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

By Roni Caryn Rabin Middle-aged and older adults who sought hospital or emergency room care because of cannabis use were almost twice as likely to develop dementia over the next five years, compared with similar people in the general population, a large Canadian study reported on Monday. When compared with adults who sought care for other reasons, the risk of developing dementia was still 23 percent higher among users of cannabis, the study also found. The study included the medical records of six million people in Ontario from 2008 to 2021. The authors accounted for health and sociodemographic differences between comparison groups, some of which play a role in cognitive decline. The data do not reveal how much cannabis the subjects had been using, and the study does not prove that regular or heavy cannabis use plays a causal role in dementia. But the finding does raise serious concerns that require further exploration, said Dr. Daniel T. Myran, the first author of the study, which was published in JAMA Neurology. “Figuring out whether or not cannabis use or heavy regular chronic use causes dementia is a challenging and complicated question that you don’t answer in one study,” said Dr. Myran, an assistant professor of family medicine at University of Ottawa. “This contributes to the literature and to a sign, or signal, of concern.” Dr. Myran’s previous research has found that patients with cannabis use disorder died at almost three times the rate of individuals without the disorder over a five-year period. He has also reported that more cases of schizophrenia and psychosis in Canada have been linked to cannabis use disorder since the drug was legalized. © 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: 29745 - Posted: 04.16.2025

Ian Sample Science editor Researchers who tracked cases of dementia in Welsh adults have uncovered the strongest evidence yet that the shingles vaccination reduces the risk of developing the devastating brain disease. Health records of more than 280,000 older adults revealed that those who received a largely discontinued shingles vaccine called Zostavax were 20% less likely to be diagnosed with dementia over the next seven years than those who went without. Pascal Geldsetzer, at Stanford University, said: “For the first time we are able to say much more confidently that the shingles vaccine causes a reduction in dementia risk. If this truly is a causal effect, we have a finding that’s of tremendous importance.” The researchers took advantage of a vaccination rollout that took place in Wales more than a decade ago. Public health policy dictated that from 1 September 2013, people born on or after 2 September 1933 became eligible for the Zostavax shot, while those who were older missed out. The policy created a natural experiment where the older population was sharply divided into two groups depending on their access to the vaccine. This allowed the researchers to compare dementia rates in older people born weeks apart but on either side of the vaccine eligibility divide. After accounting for the fact that not all those eligible for the vaccine received it, the researchers found vaccination led to a 20% reduction in dementia risk, with the strongest effect in women. Anupam Jena, a professor of healthcare policy at Harvard Medical School, said the implications were profound. © 2025 Guardian News & Media 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: 29732 - Posted: 04.05.2025

Jon Hamilton New tests of blood and spinal fluid could help doctors quickly identify patients who would most benefit from treatment. New tests of blood and spinal fluid could help doctors quickly identify patients who would most benefit from treatment. Andrew Brookes/Getty Images When doctors suspect Alzheimer's, they can order a blood test to learn whether a patient's brain contains the sticky amyloid plaques that are a hallmark of the disease. But the results of that test won't tell the whole story, says Dr. Randall Bateman, a neurology professor at Washington University in St. Louis. "People can have a head full of amyloid, but no dementia or memory loss," Bateman says. So he and a team of scientists have developed a new blood test that can show whether Alzheimer's has actually begun to affect a person's thinking and memory. It joins another new test, this one of spinal fluid, that can predict whether the brain changes associated with Alzheimer's are likely to affect cognitive function. "It's a strong indicator of memory impairment," says Tony Wyss-Coray, a neurology professor at Stanford University. Both tests, described in the journal Nature Medicine, could help doctors identify patients who are likely to benefit from drugs that can clear the brain of amyloid plaques. Both were developed with funding from the National Institutes of Health. © 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: 29725 - Posted: 04.02.2025

By Paula Span Joan Presky worries about dementia. Her mother lived with Alzheimer’s disease for 14 years, the last seven in a memory-care residence, and her maternal grandfather developed dementia, too. “I’m 100 percent convinced that this is in my future,” said Ms. Presky, 70, a retired attorney in Thornton, Colo. Last year, she spent almost a full day with a neuropsychologist, undergoing an extensive evaluation. The results indicated that her short-term memory was fine — which she found “shocking and comforting” — and that she tested average or above in every cognitive category but one. She’s not reassured. “I saw what Alzheimer’s was like,” she said of her mother’s long decline. “The memory of what she went through is profound for me.” The prospect of dementia, which encompasses Alzheimer’s disease and a number of other cognitive disorders, so frightens Americans that a recent study projecting steep increases in cases over the next three decades drew enormous public attention. The researchers’ findings, published in January in Nature Medicine, even showed up as a joke on the Weekend Update segment of “Saturday Night Live.” “Dementia is a devastating condition, and it’s very much related to the oldest ages,” said Dr. Josef Coresh, director of the Optimal Aging Institute at NYU Langone Health and the senior author of the study. “The globe is getting older.” Now the findings are being challenged by other dementia researchers who say that while increases are coming, they will be far smaller than Dr. Coresh and his co-authors predicted. © 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: 29713 - Posted: 03.22.2025

By Gina Kolata Women’s brains are superior to men’s in at least in one respect — they age more slowly. And now, a group of researchers reports that they have found a gene in mice that rejuvenates female brains. Humans have the same gene. The discovery suggests a possible way to help both women and men avoid cognitive declines in advanced age. The study was published Wednesday in the journal Science Advances. The journal also published two other studies on women’s brains, one on the effect of hormone therapy on the brain and another on how age at the onset of menopause shapes the risk of getting Alzheimer’s disease. The evidence that women’s brains age more slowly than men’s seemed compelling. Researchers, looking at the way the brain uses blood sugar, had already found that the brains of aging women are years younger, in metabolic terms, than the brains of aging men. Other scientists, examining markings on DNA, found that female brains are a year or so younger than male brains. And careful cognitive studies of healthy older people found that women had better memories and cognitive function than men of the same age. Dr. Dena Dubal, a professor of neurology at the University of California, San Francisco, set out to understand why. “We really wanted to know what could underlie this female resilience,” Dr. Dubal said. So she and her colleagues focused on the one factor that differentiates females and males: the X chromosome. Females have two X chromosomes; males have one X and one Y chromosome. Early in pregnancy, one of the X chromosomes in females shuts down and its genes go nearly silent. But that silencing changes in aging, Dr. Dubal found. © 2025 The New York Times Company

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: 29704 - Posted: 03.12.2025

By Lola Butcher Last September, Eliezer Masliah, a prominent Alzheimer’s disease researcher, stepped away from his influential position at the National Institutes of Health after the organization, where he oversaw a $2.6 billion budget for neuroscience research, found falsified or fabricated images in his scientific articles. That same month, the Securities and Exchange Commission announced neuroscientist Lindsay Burns, her boss, and their company would pay more than $40 million to settle charges they had made misleading statements about research results from their clinical trial of a possible treatment for Alzheimer’s disease. Also in September: A $30 million clinical trial to study a stroke treatment developed by Berislav Zlokovic, a well-known Alzheimer’s expert, and his colleagues was canceled amid an investigation into whether he had manipulated images and data in research publications. Shortly thereafter, Zlokovic, director of the Zilkha Neurogenetic Institute at the University of Southern California medical school, was placed on indefinite administrative leave. Is there a pattern here? And, if there is, can neurology patients trust treatments that are based on published scientific research? That is what Charles Piller, an investigative reporter for Science magazine, examines in “Doctored: Fraud, Arrogance, and Tragedy in the Quest to Cure Alzheimer’s,” and his analysis is not comforting. As for the first question — is there a pattern? — Piller’s relentless reporting reveals that dozens of neuroscientists, including some of the most prominent in the world, appear to be responsible for inaccurate images in their published research. Those problematic images have prompted many of their articles to be retracted, corrected, or flagged as being “of concern” by the journals in which they were published.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 1: Introduction: Scope and Outlook
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 1: Cells and Structures: The Anatomy of the Nervous System
Link ID: 29687 - Posted: 03.01.2025

Jon Hamilton People who inherit one very rare gene mutation are virtually guaranteed to develop Alzheimer's before they turn 50. Except for Doug Whitney. "I'm 75 years old, and I think I'm functioning fairly well," says Whitney, who lives near Seattle. "I'm still not showing any of the symptoms of Alzheimer's." Now a team of scientists is trying to understand how Whitney's brain has defied his genetic destiny. "If we are able to learn what is causing the protection here, then we could translate that to therapeutic approaches and apply that to the more common forms of the disease," says Dr. Jorge Llibre-Guerra, an assistant professor of neurology at Washington University School of Medicine in St. Louis. One possibility is high levels of heat shock proteins found in Whitney's brain, the team reports in the journal Nature Medicine. There are hints that these proteins can prevent the spread of a toxic protein that is one of the hallmarks of Alzheimer's, Llibre-Guerra says. A genetic surprise Early-onset Alzheimer's is everywhere in Whitney's family. His mother and 11 of her 13 siblings all had the disease by about age 50. "None of them lasted past 60," Whitney says. Whitney's wife, Ione, saw this up close. "We went home for Thanksgiving, and his mom couldn't remember the pumpkin pie recipe," she says. "A year later when we went back, she was already wandering off and not finding her way back home." © 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: 29675 - Posted: 02.19.2025

By Sara Reardon A man who seemed genetically destined to develop Alzheimer’s disease while still young has reached his mid-70s without any cognitive decline — in only the third recorded case of such resistance to the disease. The findings, published today in Nature Medicine1, raise questions about the role of the proteins that ravage the brain during the disease and the drugs that target them. Since 2011, a study called the Dominantly Inherited Alzheimer Network (DIAN) has been following a family in which many members have a mutation in a gene called PSEN2. The mutation causes the brain to produce versions of the amyloid protein that are prone to clumping into the sticky plaques thought to drive neurodegeneration. Family members with the mutation invariably develop Alzheimer’s at around age 50. Then, a 61-year-old man from this family showed up at the DIAN study’s clinic with full cognitive function, and the researchers were shocked to discover that he had the fateful PSEN2 mutation. The man’s mother had had the same mutation, as had 11 of her 13 siblings; all had developed dementia around age 50. The researchers were even more shocked when scans revealed that his brain looked like that of someone with Alzheimer’s. “His brain was full of amyloid,” says behavioural neurologist and study co-author Jorge Llibre-Guerra at Washington University in St. Louis, Missouri. What the man’s brain didn’t contain, however, were clusters of tau — another protein that forms tangled threads inside neurons. Positron emission tomography (PET) scans revealed that he had a small amount of abnormal tau and that it was only in the occipital lobe, a brain region involved in visual perception that is not usually affected in Alzheimer’s disease. © 2025 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: 29667 - Posted: 02.12.2025

By Laura Hercher edited by Gary Stix It is impossible, of course, to identify the precise moment we first suspected the changes in my mother were something other than normal aging. In my own imperfect memory, what rises up is the first morning of a weeklong trip to Rome, when my mother woke up at 2 A.M., got dressed and went down for breakfast. A hotel employee found her wandering from room to room, looking for toast and coffee. She was jet-lagged, my brother and I told each other uneasily. It could happen to anyone. But weren’t there cues? Didn’t she notice the darkened lobby, the stillness, the clock? If we had known then, would it have helped? To date, no U.S. Food and Drug Administration–­approved therapy exists for asymptomatic people at risk of Alzheimer’s disease (AD). My mother was not a smoker, drank in moderation, read books, took classes, and spent that week in Italy soaking up everything the tour guide told her about Caravaggio and Bernini like she was prepping for a quiz. Five years passed after that trip before my mother received a diagnosis of dementia. Today, a simple blood test can detect changes in the brain that predict AD up to 15 years before the first symptoms emerge. For researchers, tools for early detection give a peek at the full spectrum of AD, pinpointing early seeds of pathology deep inside the brain. Cognitive decline—what we typically think of as the disease itself—is merely the illness’s denouement. “Dementia is a result. Dementia is a symptom,” explains Clifford R. Jack, Jr., a neuroradiologist at the Mayo Clinic in Rochester, Minn., and chair of the Alzheimer’s Association (AA) working group responsible for recent, controversial guidelines for the diagnosis of AD based on underlying biology, not clinical presentation. Scientific American is part of Springer Nature,

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: 29657 - Posted: 02.05.2025

By Katharine Gammon Today more than 55 million people around the world have Alzheimer’s disease and other dementias, which ravage the minds of those who suffer from them and have devastating impacts on their family members. In spite of decades of research, the precise origins of these diseases continue to elude scientists, though numerous factors have been found to be associated with higher risk, including genetics and various lifestyle and environmental factors. Nautilus Members enjoy an ad-free experience. Log in or Join now . The quest has recently taken a turn to a newer model for studying the brain: brain organoids. These three-dimensional clumps of neuronal tissue derived from human stem cells have been used to study everything from epilepsy to the origins of consciousness. And now, researchers in Massachusetts are slamming them with miniature metal pistons to test out whether they can lend credence to a controversial hypothesis: that concussions might reactivate a common virus in the brain, increasing dementia risk. A decade of research suggests traumatic brain injury, whether from accidents or high-contact sports, is a standout risk factor for Alzheimer’s and other forms of neurodegenerative decline. Some estimates suggest that up to 10 percent of cases could be attributed to at least one prior head injury, but why is not fully understood. Separately, a growing body of research proposes that viral infection, including a common virus known as herpes simplex one, can also increase susceptibility to these diseases. But all three things—head trauma, viral infection, and dementia—have not been directly connected in experimental research, until now. One of the challenges in getting to the roots of dementia is that humans lead complex, messy lives. In the soup of risk factors—from high blood pressure to loneliness to genetic inheritance—it can be hard to filter out the most impactful forces that have contributed to the onset of any one dementia case. There are no ethical ways to test these questions on humans, of course, while using lab animals presents its own ethical and cost challenges. Animals are never a perfect match for humans anyway, and dementia-related findings in animals have so far not translated well to human patients. © 2025 NautilusNext Inc.,

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 19: Language and Lateralization
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 15: Language and Lateralization
Link ID: 29646 - Posted: 01.29.2025

By Meghan Rosen Baby Boomers may drive a bigger-than-expected boom in dementia cases. By 2060, 1 million U.S. adults per year will develop dementia, scientists predict January 13 in Nature Medicine. Dementia is a broad term encompassing many symptoms, including memory, reasoning and language difficulties that interfere with people’s daily lives. Researchers estimate that it currently affects more than 6 million people in the United States. “This is a huge problem,” says Josef Coresh, an epidemiologist at New York University’s Grossman School of Medicine. A rise in the projected number of dementia cases is not surprising, given the aging U.S. population ­­— but the extent of the rise stands out, he says. His team predicts that 42 percent of people in the United States who are over 55 years old will develop dementia sometime during their lifetime. That’s about double the percentage estimated by previous researchers. Coresh’s new estimate is based on a study population that’s larger — more than 15,000 people — and more diverse than earlier work. His team followed participants for years, in some cases decades, using several methods to identify dementia cases. They pored over hospital and death records, evaluated participants in person and screened them by phone. For the last decade, the researchers have been calling participants twice a year, Coresh says. That gave the team a window into people’s lives, revealing dementia cases that might otherwise have gone unreported. Though the team focused on dementia in people over age 55, risk doesn’t typically start ticking up for decades. And some populations were at greater risk than others, including women, Black people and those with a particular gene variant linked to Alzheimer’s disease. © 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: 29627 - Posted: 01.15.2025

By Angie Voyles Askham Old age is the best predictor of Alzheimer’s disease, Parkinson’s disease and many other neurodegenerative conditions. And yet, as deeply studied as those conditions are, the process of healthy brain aging is not well understood. Without that knowledge, “how can we possibly fix something that goes wrong because of it?” asks Courtney Glavis-Bloom, senior staff scientist at the Salk Institute for Biological Sciences. “We don’t have the basics. It’s like running before we walk.” That said, mounting evidence suggests that aging takes a particular toll on non-neuronal and white-matter cells in mice. For example, white-matter cells display more differentially expressed genes in aged mice than in younger ones, according to a 2023 single-cell analysis of the frontal cortex and striatum. And glia present in white matter show accelerated aging when compared with cells in the cortex across 15 different brain regions, another 2023 mouse study revealed. “Different brain regions show totally different trajectories regarding aging,” says Andreas Keller, head of the Department of Clinical Bioinformatics at the Helmholtz Institute for Pharmaceutical Research Saarland, who worked on the latter study. Some of the cell types with the most extensive aging-related changes in gene expression occur in a small region of the hypothalamus, according to a new single-cell mouse atlas, the largest and broadest to date. Rare neuronal and non-neuronal cell populations within this “hot spot” are particularly vulnerable to the aging process, says Hongkui Zeng, executive vice president and director of the Allen Institute for Brain Science, who led the work. “This demonstrates the power of using the cell-type-specific approach that will identify highly susceptible, rare populations of interest in the brain,” she says. © 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: 29620 - Posted: 01.08.2025

Kat Lay Global health correspondent Pills that prevent Alzheimer’s disease or blunt its effects are on the horizon, as the fight against dementia enters a “new era”, experts have said. Scientific advances were on the cusp of producing medicines that could be used even in the most remote and under-resourced parts of the world, thereby “democratising” care, said Jeff Cummings, professor of brain science and health at the University of Nevada. An estimated 50 million people live with dementia globally, more than two-thirds of them in low- and middle-income countries. In 2024, the first drugs that can change the course of Alzheimer’s disease entered the market. Eisai and Biogen’s lecanemab and Eli Lilly’s donanemab were approved by medicine watchdogs in many western countries, including the UK and US. “I’m just so excited about this,” said Cummings. “We are truly in a new era. We have opened the door to understanding and manipulating the biology of Alzheimer’s disease for the benefit of our patients.” Cummings conceded that high prices, complicated administration techniques and requirements for advanced technology to monitor patients meant that those newly approved drugs were “not going to be made widely available in the world”. Neither is yet available on the NHS in the UK because of the high cost – about £20,000 to £25,000 a year for each patient. They require additional tests and scans that would probably double that figure. But Cummings said they offered evidence of how to target dementia and “this learning is going to open the door to new therapies of many types, and those drugs can be exported around the world”. There are currently 127 drugs in trials for Alzheimer’s disease. © 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: 29619 - Posted: 01.08.2025

By Joshua Cohen For decades, scientists have been trying to develop therapeutics for people living with Alzheimer’s disease, a progressive neurodegenerative disease that is characterized by cognitive decline. Given the global rise in cases, the stakes are high. A study published in The Lancet Public Health reports that the number of adults living with dementia worldwide is expected to nearly triple, to 153 million in 2050. Alzheimer’s disease is a dominant form of dementia, representing 60 to 70 percent of cases. Recent approvals by the Food and Drug Administration have focused on medications that shrink the sticky brain deposits of a protein called amyloid beta. The errant growth of this protein is responsible for triggering an increase in tangled threads of another protein called tau and the development of Alzheimer’s disease — at least according to the dominant amyloid cascade hypothesis, which was first proposed in 1991. Over the past few years, however, data and drugs associated with the hypothesis have been mired in various controversies relating to data integrity, regulatory approval, and drug safety. Nevertheless, the hypothesis still dominates research and drug development. According to Science, in fiscal year 2021 to 2022, the National Institutes of Health spent some $1.6 billion on projects that mention amyloids, about 50 percent of the agency’s overall Alzheimer’s funding. And a close look at the data for recently approved drugs suggests the hypothesis is not wrong, so much as incomplete. A few years ago, Matthew Schrag, a neurologist at Vanderbilt University, discovered possible image tampering in papers that supported the hypothesis, including in an influential 2006 Nature study that was eventually retracted. At roughly the same time, the FDA had been greenlighting medications that target amyloid beta.

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: 29618 - Posted: 01.08.2025

Amy Fleming Nine years ago, Nikki Schultek, an active and healthy woman in her early 30s, experienced a sudden cascade of debilitating and agonising symptoms – including cognitive and breathing problems and heart arrhythmia – and was investigated for multiple sclerosis. But three brain scans and numerous X-rays later, there was still no diagnosis or treatment plan. “It was like living in a nightmare, imagining not watching my children – three and five years old – grow up,” says Schultek. Now, speaking on a video call from North Carolina, she is as bright as a button and shows no signs of degenerative brain disease. It turned out she had multiple chronic infections, including Borrelia burgdorferi bacteria, which causes Lyme disease and which had stealthily reached her brain. Antibiotics restored her health, but B burgdorferi is hard to eradicate once in the brain. She may need maintenance treatment to keep the disease at bay. Schultek is not the only person whose neurological disorder turned out to be caused by microbes in the brain. A recent paper she jointly lead-authored, published in Alzheimer’s and Dementia, compiled a long list of case reports where infectious disease was discovered to be the primary cause of dementia, meaning that, in many cases, the dementia was reversible. A few of the patients died, but most survived and saw significant improvements in cognitive function, including a man in his 70s who had been diagnosed with Alzheimer’s disease after his swift cognitive decline saw him unable to drive or, eventually, leave the house alone. A sample of his cerebrospinal fluid was taken and revealed a fungal infection caused by Cryptococcus neoformans. Within two years of taking antifungal medication, he was driving again and back at work as a gardener. Richard Lathe, a professor of infectious medicine at the University of Edinburgh and another lead author of the paper, says these patients “were by accident found to be suffering from various fungal, bacterial or viral infections, and when they treated the patient with antifungals, antivirals or antibiotics, the dementia went away”. He, among others, has been investigating the possibility that, like the gut, the brain hosts a community of microbes – an area of largely scientifically uncharted waters, but with huge life-saving potential. © 2024 Guardian News & Media Limited

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: 29587 - Posted: 12.04.2024

By Teddy Rosenbluth Cassava Sciences, a small biotechnology company based in Austin, Texas, announced it would stop the advanced clinical trial for an experimental Alzheimer’s drug, ending a long-contested bid for regulatory approval. The company announced on Monday that the drug, simufilam, did not significantly reduce cognitive decline in people with mild to moderate Alzheimer’s disease in the trial, which enrolled more than 1,900 patients. “The results are disappointing for patients and their families who are living with this disease and physicians who have been looking for novel treatment options,” the company’s chief executive, Richard J. Barry, said in a statement. These results were unsurprising to many dementia researchers, who had questioned why the trial had been allowed to proceed in the first place, since much of the drug’s underlying science had been called into question. Studies that once seemed to support the drug have been retracted from scientific journals. A consultant researcher who helped conduct some of the drug’s foundational studies was charged with fraud by a federal grand jury for allegedly falsifying data to obtain research grants. In September, the company settled with the Securities and Exchange Commission over allegations that Cassava had made misleading statements about the results of earlier clinical trial data. However, the company neither admitted nor denied wrongdoing. © 2024 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
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Link ID: 29577 - Posted: 11.27.2024