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

By Pam Belluck Before dawn on a March morning, Doug Whitney walked into a medical center 2,000 miles from home, about to transform from a mild-mannered, bespectacled retiree into a superhuman research subject. First, a doctor inserted a needle into his back to extract cerebral spinal fluid — “liquid gold,” a research nurse called it for the valuable biological information it contains. Then, the nurse took a sample of his skin cells. After that came an injection of a radioactive tracer followed by a brain scan requiring him to lie still for 30 minutes with a thermoplastic mask over his face. Then, another tracer injection and another brain scan. During his three-day visit to the center, at Washington University School of Medicine in St. Louis, he also had cognitive assessments, neurological evaluations and blood draws that extracted multiple tubes for analysis. For 14 years now, Mr. Whitney has been the one-person focus of exceptionally detailed scientific investigation, for which he travels periodically to St. Louis from his home in Port Orchard, Wash. It is not because he is ill. It is because he was supposed to be ill. Mr. Whitney, 76, is a scientific unicorn with potential to provide answers about one of the world’s most devastating diseases. He has a rare genetic mutation that essentially guaranteed he would develop Alzheimer’s disease in his late 40s or early 50s and would likely die within a decade. His mother and nine of her 13 siblings developed Alzheimer’s and died in the prime of their lives. So did his oldest brother, and other relatives going back generations. It is the largest family in the United States known to have an Alzheimer’s-causing mutation. “Nobody in history had ever dodged that bullet,” Mr. Whitney 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: 29962 - Posted: 10.08.2025

Gemma Conroy Whether it’s dancing the tango or playing the guitar, engaging in a creative pastime can slow brain ageing, according to a study of dancers, musicians, artists and video game players from multiple countries. The analysis used brain clocks — models that measure the difference between a person’s chronological age and the age their brain appears to be — to assess whether creative activities help to maintain neurological youth. In brain regions that are most susceptible to ageing, engaging in creative activities increased connections with different areas of the brain. Although experts had ‘younger’ brains than their less-experienced counterparts did, even learning a creative skill from scratch had an anti-ageing effect on the brain. The findings were published on 3 October in Nature Communications1. Song and dance Previous studies suggest that engaging in creative activities can help to keep the brain young and foster emotional well-being. But few have investigated the biological basis of these brain benefits or what drives them, says study co-author Agustín Ibáñez, a neuroscientist at Adolfo Ibáñez University in Santiago, Chile. “There is really poor mechanistic evidence,” he says. How fast are you ageing? Ordinary brain scans reveal the pace To address this gap, Ibáñez and his colleagues created brain clocks using neuroimaging data of brain activity taken from 1,240 participants across 10 countries. These machine-learning models used functional connectivity, a measure of how brain regions work together, to estimate brain age. The researchers then applied their brain clocks to 232 tango dancers, musicians, visual artists and video game players of different ages and experience levels to calculate their ‘brain age gap’ — the difference between their predicted brain age and their actual age. © 2025 Springer Nature 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: 29954 - Posted: 10.04.2025

Rachel Fieldhouse An analysis of 56 million people has shown that exposure to air pollution increases the risk of developing a particular form of dementia, the third most common type after Alzheimer’s disease and vascular dementia. The study, published in Science on 4 September1, suggests that there is a clear link between long-term exposure to PM2.5 — airborne particles that are smaller than 2.5 micrometres in diameter — and the development of dementia in people with Lewy body dementia or Parkinson’s disease. The study found that PM2.5 exposure does not necessarily induce Lewy body dementia, but “accelerates the development,” in people who are already genetically predisposed to it, says Hui Chen, a clinician–neuroscientist at the University of Technology Sydney in Australia. PM2.5 exposure Lewy body dementia is an umbrella term for two different types of dementia: Parkinson’s disease with dementia, and dementia with Lewy bodies. In both cases, dementia is caused by the build-up of α-synuclein (αSyn) proteins into clumps, called Lewy bodies, in the brain’s nerve cells, which cause the cells to stop working and eventually die. Studies have suggested that long-term exposure to air pollution from car-exhaust, wildfires and factory fumes, is linked with increased risks of developing neurodegenerative illnesses, including Parkinson's disease with dementia2. Study co-author Xiaobo Mao, who researches neurodegenerative conditions at Johns Hopkins University in Baltimore, Maryland, says he and his colleagues wanted to determine if PM2.5 exposure also influenced the risk of developing Lewy body dementia. They analysed 2000–2014 hospital-admissions data from 56.5 million people with Lewy body dementia and Parkinson’s disease with or without dementia. The data served to identify people with severe neurological diseases. © 2025 Springer Nature Limited

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 5: The Sensorimotor System
Link ID: 29920 - Posted: 09.06.2025

Ian Sample Science editor A three-minute brainwave test can detect memory problems linked to Alzheimer’s disease long before people are typically diagnosed, raising hopes that the approach could help identify those most likely to benefit from new drugs for the condition. In a small trial, the test flagged specific memory issues in people with mild cognitive impairment, highlighting who was at greater risk of developing Alzheimer’s. Trials in larger groups are under way. The Fastball test is a form of electroencephalogram (EEG) that uses small sensors on the scalp to record the brain’s electrical activity while people watch a stream of images on a screen. The test detects memory problems by analysing the brain’s automatic responses to images the person sees before the test. “This shows us that our new passive measure of memory, which we’ve built specifically for Alzheimer’s disease diagnosis, can be sensitive to those individuals at very high risk but who are not yet diagnosed,” said Dr George Stothart, a cognitive neuroscientist at the University of Bath, where the test was developed. The trial, run with the University of Bristol, involved 54 healthy adults and 52 patients with mild cognitive impairment (MCI). People with MCI have problems with memory, thinking or language, but these are not usually severe enough to prevent them doing their daily activities. Before the test, volunteers were shown eight images and told to name them, but not specifically to remember them or look out for them in the test. The researchers then recorded the participants’ brain activity as they watched hundreds of images flash up on a screen. Each image appeared for a third of a second and every fifth picture was one of the eight they had seen before. © 2025 Guardian News & Media Limited

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 14: Attention and Higher Cognition
Link ID: 29914 - Posted: 09.03.2025

Jon Hamilton People who inherit two copies of a gene variant called APOE4 have a 60% chance of developing Alzheimer's by age 85. Only about 2% to 3% of people in the U.S. have this genetic profile, and most of them don't know it because they've never sought genetic testing. But three scientists are among those who did get tested, and learned that they are in the high-risk group. Now, each is making an effort to protect not only their own brain, but the brains of others with the genotype known as APOE4-4. "I just felt like the end of the world," says June, who asked to use only her first name out of fear that making her genetic status public could affect her job or health insurance. June was 57 when she found out. As someone with a doctorate in biochemistry, she quickly understood what the results meant. New tests of blood and spinal fluid could help doctors quickly identify patients who would most benefit from treatment. "People with our genotype are almost destined to get the disease," she says. "We tend to get symptoms 7 to 10 years earlier than the general population, which means that I had about seven years left before I may get the disease." At first, June spent sleepless nights online, reading academic papers about Alzheimer's and genetics. She even looked into physician-assisted suicide in an effort to make sure she would not become a burden to her adult son. © 2025 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: 29913 - Posted: 09.03.2025

By Claudia López Lloreda As cats age, they may yowl more than usual at night, have trouble sleeping or sleep too much, and act generally confused or disoriented. Now a new study shows that, just like in humans with Alzheimer’s disease, amyloid-beta plaques build up in the brains of aging felines and may contribute to dementia-like behaviors. In cats, that buildup could be causing a cascade of problems within the brain, such as hyperactivation of immune and other supporting brain cells that attack the synapses that connect nerve cells, researchers report August 11 in European Journal of Neuroscience. Aged cats with and without dementia had similar features and only a small number of cats were studied. But these findings could start helping researchers better understand how cats age and potentially develop treatments for feline dementia, as well as provide new insights into how the disease progresses in humans. Earlier studies had found amyloid beta in the brains of cats, but scientists didn’t know to what extent it was disrupting brain function. Robert McGeachan, a veterinarian at the University of Edinburgh, knew that the number of synapses decreased early in Alzheimer’s disease in humans. And so he and his team decided to focus on these connections in their cat study. They looked at the postmortem brains of seven young cats and 18 older ones, including eight with behavioral signs of dementia. Using fluorescent markers that find and cling to amyloid beta, the team found that the brains of aged cats, with or without dementia, had more of the protein than the younger brain samples. The amyloid beta plaques in the older cats also tended to accumulate right around synapses. © 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: 29901 - Posted: 08.27.2025

Ian Sample Science editor Women should ensure they are getting enough omega fatty acids in their diets according to researchers, who found unusually low levels of the compounds in female patients with Alzheimer’s disease. The advice follows an analysis of blood samples from Alzheimer’s patients and healthy individuals, which revealed levels of unsaturated fats, such as those containing omega fatty acids, were up to 20% lower in women with the disease. The low levels were not seen in men with Alzheimer’s, suggesting there may be sex differences in how the disease takes hold and affects a person’s physiology. “The difference between the sexes was the most shocking and unexpected finding,” said Dr Cristina Legido-Quigley, a senior author on the study at King’s College London published in the Alzheimer’s & Dementia journal. “There’s an indication that having less of these compounds could be causal in Alzheimer’s, but we need a clinical trial to confirm that.” Alzheimer’s disease is twice as common in women as in men. Factors including women’s longer average lifespan, differences in hormones, immune responses and educational opportunities can all play a role in the development of the disease. In the latest study, researchers analysed the levels of lipids, which are fatty compounds, in the blood of 306 people with Alzheimer’s, 165 people with mild cognitive impairment and 370 people who were cognitively healthy controls. Lipids can be saturated or unsaturated, with the former generally considered unhealthy and the latter broadly healthy. © 2025 Guardian News & Media 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: 29898 - Posted: 08.23.2025