as sharp as it had ever been. He could remember upcoming appointments and recent dinners. He didn’t repeat himself in conversation. His long-term memory was at times better than Ms. Karger’s. After two years of worsening symptoms, the Kargers found Dr. Murray Grossman at the University of Pennsylvania. Dr. Grossman is short and charismatic, a quick-witted Montreal native who has mentored me since I began training in neurology. For the past several decades, he has pioneered research on neurodegenerative diseases that change behavior and language. When he saw Mr. Karger in 2007, the diagnosis was clear within the hour: Mr. Karger had a type of frontotemporal dementia. © 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: 26799 - Posted: 11.07.2019

By Andrew Joseph, STAT Chinese regulators have granted conditional approval to an Alzheimer’s drug that is derived from seaweed, potentially shaking up the field after years of clinical failures involving experimental therapies from major drug companies. The announcement over the weekend has been met with caution as well as an eagerness from clinicians and others to see full data from the drug maker, Shanghai Green Valley Pharmaceuticals. The company said its drug, Oligomannate, improved cognitive function in patients with mild to moderate Alzheimer’s compared to placebo in a Phase 3 trial, with benefits seen in patients as early as week four and persisting throughout the 36 weeks of the trial. It has been almost two decades since any Alzheimer’s drug was approved. Oligomannate has received scant attention in the United States during its development. Advertisement Although full data on the drug have not yet been made available, the conditional approval by regulators means Oligomannate, also known as GV-971, will on the market in China by the end of the year, Green Valley said. The company will have to submit additional research on the mechanism of the drug and its long-term safety and effectiveness to the country’s National Medical Products Administration, Reuters reported. Green Valley also said it would launch a global Phase 3 trial next year in hopes of filing for approval in other countries as well. “It’s good to see that drug regulators in China are prioritizing emerging treatments for Alzheimer’s, but we do still need to see more evidence that this drug is safe and effective,” Carol Routledge, the director of research at Alzheimer’s Research UK, said in a statement. “For any potential drug to gain a stamp of approval by regulators in the UK, we’ll need to see larger trials in countries around the world to back up the evidence from China.” © 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: 26795 - Posted: 11.06.2019

By Gretchen Reynolds Being physically fit may sharpen the memory and lower our risk of dementia, even if we do not start exercising until we are middle-aged or older, according to two stirring new studies of the interplay between exercise, aging, aerobic fitness and forgetting. But both studies, while underscoring the importance of activity for brain health, also suggest that some types of exercise may be better than others at safeguarding and even enhancing our memory. The scientific evidence linking exercise, fitness and brain health is already hefty and growing. Multiple studies have found that people with relatively high levels of endurance, whatever their age, tend to perform better on tests of thinking and memory than people who are out of shape. Other studies associate better fitness with less risk for developing Alzheimer’s disease. But many of these studies have been one-time snapshots of people’s lives and did not delve into whether and how changing fitness over time might alter people’s memory skills or dementia risk. They did not, in other words, tell us whether, by midlife or retirement age, it might be too late to improve our brain health with exercise. So, for the first of the new studies, which was published this month in The Lancet Public Health, researchers at the Norwegian University of Science and Technology in Trondheim, Norway, helpfully decided to look into that very issue, taking advantage of the reams of health data available on average Norwegians. They began by turning to records from a large-scale health study that had enrolled almost every adult resident in the region around Trondheim beginning in the 1980s. The participants completed health and medical testing twice, about 10 years apart, that included estimates of their aerobic fitness. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 5: The Sensorimotor System
Link ID: 26794 - Posted: 11.06.2019

By Pam Belluck The woman’s genetic profile showed she would develop Alzheimer’s by the time she turned 50. She, like thousands of her relatives, going back generations, was born with a gene mutation that causes people to begin having memory and thinking problems in their 40s and deteriorate rapidly toward death around age 60. But remarkably, she experienced no cognitive decline at all until her 70s, nearly three decades later than expected. How did that happen? New research provides an answer, one that experts say could change the scientific understanding of Alzheimer’s disease and inspire new ideas about how to prevent and treat it. In a study published Monday in the journal Nature Medicine, researchers say the woman, whose name they withheld to protect her privacy, has another mutation that has protected her from dementia even though her brain has developed a major neurological feature of Alzheimer’s disease. This ultra rare mutation appears to help stave off the disease by minimizing the binding of a particular sugar compound to an important gene. That finding suggests that treatments could be developed to give other people that same protective mechanism. “I’m very excited to see this new study come out — the impact is dramatic,” said Dr. Yadong Huang, a senior investigator at Gladstone Institutes, who was not involved in the research. “For both research and therapeutic development, this new finding is very important.” A drug or gene therapy would not be available any time soon because scientists first need to replicate the protective mechanism found in this one patient by testing it in laboratory animals and human brain cells. © 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: 26792 - Posted: 11.05.2019

By Derek Lowe So Amgen has exited the neuroscience area, with a good-sized round of layoffs at their research site Cambridge. The company has a migraine drug (Aimovig) that they’ll continue to support, and they’ll stick with their existing clinical programs, but it looks like all the early-stage stuff is gone. What does this mean? Not as much as you might think. Neuroscience is indeed hard, and Amgen’s not the only company to rethink its commitment to it (Eli Lilly did something similar last month with their neuro efforts in the UK). But there are still plenty of participants, large and small – it’s not that the field is being totally abandoned by pharma. It’s just being abandoned by Amgen, because they have other areas that look a lot more promising for them. And let’s face it, Amgen is a bit of an oddity, anyway – it’s not for nothing that they get referred to as a law firm with fume hoods. Enbrel is what pays a lot of the bills over there, and Enbrel is (and has long been) a patent-court story, not a research one. Inflammation, cardiovascular disease, and oncology are going to be the focus there, and given the company’s portfolio, that makes a lot of sense. It looks like the only neuro programs going on will be the ones that intersect with the larger inflammation area. One interesting thing that came out of the company’s statements was that management felt that a lot of the neuroscience landscape is focused on what their CFO David Meline called “orphan or niche diseases”, and that the company wants to work on things that will have a broader impact. Now, it’s not like there isn’t a neuroscience disease with a huge health impact, and it’s one that even has some inflammation and cardiovascular connections. So one of the things that Amgen is saying is “No Alzheimer’s research for us, thanks”. © 2017 American Association for the Advancement of Science

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: 26777 - Posted: 11.01.2019