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

By Annika Inampudi Once placed in sodas as a mood enhancer and eventually made into a drug for bipolar disorder, lithium is probably best known for powering the batteries in our electronics. But a new study suggests yet another potential use for this versatile metal as a treatment for Alzheimer’s disease. In a paper published today in Nature, researchers report reduced lithium levels in the brains of people with Alzheimer’s and mild cognitive impairment. They also found that a form of lithium improved memory when fed to mice with Alzheimer’s-like symptoms. The paper is a “thorough and pioneering exploration” of lithium’s role in the brain during cognitive decline, says Ashley Bush, a psychiatrist at the Florey Institute of Neuroscience and Mental Health who was not involved in the study. The work offers a new route forward for a field still eager to find new treatments despite the recent approval of antiamyloid drugs, he says. Found in extremely low concentrations in rocks and seawater, lithium enters the human body through foods such as cereals, cabbage, and tomatoes, or through drinking water that naturally flows through lithium-rich rocks. For reasons that remain unknown, lithium seems to stabilize mood, and the compound lithium carbonate has been used for decades to treat mania in bipolar disorder. Some previous studies have hinted that the metal might also have neuroprotective effects, leading researchers to propose it as a treatment for neurodegenerative conditions. But these findings come mostly from observational studies and haven’t proved lithium can change the course of Alzheimer’s. Small clinical trials in dementia patients have produced mixed results. © 2025 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: 29881 - Posted: 08.09.2025

By Pam Belluck A combination of healthy activities including exercise, nutritious diet, computer brain games and socializing can improve cognitive performance in people at risk for dementia, according to a large new study. The study, conducted in five locations across the United States over two years, is the biggest randomized trial to examine whether healthy behaviors protect brain health. “It confirms that paying attention to things like physical activity and vascular risk factors and diet are all really important ways to maintain brain health,” said Dr. Kristine Yaffe, an expert in cognitive aging at the University of California, San Francisco, who was not involved in the study. The results were presented on Monday at the Alzheimer’s Association International Conference in Toronto and published in the journal JAMA. The study involved 2,111 people, ages 60 to 79, from diverse racial and ethnic backgrounds. None were cognitively impaired. All had sedentary lifestyles, suboptimal diets and two other dementia risk factors, such as a family history of cognitive decline and high blood pressure. Half of the participants followed a structured program. They were prescribed a healthy diet, socially engaging activities and a weekly regimen of eight exercise sessions and three sessions of computerized cognitive training. They attended 38 meetings with facilitators and fellow participants. The other participants followed a self-guided program. They were given educational materials and resources, and were regularly encouraged to engage in healthy behaviors. They attended six team meetings during the study. © 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: 29870 - Posted: 08.02.2025

Smriti Mallapaty A gene variant known to increase the risk of Alzheimer’s disease also makes people vulnerable to a host of other age-related brain disorders, from Parkinson’s disease to motor neuron disease. The gene variant, a version of apolipoprotein E called APOE ε4, produces a distinct set of proteins that contribute to chronic inflammation, finds an analysis1 using the largest proteomics database for neurodegenerative disease. Neurodegenerative diseases affect more than 57 million people worldwide. Researchers know that people who carry the APOE ε4 variant have an increased risk of developing late-onset Alzheimer’s disease, but studies are beginning to implicate this version, or allele, of APOE in other neurodegenerative diseases. Caitlin Finney and Artur Shvetcov, who study neurodegenerative diseases at the Westmead Institute for Medical Research in Sydney, Australia, and their colleagues wanted to better understand how this genetic risk factor contributes to disease. They took advantage of a newly established proteomics database that allowed them to look beyond individual diseases, says Finney. The Global Neurodegeneration Proteomics Consortium (GNPC) data set2 includes samples from more than 18,600 individuals, mainly of European ancestry, including many with Alzheimer’s, Parkinson’s, a form of motor neuron disease called amyotrophic lateral sclerosis (ALS) and types of dementia, as well as individuals without neurological disorders. The consortia collected around 250 million measurements of proteins found in the blood and cerebrospinal fluid, which surrounds the brain and spinal cord, taken at some two dozen clinics across the United States and Europe. “It’s one of the most powerful databases that we have available for proteomics right now,” says Maryam Shoai, a bioinformatician at University College London. Predicting risk © 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: 29855 - Posted: 07.16.2025

By Michael A. Yassa For nearly three decades, Alzheimer’s disease has been framed as a story about amyloid: A toxic protein builds up, forms plaques, kills neurons and slowly robs people of their memories and identity. The simplicity of this “amyloid cascade hypothesis” gave us targets, tools and a sense of purpose. It felt like a clean story. Almost too clean. We spent decades chasing it, developing dozens of animal models and pouring billions into anti-amyloid therapies, most of which failed. The few that made it to market offer only modest benefits, often with serious side effects. Whenever I think about this, I can’t help but picture Will Ferrell’s Buddy the Elf, in the movie “Elf,” confronting the mall Santa: “You sit on a throne of lies.” Not because anyone meant to mislead people (though maybe some did). But because we wanted so badly for the story to be true. So what happened? This should have worked … right? I would argue it was never going to work because we have been thinking about Alzheimer’s the wrong way. For decades, we have treated it as a single disease with a single straight line from amyloid to dementia. But what if that’s not how it works? What if Alzheimer’s only looks like one disease because we keep trying to force it into a single narrative? If that’s the case, then the search for a single cause—and a single cure—was always destined to fail. ”What if Alzheimer’s only looks like one disease because we keep trying to force it into a single narrative? If that’s the case, then the search for a single cause—and a single cure—was always destined to fail. Real progress, I believe, requires two major shifts in how we think. First, we have to let go of our obsession with amyloid. © 2025 Simons Foundation

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: 29835 - Posted: 06.18.2025

Jon Hamilton Joe Walsh, 79, is waiting to inhale. He's perched on a tan recliner at the Center for Alzheimer Research and Treatment at Brigham and Women's Hospital in Boston. His wife, Karen Walsh, hovers over him, ready to depress the plunger on a nasal spray applicator. "One, two, three," a nurse counts. The plunger plunges, Walsh sniffs, and it's done. The nasal spray contains an experimental monoclonal antibody meant to reduce the Alzheimer's-related inflammation in Walsh's brain. He is the first person living with Alzheimer's to get the treatment, which is also being tested in people with diseases including multiple sclerosis, ALS and COVID-19. Sponsor Message Health A man genetically destined to develop Alzheimer's isn't showing any symptoms And the drug appears to be reducing the inflammation in Walsh's brain, researchers report in the journal Clinical Nuclear Medicine. "I think this is something special," says Dr. Howard Weiner, a neurologist at Mass General Brigham who helped develop the nasal spray, along with its maker, Tiziana Life Sciences. Whether a decrease in inflammation will bring improvements in Walsh's thinking and memory, however, remains unclear. The experimental treatment is part of a larger effort to find new ways to interrupt the cascade of events in the brain that lead to Alzheimer's dementia. Two drugs now on the market clear the brain of sticky amyloid plaques, clumps of toxic protein that accumulate between neurons. Other experimental drugs have targeted the tau tangles, a different protein that builds up inside nerve cells. © 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: 29813 - Posted: 05.31.2025

Jon Hamilton A new blood test that detects a hallmark of Alzheimer's is poised to change the way doctors diagnose and treat the disease. The test, the first of its kind to be cleared by the Food and Drug Administration, is for people 55 and older who already have memory problems or other signs and symptoms of Alzheimer's. The results show whether the brain of a person with cognitive symptoms also has amyloid plaques, clumps of toxic proteins that build up in the spaces between brain cells. The presence of plaques in a person with cognitive symptoms usually confirms an Alzheimer's diagnosis. "I think the blood test is going to really revolutionize the way people with Alzheimer's are cared for and diagnosed," says Dr. Howard Fillit, chief science officer at the Alzheimer's Drug Discovery Foundation. "Primary care physicians will now have access to something that can give them a quicker read" on whether a patient has Alzheimer's, says Maria Carrillo, chief science officer of the Alzheimer's Association. One benefit of a readily-available blood test will be more accurate diagnoses, Fillit says, noting that currently, primary care doctors correctly diagnose patients only about 60% of the time. "Specialty neurologists get it right like seventy, eighty percent of the time," He says. "With the blood test, we can get it up to over 90%." A PET scan is the gold standard for detecting the amyloid plaques associated with Alzheimer's. But the technology is costly, and unavailable in many communities. © 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: 29799 - Posted: 05.24.2025

Andrew Gregory Health editor Scientists have used living human brain tissue to mimic the early stages of Alzheimer’s disease, the most common form of dementia, in a breakthrough that will accelerate the hunt for a cure. In a world first, a British team successfully exposed healthy brain tissue from living NHS patients to a toxic form of a protein linked to Alzheimer’s – taken from patients who died from the disease – to show how it damages connections between brain cells in real time. The groundbreaking move offered a rare and powerful opportunity to see dementia developing in human brain cells. Experts said the new way of studying the disease could make it easier to test new drugs and boost the chances of finding ones that work. Dementia presents a big threat to health and social care systems across the world. The number of people affected is forecast to triple to nearly 153 million by 2050, which underlines why finding new ways to study the disease and speed up the search for treatments is a health priority. In the study, scientists and neurosurgeons in Edinburgh teamed up to show for the first time how a toxic form of a protein linked to Alzheimer’s, amyloid beta, can stick to and destroy vital connections between brain cells. Tiny fragments of healthy brain tissue were collected from cancer patients while they were undergoing routine surgery to remove tumours at the Royal Infirmary of Edinburgh. Scientists dressed in scrubs were stationed in operating theatres alongside surgical teams, ready to receive the healthy brain tissue, which would otherwise have been discarded. Once the pieces of brain were retrieved, scientists put them in glass bottles filled with oxygenated artificial spinal fluid before jumping into taxis to transport the samples to their lab a few minutes away. © 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: 29767 - Posted: 04.30.2025