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By Annabelle Timsit A new study of more than 29,000 older adults has identified six habits — from eating a variety of foods to regularly reading or playing cards — that are linked with a lower risk of dementia and a slower rate of memory decline. Eating a balanced diet, exercising the mind and body regularly, having regular contact with others, and not drinking or smoking — these six “healthy lifestyle factors” were associated with better cognitive outcomes in older adults, in a large Chinese study conducted over a decade and published in the BMJ on Wednesday. While researchers have long known that there is a link between dementia and factors such as social isolation and obesity, the size and scope of the new study adds substantial evidence to a global body of research that suggests a healthy lifestyle may help brains age better. It also suggests that the effects of a healthy lifestyle are beneficial even for people who are genetically more susceptible to memory decline — a “very hope-giving” finding for the millions of individuals around the world who carry the APOEε4 gene, a major risk factor for Alzheimer’s disease, said Eef Hogervorst, chair of biological psychology at Loughborough University, who was not involved in the study. Memory naturally declines gradually as people age. Some older people may develop dementia, an umbrella term that can include Alzheimer’s, and generally describes a deterioration in cognitive function that goes beyond the normal effects of aging. But for many, “memory loss can merely be senescent forgetfulness,” write the authors of the BMJ study — like forgetting the name of that TV program you used to love, or that pesky fact you wanted to look up. Memory loss is no less damaging for being gradual, and age-related memory decline can in some cases be an early symptom of dementia. But the good news, the researchers say, is that it “can be reversed or become stable rather than progress to a pathological state.” How do you live to be 100? Good genes, getting outside and friends.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 28644 - Posted: 01.27.2023

ByMeredith Wadman A massive data mining study has found numerous associations between common viruses like the flu and devastating neurodegenerative disorders such as Parkinson’s disease, Alzheimer’s disease, and amyotrophic lateral sclerosis (ALS, also known as Lou Gehrig’s disease). The findings expand on previous research linking individual viruses to neurological diseases. But experts caution that the study, which relied on electronic medical records rather than biological samples, merely describes correlations and doesn’t prove causation. Still, it’s “really exciting,” says Kristen Funk, a neuroimmunologist who studies Alzheimer’s at the University of North Carolina, Charlotte. Rather than homing in on, say, the relationship between herpes simplex infections and Alzheimer’s—a recent focus in her own field—“this research broadens that scope to look at different viruses and more neurodegenerative diseases.” Scientists have found connections between viruses and neurodegenerative diseases before. Previous studies uncovered ties between the influenza virus and Parkinson’s, for example, and between genital warts (caused by human papillomavirus) and dementia. A landmark project published in Science last year cemented another connection: Epidemiologists who analyzed 2 decades of data from the blood tests of 10 million U.S. soldiers reported that it’s nearly impossible to develop multiple sclerosis without first being infected with the Epstein-Barr virus—a ubiquitous pathogen long suspected of causing MS. Inspired by that paper, National Institutes of Health (NIH) researchers wondered whether they could mine other large databases to tease out more associations. They focused on viral links to six neurodegenerative diseases: Alzheimer’s, Parkinson’s, dementia, ALS, MS, and vascular dementia. (Some scientists dispute that MS and vascular dementia are neurodegenerative diseases.)

Related chapters from BN: 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 and Learning
Link ID: 28638 - Posted: 01.25.2023

Kaitlyn Radde Socially isolated older adults have a 27% higher chance of developing dementia than older adults who aren't, a new study by Johns Hopkins researchers found. "Social connections matter for our cognitive health, and it is potentially easily modifiable for older adults without the use of medication," Dr. Thomas Cudjoe, an assistant professor of medicine at Johns Hopkins and a senior author of the study, said in a news release. Published in the Journal of the American Geriatrics Society, the study tracked 5,022 dementia-free U.S. adults who were 65 or older – with an average age of 76 – and not living in a residential care facility. About 23% of participants were socially isolated. Social isolation is defined as having few relationships and few people to interact with regularly. The study measured this based on whether or not participants lived alone, talked about "important matters" with two or more people in the past year, attended religious services or participated in social events. Participants were assigned one point for each item, and those who scored a zero or one were classified as socially isolated. Over the course of nine years, researchers periodically administered cognitive tests. Overall, about 21% of the study participants developed dementia. But among those were who were socially isolated, about 26% developed dementia – compared to slightly less than 20% for those who were not socially isolated. The study did not find significant differences by race or ethnicity. However, more than 70% of the participants in the study were white – with particularly small sample sizes of Hispanic, Asian and Native participants – and the authors call for further research on the topic. © 2023 npr

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 11: Emotions, Aggression, and Stress
Link ID: 28631 - Posted: 01.18.2023

By Laurie McGinley The Food and Drug Administration on Friday approved an Alzheimer’s drug that slowed cognitive decline in a major study, offering patients desperately needed hope — even as doctors sharply debated the safety of the drug and whether it provides a significant benefit. The FDA said the drug, called lecanemab, is for patients with mild cognitive impairment or early dementia because of Alzheimer’s. The accelerated approval was based on a mid-stage trial that showed the treatment effectively removed a sticky protein called amyloid beta — considered a hallmark of the illness — from the brain. A larger trial, conducted more recently, found the drug, which will be sold under the brand name Leqembi, slowed the progression of Alzheimer’s disease by 27 percent. “This treatment option is the latest therapy to target and affect the underlying disease process of Alzheimer’s, instead of only treating the symptoms of the disease,” Billy Dunn, director of the FDA’s Office of Neuroscience, said in a statement. The approval followed a barrage of criticism endured by the FDA for its 2021 approval of Aduhelm, another amyloid-targeting drug that had been panned by the agency’s outside experts. Lecanemab is getting a warmer reception but disagreements remain. Many neurologists and advocates hailed lecanemab, given intravenously twice a month, as an important advance — one that follows years of failure involving Alzheimer’s drugs. They said the treatment will allow patients to stay longer in the milder stages of the fatal, neurodegenerative disorder, which afflicts more than 6 million people in the United States.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 28622 - Posted: 01.07.2023

Linda Geddes Science correspondent Scientists have developed a blood test to diagnose Alzheimer’s disease without the need for expensive brain imaging or a painful lumbar puncture, where a sample of cerebrospinal fluid (CSF) is drawn from the lower back. If validated, the test could enable faster diagnosis of the disease, meaning therapies could be initiated earlier. Alzheimer’s is the most common form of dementia, but diagnosis remains challenging – particularly during the earlier stages of the disease. Current guidelines recommend detection of three distinct markers: abnormal accumulations of amyloid and tau proteins, as well as neurodegeneration – the slow and progressive loss of neuronal cells in specified regions of the brain. This can be done through a combination of brain imaging and CSF analysis. However, a lumbar puncture can be painful and people may experience headaches or back pain after the procedure, while brain imaging is expensive and takes a long time to schedule. Prof Thomas Karikari at the University of Pittsburgh, in Pennsylvania, US, who was involved in the study, said: “A lot of patients, even in the US, don’t have access to MRI and PET scanners. Accessibility is a major issue.” The development of a reliable blood test would be an important step forwards. “A blood test is cheaper, safer and easier to administer, and it can improve clinical confidence in diagnosing Alzheimer’s and selecting participants for clinical trial and disease monitoring,” Karikari said. Although current blood tests can accurately detect abnormalities in amyloid and tau proteins, detecting markers of nerve cell damage that are specific to the brain has been harder. Karikari and his colleagues around the world focused on developing an antibody-based blood test that would detect a particular form of tau protein called brain-derived tau, which is specific to Alzheimer’s disease. © 2022 Guardian News & Media Limited

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 28616 - Posted: 12.28.2022

By Anthea Rowan To many, the word “hobby” signifies something lightweight or trivial. Yet taking on a new hobby as one ages might provide an important defense against dementia, some experts say. About 5.8 million adults over 65 in the United States live with Alzheimer’s disease or other dementia disorders, according to the Centers for Disease Control and Prevention. One in 9 Americans over 65 has Alzheimer’s, according to the Alzheimer’s Association. And although the rate of dementia may be falling thanks to lifestyle changes, more of us are living longer, which means the societal burden of dementia is rising. David Merrill, an adult and geriatric psychiatrist and director of the Pacific Brain Health Center in Santa Monica, Calif., suggests we use the word “pursuit” instead of “hobby,” as it elevates the concept of an activity to something demanding, something requiring concentration or collaboration. Something we ought to chase down. Activities that demand focus and industry are the whetstone to keeping cognition sharp, Merrill says. Our brains, he continues, are like any other part of our body. “‘Use it or lose it’ is not just a hypothesis, it’s a basic biologic fact that holds as true for our brains as our muscles or our bones.” While there is as yet no surefire way to prevent dementia or cure it, the Lancet in 2020 identified 12 potentially modifiable risk factors for the condition; they include physiological (blood pressure, diabetes, hearing loss), lifestyle choices (smoking, drinking, physical inactivity), environmental (air pollution) depression, social isolation and a lower level of education. The Alzheimer Society of Canada is also clear about what we can do to help minimize our dementia risk: keep cognitively engaged, learn new things, meet new people, keep a diary, remain curious and engage in conversations.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 13: Memory and Learning
Link ID: 28605 - Posted: 12.21.2022

Patrick Barkham Three species of cetacean stranded off the coast of Scotland, including a bottlenose dolphin and a long-finned pilot whale, have been found to have the classic markers of Alzheimer’s disease, according to a study. Although types of dementia have been fairly widely detected in other animals, Alzheimer’s disease has not been found to occur naturally in species other than humans. But researchers from the University of Glasgow, the universities of St Andrews and Edinburgh and the Moredun Research Institute in Scotland were surprised to find that postmortem tests of 22 toothed whales, or odontocetes, detected three key brain changes associated with human Alzheimer’s disease in three animals. Scientists do not know the cause of this brain degeneration but it could support one theory about why some groups or pods of whales and dolphins run aground in shallow water. Some mass strandings have been linked to increasing anthropogenic noise in the oceans, but Alzheimer’s-like signs in the brain could support a “sick leader” theory, whereby mostly healthy cetaceans are stranded because they follow a group leader that has become confused or lost. The researchers found signs of Alzheimer’s in three of 22 stranded odontocetes: a white-beaked dolphin, a bottlenose dolphin and a long-finned pilot whale, also a member of the dolphin family.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 28604 - Posted: 12.21.2022

By Yasemin Saplakoglu It’s often subtle at first. A lost phone. A forgotten word. A missed appointment. By the time a person walks into a doctor’s office, worried about signs of forgetfulness or failing cognition, the changes to their brain have been long underway — changes that we don’t yet know how to stop or reverse. Alzheimer’s disease, the most common form of dementia, has no cure. “There’s not much you can do. There are no effective treatments. There’s no medicine,” said Riddhi Patira, a behavioral neurologist in Pennsylvania who specializes in neurodegenerative diseases. That’s not how the story was supposed to go. Three decades ago, scientists thought they had cracked the medical mystery of what causes Alzheimer’s disease with an idea known as the amyloid cascade hypothesis. It accused a protein called amyloid-beta of forming sticky, toxic plaques between neurons, killing them and triggering a series of events that made the brain waste away. The amyloid cascade hypothesis was simple and “seductively compelling,” said Scott Small, the director of the Alzheimer’s Disease Research Center at Columbia University. And the idea of aiming drugs at the amyloid plaques to stop or prevent the progression of the disease took the field by storm. Decades of work and billions of dollars went into funding clinical trials of dozens of drug compounds that targeted amyloid plaques. Yet almost none of the trials showed meaningful benefits to patients with the disease. That is, until September, when the pharmaceutical giants Biogen and Eisai announced that in a phase 3 clinical trial, patients taking the anti-amyloid drug lecanemab showed 27% less decline in their cognitive health than patients taking a placebo did. Last week, the companies revealed the data, now published in the New England Journal of Medicine, to an excited audience at a meeting in San Francisco. Simons Foundation © 2022

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 28595 - Posted: 12.15.2022

Kristine Zengeler Many neurodegenerative diseases, or conditions that result from the loss of function or death of brain cells, remain largely untreatable. Most available treatments target just one of the multiple processes that can lead to neurodegeneration, which may not be effective in completely addressing disease symptoms or progress, if at all. But what if researchers harnessed the brain’s inherent capabilities to cleanse and heal itself? My colleagues and I in the Lukens Lab at the University of Virginia believe that the brain’s own immune system may hold the key to neurodegenerative disease treatment. In our research, we found a protein that could possibly be leveraged to help the brain’s immune cells, or microglia, stave off Alzheimer’s disease. No available treatments for neurodegenerative diseases stop ongoing neurodegeneration while also helping affected areas in the body heal and recuperate. In terms of failed treatments, Alzheimer’s disease is perhaps the most infamous of neurodegenerative diseases. Affecting more than 1 in 9 U.S. adults 65 and older, Alzheimer’s results from brain atrophy with the death of neurons and loss of the connections between them. These casualties contribute to memory and cognitive decline. Billions of dollars have been funneled into researching treatments for Alzheimer’s, but nearly every drug tested to date has failed in clinical trials.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 11: Emotions, Aggression, and Stress
Link ID: 28590 - Posted: 12.13.2022

By Gina Kolata In a bold attempt to stop the progress of some cases of Alzheimer’s disease, a group of researchers is trying something new — injecting a protective gene into patients’ brains. The trial involved just five patients with a particular genetic risk for Alzheimer’s. They received a very low dose of the gene therapy — a test of safety, which the treatment passed. But the preliminary results, announced Friday during the Clinical Trials on Alzheimer’s Disease conference, showed that proteins from the added gene appeared in the patients’ spinal fluid, and levels in the brain of two markers of Alzheimer’s disease, tau and amyloid, fell. Those findings were promising enough to advance the clinical trial into its next phase. Treatment of another five patients at a higher dose is underway, and the work, initially funded by the nonprofit Alzheimer’s Drug Discovery Foundation, is supported by Lexeo Therapeutics, a fledgling company founded by Dr. Ronald Crystal, who is also chairman of the department of genetic medicine at Weill Cornell Medicine in New York. The hope is to get a stronger response, eventually leading to a treatment that might slow the disease in whom it has started or, even better, protect people at high risk who have no symptoms. “It’s a very provocative, very intriguing approach,” said Dr. Eliezer Masliah, director of the neuroscience division at the National Institute on Aging. Participants in the study are among the approximately 2 percent of people who have inherited a pair of copies of a gene, APOE4, which markedly increases their risk of Alzheimer’s. For the study subjects, the first symptoms of Alzheimer’s had already emerged — their genetic risk had played out, and they had few options. There is no treatment that is directed specifically at APOE4-driven Alzheimer’s, nor is one on the near horizon. © 2022 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 28575 - Posted: 12.03.2022

By Pam Belluck The hotly anticipated results of a clinical trial of an experimental Alzheimer’s drug suggest that the treatment slowed cognitive decline somewhat for people in the early stages of the disease but also caused some patients to experience brain swelling or brain bleeding. The new data, released Tuesday evening, offered the first detailed look at the effects of the drug, lecanemab, and comes two months after its manufacturers, Eisai and Biogen, stoked excitement by announcing that the drug had shown positive results. Alzheimer’s experts said the new information showed reason for both optimism and caution. “The benefit is real; so too are the risks,” said Dr. Jason Karlawish, a co-director of the University of Pennsylvania’s Penn Memory Center, who was not involved in the research. A report of the findings published in the New England Journal of Medicine said that over 18 months, lecanemab “resulted in moderately less decline on measures of cognition and function,” compared with patients receiving a placebo. Still, the study of nearly 1,800 patients with mild symptoms, which was funded by the companies and co-written by scientists at Eisai, concluded that “longer trials are warranted to determine the efficacy and safety of lecanemab in early Alzheimer’s disease.” The companies’ initial announcement in September had sent their stock prices soaring because the field of Alzheimer’s drug development has been marked by years of failures. © 2022 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 28572 - Posted: 11.30.2022

Ian Sample Science editor At the end of November, thousands of researchers from around the world will descend on San Francisco for the annual Clinical Trials on Alzheimer’s Disease meeting. The conference is a mainstay of the dementia research calendar, the place where the latest progress – and all too often, setbacks – in the quest for Alzheimer’s treatments are made public for the first time. This year’s meeting is poised to be a landmark event. After more than a century of research into Alzheimer’s, scientists expect to hear details of the first treatment that can unambiguously alter the course of the disease. Until now, nothing has reversed, halted or even slowed the grim deterioration of patients’ brains. Given that dementia and Alzheimer’s are the No 1 killer in the UK, and the seventh largest killer worldwide, there is talk of a historic moment. The optimism comes from a press statement released in September from Eisai, a Japanese pharmaceutical firm, and Biogen, a US biotech. It gave top-line results from a major clinical trial of an antibody treatment, lecanemab, given to nearly 2,000 people with early Alzheimer’s disease. The therapy slowed cognitive decline, the statement said, raising hopes that a drug might finally apply the brakes to Alzheimer’s and provide “a clinically meaningful impact on cognition and function”. The announcement was greeted, broadly, with delight and relief from researchers who have endured failure after failure in the long search for Alzheimer’s drugs. But even the most enthusiastic conceded that significant questions remained. With only a press release to go on, it was hard to be sure the claims stood up. The answer will come on 29 November when researchers leading the trial, named Clarity AD, present their results at the San Francisco meeting. © 2022 Guardian News & Media Limited

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 28562 - Posted: 11.23.2022

By Laurie McGinley Few illnesses instill as much fear as Alzheimer’s, a fatal neurodegenerative disease that destroys memory and identity. The dread is compounded by the uncertainty that often surrounds the diagnosis of the most common form of dementia. Brain autopsies remain the only way to know for sure whether someone had the disease, which the Centers for Disease Control and Prevention estimates affects 6.5 million people in the United States. Over the past several years, sophisticated tests such as spinal taps and specialized PET scans have become available — but they are invasive and costly and not routinely used. As a result, Alzheimer’s is frequently misdiagnosed, especially in the early stages. Other illnesses, including depression, can have similar symptoms and require other treatments. But simple blood tests designed to help doctors diagnose Alzheimer’s now are on the market. More are on the way. The tests are seen as an important scientific advance, but have ignited debate about how and when they should be used. Some experts say much more research is needed before the new tests can be widely deployed, especially in primary-care settings. Others say there already is sufficient information on the accuracy of some tests. All agree that no single test is perfect and physicians still should perform a complete clinical assessment. Widespread use of the tests may be some time off in the future — after insurance coverage improves and even more accurate next-generation tests become available. For now, none is covered by Medicare, and private insurance coverage is patchy. In the past few years, scientific and technological advances have made it possible to detect in the blood tiny fragments of brain proteins implicated in Alzheimer’s. That has prompted experts in academia and industry to develop blood tests for the disease. Some of the tests detect a sticky protein called amyloid beta, while others look for another protein called tau. Some search for both or other markers of disease. The abnormal accretions of amyloid plaques and tau tangles are the defining characteristics of Alzheimer’s. washingtonpost.com © 1996-2022

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 28560 - Posted: 11.19.2022

By Elie Dolgin, No gene variant is a bigger risk factor for Alzheimer’s disease than one called APOE4. But exactly how the gene spurs brain damage has been a mystery. A study has now linked APOE4 with faulty cholesterol processing in the brain, which in turn leads to defects in the insulating sheaths that surround nerve fibres and facilitate their electrical activity. Preliminary results hint that these changes could cause memory and learning deficits. And the work suggests that drugs that restore the brain’s cholesterol processing could treat the disease. “This fits in with the picture that cholesterol needs to be in the right place,” says Gregory Thatcher, a chemical biologist at the University of Arizona in Tucson. Inheriting a single copy of APOE4 raises the risk of developing Alzheimer’s around 3-fold; having two copies boosts the chances 8- to 12-fold. Interactions between the protein encoded by APOE4 and sticky plaques of amyloid—a substance tied to brain cell death—in the brain partially explain the connection. But those interactions are not the whole story. As neuroscientist Li-Huei Tsai at the Massachusetts Institute of Technology (MIT) in Cambridge and her colleagues report today in Nature, APOE4 triggers insulation-making brain cells known as oligodendrocytes to accumulate the fatty molecule cholesterol—a type of lipid—in all the wrong places. This interferes with the cells’ ability to cover nerve fibres in a protective wrapper made of a lipid-rich material called myelin. Electrical signalling in the brain then slows, and cognition usually suffers. Tsai’s team had previously linked lipid changes to malfunctions in other cell types, including some that offer structural support to neurons and others that provide immune protection for the brain. The latest findings add oligodendrocytes and their essential myelin function to the mix. © 2022 Scientific American

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 28558 - Posted: 11.19.2022

By Laurie McGinley An experimental Alzheimer’s drug designed to slow cognitive decline failed to meet the goals of two closely watched clinical trials, a discouraging development that underscores the challenges of developing treatments for the memory-robbing disease. Genentech, a division of health-care giant Roche, said in a news release Monday that the treatment, called gantenerumab, slowed the pace of decline in patients with early-stage disease but not enough to be statistically significant. The therapy was tested in identical late-stage trials, each with 1,000 participants. Half received placebos and half got the treatment. The studies lasted 27 months. The drug, a monoclonal antibody, is designed to remove from the brain clumps of an abnormal version of a protein called amyloid beta, a hallmark of the disease. The company said Monday that the treatment removed less amyloid beta than expected. Some scientists have thought for years that amyloid-busting medicines could slow the fatal neurodegenerative disease, but there have been multiple failures, and just a few encouraging signs, involving amyloid-busting drugs. “So many of our families have been directly affected by Alzheimer’s, so this news is very disappointing to deliver,” Levi Garraway, Roche’s chief medical officer and head of global product development, said in a statement. He said the company looks forward to sharing more information about the results “as we continue to search for new treatments for this complex disease.” Genentech said that 25 percent of the patients who received gantenerumab experienced a side effect that can cause brain swelling and bleeding but that most did not have symptoms and few needed to stop taking the drug. The company said it planned to present more data from the trials at an Alzheimer’s conference this month. The company assessed the drug by measuring trial participants’ performance on an 18-point measure of memory and cognition, called the Clinical Dementia Rating scale — Sum of Boxes. The news on gantenerumab is a disappointment for patients, physicians and researchers desperate for effective treatments for a disease that affects 6.5 million Americans.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 28554 - Posted: 11.16.2022

Jon Hamilton An idea that has propelled Alzheimer's research for more than 30 years is approaching its day of reckoning. Scientists are launching a study designed to make or break the hypothesis that Alzheimer's is caused by a sticky substance called beta-amyloid. The study will give an experimental anti-amyloid drug to people as young as 18 who have gene mutations that often cause Alzheimer's to appear in their 30s or 40s. The study comes after several experimental drugs have failed to prevent declines in memory and thinking even though they succeeded in removing amyloid from the brains of patients in the early stages of Alzheimer's. Those failures have eroded support for the idea that amyloid is responsible for a cascade of events that eventually lead to the death of brain cells. "Many of us think of that as the ultimate test of the amyloid hypothesis," says Dr. Randall Bateman, a professor of neurology at Washington University School of Medicine in St. Louis."If that doesn't work, nothing will work." The new experiment, called the DIAN-TU primary Prevention Trial, is scheduled to begin enrolling patients by the end of the year. The amyloid hypothesis can be traced to Dr. Alois Alzheimer, a pathologist who first described the disease that would bear his name in 1906. Alzheimer was working at a psychiatric clinic in Munich, where he had the chance to conduct an autopsy on a woman who died at 50 after experiencing memory loss, disorientation, and hallucinations. He observed that the woman's brain had an "unusual disease of the cerebral cortex," including "senile plaque" usually seen in much older people. © 2022 npr

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 28534 - Posted: 11.02.2022

Nina Lakhani The mystery behind the astronomical rise in neurological disorders like Parkinson’s disease and Alzheimer’s could be caused by exposure to environmental toxins that are omnipresent yet poorly understood, leading doctors warn. At a conference on Sunday, the country’s leading neurologists and neuroscientists will highlight recent research efforts to fill the gaping scientific hole in understanding of the role environmental toxins – air pollution, pesticides, microplastics, forever chemicals and more – play in increasingly common diseases like dementias and childhood developmental disorders. Humans may encounter a staggering 80,000 or more toxic chemicals as they work, play, sleep and learn – so many that it is almost impossible to determine their individual effects on a person, let alone how they may interact or the cumulative impacts on the nervous system over a lifespan. Some contact with environmental toxins is inevitable given the proliferation of plastics and chemical pollutants, as well as America’s hands off regulatory approach, but exposure is unequal. In the US, communities of color, Indigenous people and low income families are far more likely to be exposed to a myriad of pollutants through unsafe housing and water, manufacturing and agricultural jobs, and proximity to roads and polluting industrial plants, among other hazards. It’s likely genetic makeup plays a role in how susceptible people are to the pathological effects of different chemicals, but research has shown higher rates of cancers and respiratory disease in environmentally burdened communities. © 2022 Guardian News & Media Limited

Related chapters from BN: 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 and Learning
Link ID: 28526 - Posted: 10.26.2022

Andrew Gregory Health editor Scientists have discovered that it may be possible to spot signs of dementia as early as nine years before patients receive an official diagnosis. The findings raise the possibility that, in the future, at-risk people could be screened to help select those who could benefit from interventions, or help identify patients suitable for clinical trials for new treatments. Researchers at Cambridge University published the study – funded by the Medical Research Council with support from the NIHR Cambridge Biomedical Research Centre – in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association. Dr Richard Oakley, associate director of research at the Alzheimer’s Society, said the “important” findings suggested that “for some people who go on to develop Alzheimer’s disease, memory and thinking problems can begin up to nine years before they receive a diagnosis”. Advertisement He added: “This opens up the possibility of screening programmes in the future to help identify people at risk and who may benefit from interventions, and identify more people suitable for clinical trials for new dementia treatments, which are both so desperately needed.” The study’s first author, Nol Swaddiwudhipong, said: “When we looked back at patients’ histories, it became clear that they were showing some cognitive impairment several years before their symptoms became obvious enough to prompt a diagnosis. The impairments were often subtle, but across a number of aspects of cognition. “This is a step towards us being able to screen people who are at greatest risk – for example, people over 50 or those who have high blood pressure or do not do enough exercise – and intervene at an earlier stage to help them reduce their risk.” Man in bed with pillow over his head. © 2022 Guardian News & Media Limited

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 28513 - Posted: 10.15.2022

McKenzie Prillaman Some researchers are celebrating this week’s announcement that a drug candidate for Alzheimer’s disease slowed the rate of cognitive decline for people in a clinical trial by 27%. Others, however, remain hesitant, wanting to see data beyond what was disclosed in a 27 September press release. If the results stand up, the treatment — called lecanemab — would be the first of its kind to show a strong signal of cognitive benefit in a robust trial. “It’s such a win for our field,” says Liana Apostolova, a neurologist at the Indiana University School of Medicine in Indianapolis. The results are “quite promising”, says Caleb Alexander, an internal-medicine specialist and epidemiologist at the Johns Hopkins Bloomberg School of Public Health in Baltimore, Maryland, and an advisory committee member for the US Food and Drug Administration (FDA). But, he adds, “we’ll have to see what the full analysis of the trial suggests”. Alexander and others also note that, although the results indicate that lecanemab does provide some clinical benefit, the degree to which it does so is small. Developed by Eisai, a pharmaceutical company in Tokyo, and biotechnology firm Biogen in Cambridge, Massachusetts, lecanemab is a monoclonal antibody designed to clear clumps of protein from the brain that many think are a root cause of Alzheimer’s disease. This theory, known as the ‘amyloid hypothesis’, holds that the protein amyloid-β accumulates into toxic deposits as the disease progresses, ultimately causing dementia. Whether or not lecanemab confirms the amyloid hypothesis remains to be seen, researchers say. “I don’t think one study will prove a very long-standing controversial hypothesis,” says Brent Forester, director of the Geriatric Psychiatry Research Program at McLean Hospital in Belmont, Massachusetts, who helped to run the clinical trial for lecanemab. “But one positive study supports the hypothesis.” Amyloid is “associated with the problem, but it isn’t ‘the’ problem”, says George Perry, a neurobiologist at the University of Texas at San Antonio and a sceptic of the amyloid hypothesis. “If you modulate it, of course you can have some small benefit.” © 2022 Springer Nature Limited

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 28497 - Posted: 10.01.2022

Terriline Porelle is puzzling over two mysteries. The first is: what’s plaguing her? For the past two years, the formerly healthy, active, 34-year-old resident of Cocagne, N.B. has been experiencing many strange and alarming symptoms, including muscle twitches and blurred vision, auditory hallucinations, brain fog and loss of balance and co-ordination. The second mystery is why health authorities no longer seem interested in finding out why she’s ill. “It’s like nobody’s really looking to see what’s going on and it doesn’t make any sense,” she said. Ms. Porelle is one of 48 people who were initially identified between late 2020 and May, 2021, as being part of a cluster of patients in New Brunswick who all had a mysterious brain illness, which the province referred to as a “potential neurological syndrome of unknown cause.” Doctors and researchers puzzled over the cases for months. Then, in a February report, the province announced that there was no mystery illness, and that its investigation into the matter had concluded. An independent oversight committee had found that the 48 patients were likely suffering from various previously known diseases that had simply been misdiagnosed, the report said. But some of the patients and their families say their suffering remains very real – and that it’s made worse by the fact that they’re no closer to getting answers about what’s causing it. The province’s report said neurologists on the oversight committee had provided potential alternative diagnoses for 41 of the 48 patients, including Alzheimer’s disease and other types of dementia, post-concussion syndrome, chronic severe anxiety disorder and cancer. It recommended that patients contact their primary caregivers for referrals to further treatment, or that they seek help from a specialized clinic in Moncton called the Moncton Interdisciplinary Neurodegenerative Diseases (MIND) Clinic.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 28491 - Posted: 09.28.2022