By Pam Belluck Since the approval of new Alzheimer’s drugs in recent years, there has been a lingering question: While data indicated that they could modestly slow cognitive decline for some patients, would that effect be meaningful or too slight to make difference? A new review of research spanning a decade, published on Wednesday, concluded that the clinical benefit of these and similar drugs is negligible. But the way the review was conducted spurred heated criticism from many Alzheimer’s experts, including some who had been skeptical of some of them. The review, published by Cochrane, an international network of health researchers, evaluated studies that were conducted on seven monoclonal antibody drugs developed over the last two decades to target amyloids, proteins that form plaques in the brains of people who have Alzheimer’s disease. Some Alzheimer’s experts said the conclusions were meaningless because the review swept under one umbrella drugs that had shown very dissimilar results and worked differently. The experts noted that data from the two most recent drugs studied — Leqembi and Kisunla — showed they could slow cognitive decline, which led to approval from the Food and Drug Administration and made them the only anti-amyloid drugs available to patients. But a vast majority of the studies analyzed in the review involved four earlier drugs that had failed clinical trials or were never approved and a fifth drug that was pulled from the market. “The problem with the review is the mix of ingredients,” said Dr. Jason Karlawish, a director of the Penn Memory Center at the University of Pennsylvania, who has been skeptical or cautious toward some of the drugs over the years. “They took some of the rotten ingredients and mixed it in with the fresh food, and the result is a stinky stew.” © 2026 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: 30206 - Posted: 04.18.2026

By Jennie Erin Smith For a person who may be in the early stages of Alzheimer’s disease, getting a clear diagnosis is simpler than ever. Blood tests that detect biological changes linked to the disease are now considered reliable alternatives to brain imaging and invasive spinal fluid tests. And one biomarker, called phosphorylated tau 217 (p-tau217), has risen to the top. More accurate than other blood-based measures, p-tau217 is widely used in research, and the first commercial test was approved in the United States last year. Guidance from the influential Alzheimer’s Association says a positive result in a patient with cognitive symptoms can justify starting therapy with antibody drugs recently approved for the disease. “P-tau217 is the biomarker of the day,” says Alzheimer’s researcher Lon Schneider of the University of Southern California. But its success has sparked worries among some researchers and clinicians about inappropriate use of the test. Some doctors have begun to use it in people without confirmed symptoms, and telehealth companies peddle p-tau217 testing, for as little as a few hundred dollars, to anyone concerned about their memory. A positive result doesn’t mean a person will develop cognitive impairment or dementia, Schneider and other researchers warn. And some fear the tests will be used to push people without symptoms toward pricey infusion drugs that they may not need. At the Alzheimer’s Disease and Parkinson’s Disease (AD/PD) meeting last month in Copenhagen, Denmark, scientists seemed to agree that for better or for worse, p-tau217 is poised to become a widespread screening tool for healthy people. That assumption is driving an ongoing trial called TRAILBLAZER-3, in which people with positive p-tau217 but no symptoms are taking the antiamyloid drug donanemab to see whether it delays the onset of cognitive impairment. “People keep thinking or talking about early treatment,” says neurologist Richard Mayeux of Columbia University, who is not involved with that study. “What you want to do is get to that fine area just before cognitive impairment starts to occur.” © 2026 American Association for the Advancement of Science.

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: 30185 - Posted: 04.01.2026

Rachel Fieldhouse A group of specialized cells play a crucial part in clearing toxic proteins from inside the brain1. But in people with Alzheimer’s disease, these cells malfunction, leading to the build up of tau proteins — a hallmark of the disease. Tanycytes, specialized cells that line the third ventricle of the brain, are unique because they are in direct contact with both the bloodstream and the cerebrospinal fluid (CSF). This means that they can circumvent the blood–brain barrier to allow molecules into and out of the brain. “Tanycytes are highways for the brain,” says Vincent Prévot, a neuroendocrinologist based in Paris at Inserm, the French National Institute of Health and Medical Research. Although it was known that tanycytes transport molecules into the CSF, Prévot and his colleagues are the first to show that tanycytes also transport molecules out of the CSF. In particular, they move tau proteins from the CSF surrounding the brain into the bloodstream. The findings are fascinating, says Amy Brodtmann, a cognitive neurologist and researcher at Monash University in Melbourne, Australia. “No one has looked at these cells before” in relation to Alzheimer’s disease, she adds. The works shows a potential explanation for how abnormal tau proteins accumulate in the brain, she adds. Tau proteins usually help to support the internal structure of cells and make them stronger, including cells in the brain. But in people with Alzheimer’s disease, the protein stops working properly. Brodtmann says tau then becomes “sticky”, forming clumps in the cells and causing them to die. These tau tangles tend to accumulate in regions of the brain that are involved in memory. © 2026 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: 30152 - Posted: 03.07.2026

Rachel Fieldhouse Alzheimer’s disease is about to become a big problem for China. Nearly 30% of all people with the condition or related forms of dementia already live in the country. And with its ageing population and falling birth rate, the burden on health and social welfare is expected to multiply dramatically in the coming decades. The Chinese government has responded with programmes and funding that are aimed at improving screening, diagnosis and treatment of Alzheimer’s disease by 2030. And the research has started to take off. Scientists have been working on new drugs and innovative — if controversial — surgical techniques. The government has also encouraged the development of drugs derived from traditional Chinese medicine. And researchers are accelerating the search for biological markers that precede the onset of Alzheimer’s disease, including genetic contributors, which could explain how the condition develops and reveal the best way to identify it early. Although the investments don’t yet match the level of funding in the United States, the improving quality and quickening pace of clinical and preclinical research has attracted attention from researchers around the world. “Maybe China is the next place that will take the lead,” says John Hardy, a neurogeneticist at the UK Dementia Research Institute in London, who is also affiliated with the Hong Kong Center for Neurodegenerative Diseases. Treating the root of the problem Nearly 17 million people in China had Alzheimer’s disease and related dementias in 2021 — about 9 in 1,000, according to a report published last year1. Projections suggest that this number could reach as high as 66 million by 2050 (see ‘Dementia’s rise’) or even exceed 100 million by then2,3. The problem is compounded by China’s low fertility rate, which means that there will be fewer people of working age to support the growing population of older individuals with debilitating conditions. © 2026 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: 30139 - Posted: 02.25.2026

Heidi Ledford A simple blood test might one day serve as a molecular ‘clock’ that predicts not only whether someone will develop Alzheimer’s disease — but when. Blood tests are now approved for Alzheimer’s: how accurate are they? The test, published in Nature Medicine on 19 February1, is based on an abnormal form of a protein called tau that circulates in the blood, and begins to accumulate in the brains of people with Alzheimer’s well before symptoms such as memory loss appear. If validated in larger studies, the test could provide a way to intervene in the neurodegenerative disease at an earlier stage, when treatment is more likely to be effective. It could also provide a measurable biological marker, or ‘biomarker’, to make clinical trials of potential Alzheimer’s disease treatments easier and cheaper. “Predicting if and when patients are likely to develop Alzheimer’s symptoms could be useful in designing trials of interventions to prevent or delay symptom onset,” says Howard Fink, a physician at the Minneapolis Veterans Affairs Health Care System in Minnesota. But until further studies are done, people should not take the test themselves, says Suzanne Schindler, a neurologist at Washington University School of Medicine in St. Louis, Missouri, and lead author of the study. (In-home blood tests for the form of tau that the study focuses on are available to consumers.) “At this point, we do not recommend that any cognitively unimpaired individuals have any Alzheimer’s disease biomarker test,” Schindler adds. Abnormal tau proteins can form tangled fibres that disrupt communication among the brain’s nerve cells. Brain-imaging tests that detect tangled tau are sometimes used when diagnosing Alzheimer’s, and preliminary studies suggest that such tests might also be able to predict when a person’s Alzheimer’s symptoms will appear2,3. © 2026 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: 30130 - Posted: 02.21.2026

Jon Hamilton A little brain training today may help stave off Alzheimer's disease and other forms of dementia for at least 20 years. That's the conclusion of a study of older adults who participated in a cognitive exercise experiment in the 1990s that was designed to increase the brain's processing speed. The federally funded study of 2,802 people found that those who did eight to 10 roughly hourlong sessions of cognitive speed training, as well as at least one booster session, were about 25% less likely to be diagnosed with dementia over the next two decades. "We now have a gold-standard study that tells us that there is something we can do to reduce our risk for dementia," says Marilyn Albert, an author of the study and a professor of neurology at Johns Hopkins University School of Medicine. "It's super-exciting to see that these effects are still holding 20 years out," says Jennifer O'Brien, an associate professor of psychology at the University of South Florida who was not involved in the research. The study appears in the journal Alzheimer's & Dementia: Translational Research & Clinical Interventions. The result is good news for people like George Kovach, 74, who started doing cognitive speed training a decade ago. This illustration shows a pink human brain with stick legs and stick arms. The pink stick arms are holding up a black barbell with black disk-shaped weights on each end. © 2026 npr

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: 30127 - Posted: 02.18.2026

Andrew Gregory Health editor Reading, writing and learning a language or two can lower your risk of dementia by almost 40%, according to a study that suggests millions of people could prevent or delay the condition. Dementia is one of the world’s biggest health threats. The number of people living with the condition is forecast to triple to more than 150 million globally by 2050, and experts say it presents a big and rapidly growing threat to future health and social care systems in every community, country and continent. US researchers found that engaging in intellectually stimulating activities throughout life, such as reading, writing or learning a new language, was associated with a lower risk of Alzheimer’s disease, the most common form of dementia, and slower cognitive decline. The study author Andrea Zammit, of Rush University Medical Center in Chicago, said the discovery suggested cognitive health in later life was “strongly influenced” by lifelong exposure to intellectually stimulating environments. “Our findings are encouraging, suggesting that consistently engaging in a variety of mentally stimulating activities throughout life may make a difference in cognition. Public investments that expand access to enriching environments, like libraries and early education programs designed to spark a lifelong love of learning, may help reduce the incidence of dementia.” Researchers tracked 1,939 people with an average age of 80 who did not have dementia at the start of the study. They were followed for an average of eight years. Participants completed surveys about cognitive activities and learning resources during three stages. © 2026 Guardian News & Media Limited

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: 30121 - Posted: 02.14.2026

Heidi Ledford For decades, researchers have noted that cancer and Alzheimer’s disease are rarely found in the same person, fuelling speculation that one condition might offer some degree of protection from the other. Now, a study in mice provides a possible molecular solution to the medical mystery: a protein produced by cancer cells seems to infiltrate the brain, where it helps to break apart clumps of misfolded proteins that are often associated with Alzheimer’s disease. The study, which was 15 years in the making, was published on 22 January in Cell1 and could help researchers to design drugs to treat Alzheimer’s disease. “They have a piece of the puzzle,” says Donald Weaver, a neurologist and chemist at the Krembil Research Institute at the University of Toronto in Canada, who was not involved in the study. “It’s not the full picture by any stretch of the imagination. But it’s an interesting piece.” Alzheimer’s mystery Weaver has been interested in that puzzle ever since he began his medical training, when a senior pathologist made an offhand comment: “If you see someone with Alzheimer’s disease, they’ve never had cancer.” The remark stuck with Weaver over the years as he diagnosed thousands of people with Alzheimer’s disease. “I can’t remember a single one that has had cancer,” he says. Epidemiological data do not draw such a clear divide, but a 2020 meta-analysis of data from more than 9.6 million people found that cancer diagnosis was associated with an 11% decreased incidence of Alzheimer’s disease2. It has been a difficult relationship to unpick: researchers must control for a variety of external factors. For example, people might die of cancer before they are old enough to develop symptoms of Alzheimer’s disease, and some cancer treatments can cause cognitive difficulties, which could obscure an Alzheimer’s diagnosis. © 2026 Springer Nature Limited

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: 30092 - Posted: 01.24.2026

Ian Sample Science editor New therapies for Alzheimer’s disease should target a particular gene linked to the condition, according to researchers who said most cases would never arise if its harmful effects were neutralised. The call to action follows the arrival of the first wave of drugs that aim to treat Alzheimer’s patients by removing toxic proteins from the brain. While the drugs slow the disease down, the benefits are minor, and they have been rejected for widespread use by the UK’s National Institute for Health and Care Excellence (Nice). In searching for alternative therapies, scientists at UCL say drug developers should focus on two risk-raising variants of a gene named Apoe. Therapies designed to block the variants’ impact have “vast potential” for preventing the disease, they claim. Dr Dylan Williams, a genetic epidemiologist at UCL, said: “Most Alzheimer’s disease cases would not arise without the contribution of just this single gene: Apoe. We need to think about it as a direct target. Almost all potential Alzheimer’s cases could benefit from Apoe-related interventions.” More than half a million people in the UK, and more than 40 million worldwide, are living with Alzheimer’s disease, the most common form of dementia. Several genes contribute to Alzheimer’s risk and lifestyle is important too: smoking, obesity, diabetes, high blood pressure and cholesterol all make the disease more likely. Williams and his colleagues analysed medical records from more than 450,000 people of European ancestry to calculate how much Alzheimer’s disease arose due to different variants of the Apoe gene. People inherit two copies of the gene – one from each parent – and there are three main variants: Apoe2, 3 and 4. © 2026 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: 30074 - Posted: 01.10.2026

Amelia Hill One in 10 people in the UK aged 70 and older could have Alzheimer’s-like changes in their brain, according to the clearest, real-world picture of how common the disease’s brain changes are in ordinary, older people. The detection of the proteins linked with the disease is not a diagnosis. But the findings indicate that more than 1 million over-70s would meet Nice’s clinical criteria for anti-amyloid therapy – a stark contrast to the 70,000 people the NHS has estimated could be eligible if funding were available. Experts, including those from Alzheimer’s Research UK, have said the findings from the first-ever population-based research into the disease have huge potential for early and accurate diagnosis. “High-quality studies like this are crucial to enhancing our understanding of how blood tests for Alzheimer’s could be used in clinical practice,” said David Thomas, the head of policy and public affairs at Alzheimer’s Research UK. “We need to generate more evidence so we can use these tests in the NHS.” The lead author of the research, conducted by King’s College London, Stavanger University hospital and the University of Gothenburg, said the findings could be a “gamechanger in the understanding of the disease”. The findings also challenge some long-held assumptions about dementia, including the idea that it is mainly a disease that mainly affects women. Dag Aarsland, a professor of old age psychiatry at the Institute of Psychiatry, Psychology and Neuroscience at King’s College London and the study’s lead author, said: “In an ageing global population, the assessment and treatment of dementia presents a significant challenge. Our study used a simple blood test to establish changes that contribute to cognitive impairment in those with dementia.” © 2025 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: 30057 - Posted: 12.20.2025

By Jennie Erin Smith More than a decade ago, when researchers discovered a ghostly network of microscopic channels that push fluid through the brain, they began to wonder whether the brain’s plumbing, as they sometimes refer to it, might be implicated in neurodegenerative diseases such as Alzheimer’s. Now, they are testing a host of ways to improve it. At the Society for Neuroscience (SfN) meeting last month in San Diego, several teams reported early promise for drugs and other measures that improve fluid flow, showing they can remove toxic proteins from animal or human brains and reverse symptoms in mouse models of neurological disease. Plastic surgeons in China, meanwhile, have gone further, conducting experimental surgeries that they say help flush out disease-related proteins in people with Alzheimer’s. The trials have generated excitement but also concern over their bold claims of success. A group of academic surgeons in the United States is planning what they say will be a more rigorous clinical trial, also in Alzheimer’s patients, that could begin recruiting as early as next year. The surgical approach “sounds unbelievable,” says neuroscientist Jeffrey Iliff of the University of Washington. “But I’m not going to say I know it can’t work. Remember, 13 years ago we didn’t know any of this existed.” In 2012, Iliff, with pioneering Danish neuroscientist Maiken Nedergaard and colleagues, described a previously unrecognized set of fluid channels in the brain that they dubbed the glymphatic system. Three years later, other groups revealed a second, related system of fluid transport: a matrix of tiny lymphatic vessels in the meninges, or membranes covering the brain. © 2025 American Association for the Advancement of Science.

Related chapters from BN: Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 10: Biological Rhythms and Sleep
Link ID: 30037 - Posted: 12.03.2025

By Pam Belluck A recently recognized form of dementia is changing the understanding of cognitive decline, improving the ability to diagnose patients and underscoring the need for a wider array of treatments. Patients are increasingly being diagnosed with the condition, known as LATE, and guidelines advising doctors how to identify it were published this year. LATE is now estimated to affect about a third of people 85 and older and 10 percent of those 65 and older, according to those guidelines. Some patients who have been told they have Alzheimer’s may actually have LATE, dementia experts say. “In about one out of every five people that come into our clinic, what previously was thought to maybe be Alzheimer’s disease actually appears to be LATE,” said Dr. Greg Jicha, a neurologist and an associate director of the University of Kentucky’s Sanders-Brown Center on Aging. “It can look like Alzheimer’s clinically — they have a memory problem,” Dr. Jicha said. “It looks like a duck, walks like a duck, but then it doesn’t quack, it snorts instead. ” On its own, LATE, shorthand for Limbic-predominant age-related TDP-43 encephalopathy, is usually less severe than Alzheimer’s and unfolds more slowly, said Dr. Pete Nelson, an associate director of the Sanders-Brown Center, who helped galvanize efforts to identify the disorder. That can be reassuring to patients and their families. But there is no specific treatment for LATE. Also, many older people have more than one type of dementia pathology, and when LATE occurs in conjunction with Alzheimer’s, it exacerbates symptoms and speeds decline, he said. © 2025 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: 30033 - Posted: 11.29.2025

By Gina Kolata Hopes were high. In retrospect, perhaps too high. On Monday, Novo Nordisk announced that two large studies failed to find any effect of the drug semaglutide on cognition and functioning in people with mild cognitive impairment — an early stage of Alzheimer’s — or with dementia. The participants were randomly assigned to take a pill of semaglutide, the compound at the heart of the weight-loss injections Ozempic and Wegovy, or a placebo for two years. “Today we announced that our efforts to slow down the progression of Alzheimer’s disease has come to an end,” said Maziar Mike Doustdar, chief executive at Novo Nordisk, in a video posted on LinkedIn. He added, “Based on the indicative data points we had, this is not the outcome we had hoped for.” The studies, involving 1,855 people in one trial and 1,953 in the other, seemed to stem an initial phase of optimism. The drugs appeared miraculous in their treatment of obesity, diabetes, heart disease and kidney disease. Alzheimer’s and other brain illnesses looked like the next frontier. But there had been other recent warnings, in two smaller studies of brain diseases. One, done by researchers in Britain, asked if a similar drug could help with Parkinson’s disease. That drug had no effect. Another study found that semaglutide did not help with cognitive impairment in people with major depression, a severe form of the disease. The company will present more detailed results from its Alzheimer’s study at a conference on Dec. 3, and another in March of 2026. Novo Nordisk’s stock was down nearly 6 percent on Monday, deepening a monthslong slump for the once-surging company. “We always knew there would be a low likelihood of success, but it was important to determine if semaglutide could take on one of medicine’s most challenging frontiers,” Mr. Doustdar said. © 2025 The New York Times Company

Related chapters from BN: 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 and Learning; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 30026 - Posted: 11.26.2025

By Meghan Rosen Taking just a few thousand steps daily could potentially stave off Alzheimer’s disease. People with the disease tend to experience debilitating cognitive challenges, like memory loss and difficulty communicating, that worsen over time. But physical activity may slow that steady downward march. In an observational study of people at risk for Alzheimer’s, researchers linked walking between 3,000 and 5,000 steps per day to a three-year delay in cognitive decline, compared with sedentary individuals. For people who walked between 5,000 and 7,500 steps per day, the reprieve appeared to last even longer — seven years, Harvard Medical School behavioral neurologist Jasmeer Chhatwal and his colleagues report November 3 in Nature Medicine. The association still needs to be tested in a clinical trial, Chhatwal says, but his team’s results hint at something important. Quality of life for people with Alzheimer’s and their families often plummets in the later stages of the disease. “If the disease can be delayed,” he says, “that can have a very big impact on people’s lives.” Previous studies have reported links between physical activity and delayed Alzheimer’s progression, says Deborah Barnes, an epidemiologist who studies dementia at the University of California, San Francisco, and who was not part of the research team. But the new study pinpoints the step count where people begin to see benefits. It also “helps to explain how,” she says. Chhatwal’s team reported a connection between exercise and less accumulation of certain Alzheimer’s proteins in the brain. It’s a mechanism that illustrates how physical activity probably works to slow Alzheimer’s progression, Barnes says. © Society for Science & the Public 2000–2025

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: 30025 - Posted: 11.26.2025

By Paula Span For years, the two patients had come to the Penn Memory Center at the University of Pennsylvania, where doctors and researchers follow people with cognitive impairment as they age, as well as a group with normal cognition. Both patients, a man and a woman, had agreed to donate their brains after they died for further research. “An amazing gift,” said Dr. Edward Lee, the neuropathologist who directs the brain bank at the university’s Perelman School of Medicine. “They were both very dedicated to helping us understand Alzheimer’s disease.” The man, who died at 83 with dementia, had lived in the Center City neighborhood of Philadelphia with hired caregivers. The autopsy showed large amounts of amyloid plaques and tau tangles, the proteins associated with Alzheimer’s disease, spreading through his brain. Researchers also found infarcts, small spots of damaged tissue, indicating that he had suffered several strokes. By contrast, the woman, who was 84 when she died of brain cancer, “had barely any Alzheimer’s pathology,” Dr. Lee said. “We had tested her year after year, and she had no cognitive issues at all.” The man had lived a few blocks from Interstate 676, which slices through downtown Philadelphia. The woman had lived a few miles away in the suburb of Gladwyne, Pa., surrounded by woods and a country club. The amount of air pollution she was exposed to — specifically, the level of fine particulate matter called PM2.5 — was less than half that of his exposure. Was it a coincidence that he had developed severe Alzheimer’s while she had remained cognitively normal? With increasing evidence that chronic exposure to PM2.5, a neurotoxin, not only damages lungs and hearts but is also associated with dementia, probably not. © 2025 The New York Times Company

Related chapters from BN: 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 and Learning; Chapter 4: Development of the Brain
Link ID: 30000 - Posted: 11.05.2025

Ian Sample Science editor Even modest amounts of daily exercise may slow the progression of Alzheimer’s disease in older people who are at risk of developing the condition, researchers have said. People are often encouraged to clock up 10,000 steps a day as part of a healthy routine, but scientists found 3,000 steps or more appeared to delay the brain changes and cognitive decline that Alzheimer’s patients experience. Results from the 14-year-long study showed cognitive decline was delayed by an average of three years in people who walked 3,000 to 5,000 steps a day, and by seven years in those who managed 5,000 to 7,000 steps daily. “We’re encouraging older people who are at risk of Alzheimer’s to consider making small changes to their activity levels, to build sustained habits that protect or benefit their brain and cognitive health,” said Dr Wai-Ying Yau, the first author on the study at Mass General Brigham hospital in Boston. Dementia affects an estimated 50 million people worldwide, with Alzheimer’s disease the most common cause. In the UK, more than 500,000 people have Alzheimer’s. The condition is linked to the buildup of two toxic forms of proteins in the brain, namely amyloid-beta plaques and tau tangles. Yau and her colleagues analysed data from 296 people aged 50 to 90 who were cognitively unimpaired at the beginning of the study. The data included annual cognitive assessments, step counts measured by pedometers, and PET imaging to detect levels of amyloid and tau in the volunteers’ brains. People with little brain amyloid at the start showed very little cognitive decline or buildup of tau protein over the course of the study. The risk of Alzheimer’s was greater for those with elevated amyloid at baseline, and among them, higher step counts were linked to slower rates of cognitive decline and a delayed buildup of tau proteins. In sedentary individuals, the buildup of tau and cognitive decline was substantially faster, the researchers report in the journal Nature Medicine. © 2025 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: 29998 - Posted: 11.05.2025

Jon Hamilton In April, the future was looking bleak for an experimental Alzheimer's drug called valiltramiprosate, or ALZ-801. Researchers had just released topline results of a study of more than 300 people age 50 or older, who were genetically predisposed to Alzheimer's. Overall, those who got the drug did no better than those given a placebo. But in September, a closer look at the results revealed benefits for a subgroup of 125 people who had only mild memory problems when they started taking the drug. Those participants, initially diagnosed with mild cognitive impairment rather than mild dementia, "showed very meaningful responses," says Dr. Susan Abushakra, chief medical officer of Alzheon, the drug's maker. By one measure, the drug slowed cognitive decline by 52% in people with mild cognitive impairment. That result appears comparable with benefits from the two Alzheimer's drugs now on the market: lecanemab and donabemab. But the true effect of ALZ-801 is hard to quantify because of the relatively small number of participants in the group with mild cognitive impairment. Three scientists learned they carry genes that significantly increase their risk for Alzheimer’s. Here's how they're grapping with the news, and working to keep their brains healthy. More robust results came from measures of brain atrophy — the shrinkage that tends to come with Alzheimer's. © 2025 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: 29987 - Posted: 10.29.2025

Jon Hamilton Scientists are reporting the first compelling evidence in people that cognitive training can boost levels of a brain chemical that typically declines with age. A 10-week study of people 65 or older found that doing rigorous mental exercises for 30 minutes a day increased levels of the chemical messenger acetylcholine by 2.3% in a brain area involved in attention and memory. This illustration shows a pink human brain with stick legs and stick arms. The pink stick arms are holding up a black barbell with black disk-shaped weights on each end. The background is light blue. Your Health Even healthy brains decline with age. Here's what you can do The increase "is not huge," says Étienne de Villers-Sidani, a neurologist at McGill University in Montreal. "But it's significant, considering that you get a 2.5% decrease per decade normally just with aging." So, at least in this brain area, cognitive training appeared to turn back the clock by about 10 years. The chemical change observed after intensive brain training is persuasive, says Michael Hasselmo, director of the Center for Systems Neuroscience at Boston University, who was not involved in the study. "It was compelling enough that I thought, 'Maybe I need to be doing this,'" he says. The result backs earlier research in animals showing that environments that stimulate the brain can increase levels of certain neurotransmitters. Studies of people have suggested that cognitive training can improve thinking and memory. Never skip brain day The study, funded by the National Institutes of Health, comes amid a proliferation of online brain-training programs, including Lumosity, Elevate, Peak, CogniFit and BrainHQ. © 2025 npr

Related chapters from BN: Chapter 17: Learning and Memory; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 13: Memory and Learning
Link ID: 29976 - Posted: 10.22.2025

Jon Hamilton In Alzheimer's, brain cells die too soon. In cancer, dangerous cells don't die soon enough. That's because both diseases alter the way cells decide when to end their lives, a process called programmed cell death. "Cell death sounds morbid, but it's essential for our health," says Douglas Green, who has spent decades studying the process at St. Jude Children's Research Hospital in Memphis, Tennessee. For example, coaxing nerve cells to live longer could help people with Alzheimer's disease, Parkinson's disease or ALS (Lou Gehrig's disease), he says, while getting tumor cells to die sooner could help people with cancer. So researchers have been searching for disease treatments that "modify or modulate the tendency of a cell to die," Green says. One of these researchers is Randal Halfmann at the Stowers Institute for Medical Research in Kansas City, Missouri. He has been studying immune cells that self-destruct when they come into contact with molecules that present a threat to the body. "They have to somehow recognize that [threat] in this vast array of other complex molecules," he says, "and then within minutes, kill themselves." They do this much the way a soldier might dive on a grenade to save others' lives. Halfmann's team has been focusing on special proteins inside cells that can trigger this process. When these proteins recognize molecules associated with a virus or some other pathogen, he says, "they implode." The proteins crumple and begin linking up with other crumpled proteins to form a structure called a "death fold" polymer. That starts a chain reaction of polymerization that ultimately kills the cell. Halfmann's team knew this process takes a burst of energy. But they couldn't locate the source. © 2025 npr

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: 29973 - Posted: 10.18.2025

Rachel Fieldhouse During ageing, men experience a greater reduction in volume across more regions of the brain than women do, according to a longitudinal study published today in the Proceedings of the National Academy of Sciences1. The authors suggest this means that age-related brain changes do not explain why women are more frequently diagnosed with Alzheimer’s disease than men are. “It’s really important that we understand what happens in the healthy brain so that we can better understand what happens when people get these neurodegenerative conditions,” says Fiona Kumfor, a clinical neuropsychologist at the University of Sydney, Australia. This study adds to scientists’ understanding of typical brain ageing, she adds. Nearly twice as many women are diagnosed with Alzheimer’s disease as men, and ageing is the biggest risk factor for the disease. This has prompted research into age-related sex differences in the brain. “If women’s brains declined more, that could have helped explain their higher Alzheimer’s prevalence,” says co-author Anne Ravndal, a PhD student at the University of Oslo. Previous research investigating sex differences in brain ageing has shown mixed results, Ravndal adds. Several studies have found that men experience greater loss of total grey matter and hippocampus size compared with women, whereas other work has reported a sharper decline of grey matter in women. Brain scans The latest study included more than 12,500 magnetic resonance imaging (MRI) brain scans from 4,726 people — at least two scans per person, taken an average of three years apart — who did not have Alzheimer’s disease or any cognitive impairments and were control participants in 14 larger data sets. The researchers compared how the individuals’ brain structures changed over time, looking at factors including the thickness of grey matter and the size of areas that are associated with Alzheimer’s disease, such as the hippocampus, which is essential to memory. © 2025 Springer Nature Limited

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 8: Hormones and Sex
Link ID: 29968 - Posted: 10.15.2025