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
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 29577 - Posted: 11.27.2024

By Jennifer Couzin-Frankel Two esteemed hospitals in the midwestern United States are a 5-hour drive apart, but when it comes to how they’re prescribing new drugs for Alzheimer’s disease, they might as well be on different planets. “I’ve been worrying about these therapies for a long time,” says Alberto Espay, a neurologist at the University of Cincinnati Medical Center, where, to his knowledge, not a single patient has gotten the monoclonal antibody lecanemab or its more recently approved cousin donanemab. Both therapies clear the brain of the protein beta amyloid, which is widely thought to fuel the disease’s symptoms. In June, Espay wrote to his Alzheimer’s patients urging them to steer clear. “The risks are high,” his letter said, citing brain swelling and bleeding. “True benefits are minuscule.” But travel a few states west, to Washington University in St. Louis (WUSTL), and the vibe is completely different. “Any patient I see with mild Alzheimer’s disease, I’m at least asking myself, ‘Should we recommend this?’” says Joy Snider, a neurologist at the university, where 230 people have received lecanemab. (Donanemab isn’t widely available yet.) “We don’t want to overplay these drugs,” Snider says. “It’s a small effect, but it’s compelling.” The contrasting views underscore deep divisions and uncertainty. The treatments are the first that have been shown to change the course of a shattering and ultimately deadly disease. But their effectiveness is under debate and they can cause sometimes severe brain swelling and bleeding. Clinicians at centers offering the drugs meet regularly to discuss patient side effects, consider whether people with other health conditions can safely get the treatments, and experiment with lower doses or extra monitoring for higher risk patients. As Alzheimer’s experts converge in Madrid this week for the Clinical Trials on Alzheimer’s Disease (CTAD) conference, the antibodies’ real-world rollout is causing a stir.

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: 29529 - Posted: 10.30.2024

By Walt Bogdanich and Carson Kessler By 2021, nearly 2,000 volunteers had answered the call to test an experimental Alzheimer’s drug known as BAN2401. For the drugmaker Eisai, the trial was a shot at a windfall — potentially billions of dollars — for defanging a disease that had confounded researchers for more than a century. To assess the drug’s effectiveness and safety, Eisai sought to include people whose genetic profiles made them especially prone to develop Alzheimer’s. But these same people were also more vulnerable to brain bleeding or swelling if they received the drug. To identify these high-risk volunteers, Eisai told everyone that they would be given a genetic test. But the results, the company added, would remain secret. In all, 274 volunteers joined the trial without Eisai telling them they were at an especially high risk for brain injuries, documents obtained by The New York Times show. One of them was Genevieve Lane, a 79-year-old resident of the Villages in Florida who died in September 2022 after three doses of the drug, her brain riddled with 51 microhemorrhages. An autopsy determined that the drug’s side effects had contributed to her death. Her final hours were spent thrashing so violently that nurses had to tie her down. Another high-risk trial volunteer died, and more than 100 others suffered brain bleeding or swelling. While most of those injuries were mild and asymptomatic, some were serious and life-threatening. “This is a medication that has some significant side effects, and we need to be aware of them,” said Dr. Matthew Schrag, the Vanderbilt University neurologist who assisted with Ms. Lane’s autopsy. This past July, the agency approved a second, similar drug, Kisunla. In a clinical trial, its maker, Eli Lilly, also chose not to tell 289 volunteers that their genetic profiles made them vulnerable to brain injuries, The Times found. Dozens experienced what Lilly classified as “severe” brain bleeding. © 2024 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: 29528 - Posted: 10.26.2024

By Laurie McGinley When Dennis Carr learned he had early Alzheimer’s disease, he immediately thought of his older brother who had died of the illness in 2023. “There was not much anyone could do,” Carr said of his brother’s long decline. “You could see him diminishing.” Today, Carr is trying a new treatment called Leqembi that has been shown to modestly slow the disease for people in the initial stages of Alzheimer’s. Carr knows it is not a cure but he wants to buy time — to be with his family, to work and to give scientists a chance to find more solutions. “I’m hoping this is the first steppingstone to something better,” said Carr, 74, an electrical contractor in Montgomery County, Pa. Carr’s experience offers a glimpse of the shifting landscape of Alzheimer’s, a memory-robbing disease that affects more than 6 million Americans and is the seventh leading cause of death in the United States. Two new treatments, including Carr’s, target toxic clumps of a protein called amyloid beta in the brain and are the first to slow progression of the illness. Blood tests could revolutionize the way the illness is diagnosed. Lifestyle factors such as diet and exercise are showing promise in helping reduce the risk of cognitive decline. “Progress against Alzheimer’s has been unprecedented,” said Howard Fillit, co-founder and chief science officer of the Alzheimer’s Drug Discovery Foundation, a nonprofit that funds the development of drugs and diagnostics. “But we have a long way to go.” The new FDA-approved Alzheimer’s treatment Leqembi is prepared at Abington Neurological Associates in Abington, Pa., on Nov. 7. (Hannah Yoon for The Washington Post) Doctors used to refer to Alzheimer’s as “diagnose and adios” because they had little to offer patients, said Adam Boxer, a neurologist at the University of California at San Francisco. “But now we see light at the end of the tunnel,” he said. “We might be able to have a big impact.”

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: 29510 - Posted: 10.09.2024

Alzheimer’s disease impairs a patient by destroying neurons, which otherwise live for decades, and by disrupting communication among the remaining brain cells. As neurons die, the areas of the brain they constitute begin to atrophy. A detailed picture of the progression is still under investigation, and the disease follows different tracks in different patients, but researchers have found brains afflicted with Alzheimer’s typically atrophy along the same basic pattern. A better understanding of that pattern may provide the foundation for methods to diagnose the disease earlier, which in turn would give medication and lifestyle changes the best chance of slowing dementia. In broad strokes, here’s how Alzheimer’s tends to change a brain. © 2024 SCIENTIFIC AMERICAN,

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 29476 - Posted: 09.11.2024

Jon Hamilton Aging and Alzheimer's leave the brain starved of energy. Now scientists think they've found a way to aid the brain's metabolism — in mice. PM Images/Getty Images The brain needs a lot of energy — far more than any other organ in the body — to work properly. And aging and Alzheimer’s disease both seem to leave the brain underpowered. But an experimental cancer drug appeared to re-energize the brains of mice that had a form of Alzheimer’s — and even restore their ability to learn and remember. The finding, published in the journal Science, suggests that it may eventually be possible to reverse some symptoms of Alzheimer’s in people, using drugs that boost brain metabolism. The results also offer an approach to treatment that’s unlike anything on the market today. Current drugs for treating Alzheimer’s, such as lecanemab and donanemab, target the sticky amyloid plaques that build up in a patient’s brain. These drugs can remove plaques and slow the disease process, but do not improve memory or thinking. The result should help “change how we think about targeting this disease,” says Shannon Macauley, an associate professor at the University of Kentucky who was not involved in the study. The new research was prompted by a lab experiment that didn’t go as planned. A team at Stanford was studying an enzyme called IDO1 that plays a key role in keeping a cell’s metabolism running properly. They suspected that in Alzheimer’s disease, IDO1 was malfunctioning in a way that limited the brain’s ability to turn nutrients into energy. © 2024 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: 29462 - Posted: 09.04.2024

Juliana Ki In the United States, it's estimated that about 7 million people are living with Alzheimer's disease and related dementias. But the number of people with a formal diagnosis is far less than that. Now, a new study suggests the likelihood of getting a formal diagnosis may depend on where a person lives. Researchers at the University of Michigan and Dartmouth College found that diagnosis rates vastly differ across the country and those different rates could not simply be explained by dementia risk factors, like if an area has more cases of hypertension, obesity and diabetes. The reasons behind the disparity aren't clear, but researchers speculate that stigma as well as access to primary care or behavioral neurological specialists may impact the odds of getting a formal diagnosis. Sponsor Message "We tell anecdotes about how hard it is to get a diagnosis and maybe it is harder in some places. It's not just your imagination. It actually is different from place to place," said Julie Bynum, the study's lead author and a geriatrician at the University of Michigan Medical School. Those differences may have potential consequences. That's because a formal diagnosis of Alzheimer's opens up access to treatments that may slow down the brain changes associated with the disease. Without that formal diagnosis, patients also would not be eligible for clinical trials or insurance coverage for certain medications. Even in cases of dementia where treatment is not an option, a diagnosis can also help in the planning for a patient's care. The findings, published last week in the journal Alzheimer's & Dementia, emerged from two main questions: What percent of older adults are being diagnosed with dementia across communities in the U.S.? And is the percent we see different from what we would expect? © 2024 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: 29444 - Posted: 08.21.2024

By Charles Q. Choi Tangles of tau protein track with cognitive impairments in Alzheimer’s disease. But even though tau is expressed throughout the brain, it clumps mainly in specific regions, such as the cortex and hippocampus. Other areas, such as the cerebellum and brainstem, are largely spared. Why tau aggregates this way has remained a mystery, but the answer may have to do with a previously overlooked, oversized and naturally occurring variant of the protein called “big tau,” according to a preprint posted 31 July on bioRxiv. Most tau isoforms range from 352 to 441 amino acids in size, but big tau comprises 758 amino acids. This supersized version is significantly more abundant in the cerebellum and brainstem than in the cortex and hippocampus of mice—and it is much less likely to form abnormal clumps than its smaller counterparts, the preprint shows. “Big tau can resist several key pathological changes related to [Alzheimer’s disease],” wrote study investigator Dah-eun Chloe Chung, a postdoctoral researcher in Huda Zoghbi’s lab at Baylor College of Medicine, in a post on X about the work. (Zoghbi declined to comment for this article because she says the study is currently under review for potential publication, and Chung did not respond to email requests for comment.) Scientists identified big tau in the peripheral nervous system in the 1990s, and it is the predominant tau isoform there. But most research on tau since then “ignores the existence of big tau,” according to a 2020 review. “No one has bothered to study this protein in the context of neurodegeneration,” says Veera Rajagopal, a research scientist at Regeneron, who did not take part in the new work. “All tau-related research has been focused on the shorter isoforms that play a key role in the tauopathies like Alzheimer’s disease, frontotemporal dementia and so on. Now many will go after this big guy.” © 2024 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: 29440 - Posted: 08.19.2024

By Greg Donahue In late 2018, after an otherwise-normal Christmas holiday, Laurie Beatty started acting strange. An 81-year-old retired contractor, he grew unnaturally quiet and began poring over old accounting logs from a construction business he sold decades earlier, convinced that he had been bilked in the deal. Listen to this article, read by Robert Petkoff Over the course of several days, Beatty slipped further into unreality. He told his wife the year was 1992 and wondered aloud why his hair had turned white. Then he started having seizures. His arms began to move in uncontrollable jerks and twitches. By the end of May, he was dead. Doctors at the Georges-L.-Dumont University Hospital Center in Moncton, the largest city in the province of New Brunswick, Canada, zeroed in on an exceedingly rare condition — Creutzfeldt-Jakob disease, caused by prions, misfolding proteins in the brain — as the most likely culprit. The doctors explained this to Beatty’s children, Tim and Jill, and said they would run additional tests to confirm the post-mortem diagnosis. Three months later, when the siblings returned to the office of their father’s neurologist, Dr. Alier Marrero, that’s what they were expecting to hear. Instead, Marrero told them that Laurie’s Creutzfeldt-Jakob test had come back negative. “We were all looking at one another,” Tim says, “because we were all very confused.” If Creutzfeldt-Jakob hadn’t killed their father, then what had? What Marrero said next was even more unsettling. “There’s something going on,” they recall him saying. “And I don’t know what it is.” It turned out that Laurie Beatty was just one of many local residents who had gone to Marrero’s office exhibiting similar, inexplicable symptoms of neurological decline — more than 20 in the previous four years. The first signs were often behavioral. One patient fell asleep for nearly 20 hours straight before a friend took her to the hospital; another found himself afraid to disturb the stranger who had sat down in his living room, only to realize hours later that the stranger was his wife. © 2024 The New York Times Company

Related chapters from BN: Chapter 17: Learning and Memory; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 14: Attention and Higher Cognition
Link ID: 29434 - Posted: 08.15.2024

Andrew Gregory Health editor Almost half of dementia cases worldwide could be prevented or delayed, a study has found, as experts named 14 risk factors. The number of people living with dementia globally is forecast to nearly triple to 153 million by 2050, and researchers warn this presents a rapidly growing threat to health and social care systems. Global health and social costs linked to dementia exceed $1tn (£780bn) a year, the research shows. However, in a seismic report published by the Lancet, 27 of the world’s leading dementia experts concluded that far more cases could be avoided or delayed than previously thought. Addressing 14 modifiable risk factors, starting in childhood and continuing throughout life, could prevent or delay 45% of dementia cases, even as people live longer, the Lancet commission on dementia said. The findings were presented at the Alzheimer’s Association international conference in the US. In an interview with the Guardian, the lead author of the research, Prof Gill Livingston, said it was increasingly clear that there was much more that millions of people could and should do to reduce the risk of dementia. Speaking from the conference in Philadelphia, Livingston said: “Many people around the world believe dementia is inevitable but it’s not. Our report concludes that you can hugely increase the chances of not developing dementia or pushing back its onset. “It’s also important to stress that while we now have stronger evidence that longer exposure to risk has a greater effect … it’s never too early or too late to take action.” © 2024 Guardian News & Media Limited

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 13: Memory and Learning
Link ID: 29420 - Posted: 08.03.2024

By Laura Sanders Alzheimer’s disease is hard to diagnose. But proteins in the blood might provide clarity. A series of recent findings, presented at the annual Alzheimer’s Association International Conference in Philadelphia and in research papers, raise the possibility of a simple blood draw to help doctors figure out if a person’s cognitive problems are caused by Alzheimer’s — or something else. Decades ago, the only definitive way to get a diagnosis was an autopsy. Since then, scientists have figured out how to see the disease in living people. Spinal taps reveal levels of key proteins associated with the disease. And brain scans can illuminate the characteristic plaques and tangles that mar the brain in a person with Alzheimer’s disease. But spinal taps and brain scans are expensive and uncomfortable. A blood draw would lower barriers to diagnosis even further. That matters, because while Alzheimer’s has no cure, an easier, faster way to spot the disease could give people more time to discuss therapy options, including the newly available drugs that lower levels of amyloid, the sticky protein that accumulates in the brain in Alzheimer’s (SN: 7/17/23). Those drugs moderately slow the progression of the disease, but they come with serious side effects (SN: 6/7/21). “It’s an exciting moment,” says neuropathologist Eliezer Masliah of the National Institute on Aging in Bethesda, Md. “It’s an explosive moment,” one that has the potential to help reshape the diagnosis and treatment of the nearly 7 million people with Alzheimer’s in the United States, and millions more worldwide, he says. © Society for Science & the Public 2000–2024.

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: 29419 - Posted: 08.03.2024

By Laura Hercher 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 assured 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 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 the week soaking up everything the tour guide had to tell her about Caravaggio and Bernini like she was prepping for the quiz. It was five years 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 an end-stage 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 new and controversial guidelines for the diagnosis of AD based on the underlying biology, not clinical presentation. Biomarkers for AD—signs of the physical changes in the brain that contribute to disease progression—have been available for more than two decades. In 2007 an international working group (IWG) of dementia experts described biomarkers as supporting evidence for a diagnosis of the disease, defined at that point largely as it was by neuropathologist Alois Alzheimer back in 1906: progressive memory loss, confusion and personality changes caused by distinctive plaques and tangles in the brain. For almost a century, those brain changes could only be confirmed on autopsy. While the affected person was alive, the label was merely presumptive. In fact, postmortem studies have found that up to 30 percent of people who received a clinical diagnosis of AD did not have the characteristic plaques and tangles.

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: 29416 - Posted: 08.02.2024

Jon Hamilton A key protein that helps assemble the brain early in life also appears to protect the organ from Alzheimer’s and other diseases of aging. A trio of studies published in the past year all suggest that the protein Reelin helps maintain thinking and memory in ailing brains, though precisely how it does this remains uncertain. The studies also show that when Reelin levels fall, neurons become more vulnerable. There’s growing evidence that Reelin acts as a “protective factor” in the brain, says Li-Huei Tsai, a professor at MIT and director of the Picower Institute for Learning and Memory. “I think we’re on to something important for Alzheimer’s,” Tsai says. Various pieces of colorful trash, such as plastic bottle caps and plastics forks, are arranged in the shape of a human brain, on a light blue background. The research has inspired efforts to develop a drug that boosts Reelin or helps it function better, as a way to stave off cognitive decline. “You don't have to be a genius to be like, ‘More Reelin, that’s the solution,’” says Dr. Joseph Arboleda-Velasquez of Harvard Medical School and Massachusetts Eye and Ear. “And now we have the tools to do that.” From Colombia, a very special brain Reelin became something of a scientific celebrity in 2023, thanks to a study of a Colombian man who should have developed Alzheimer’s in middle age but didn’t. The man, who worked as a mechanic, was part of a large family that carries a very rare gene variant known as Paisa, a reference to the area around Medellin where it was discovered. Family members who inherit this variant are all but certain to develop Alzheimer’s in middle age. © 2024 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: 29413 - Posted: 07.31.2024

By Pam Belluck Scientists have made another major stride toward the long-sought goal of diagnosing Alzheimer’s disease with a simple blood test. On Sunday, a team of researchers reported that a blood test was significantly more accurate than doctors’ interpretation of cognitive tests and CT scans in signaling the condition. The study, published Sunday in the journal JAMA, found that about 90 percent of the time the blood test correctly identified whether patients with memory problems had Alzheimer’s. Dementia specialists using standard methods that did not include expensive PET scans or invasive spinal taps were accurate 73 percent of the time, while primary care doctors using those methods got it right only 61 percent of the time. “Not too long ago measuring pathology in the brain of a living human was considered just impossible,” said Dr. Jason Karlawish, a co-director of the Penn Memory Center at the University of Pennsylvania who was not involved in the research. “This study adds to the revolution that has occurred in our ability to measure what’s going on in the brain of living humans.” The results, presented Sunday at the Alzheimer’s Association International Conference in Philadelphia, are the latest milestone in the search for affordable and accessible ways to diagnose Alzheimer’s, a disease that afflicts nearly seven million Americans and over 32 million people worldwide. Medical experts say the findings bring the field closer to a day when people might receive routine blood tests for cognitive impairment as part of primary care checkups, similar to the way they receive cholesterol tests. “Now, we screen people with mammograms and PSA or prostate exams and other things to look for very early signs of cancer,” said Dr. Adam Boxer, a neurologist at the University of California, San Francisco, who was not involved in the study. “And I think we’re going to be doing the same thing for Alzheimer’s disease and hopefully other forms of neurodegeneration.” © 2024 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: 29410 - Posted: 07.31.2024

Richard Luscombe Federal health authorities on Tuesday gave approval to an experimental new drug that has shown to delay the onset of Alzheimer’s disease in trials. Donanemab, manufactured by Eli Lilly, is the second medication that has won the blessing of the Food and Drug Administration (FDA) to treat patients showing early symptoms of the disease, most prominently cognitive impairment. Last year, authorities cleared the drug lecanemab, marketed under the brand name Leqembi, after it demonstrated a similar decline in the progression of Alzheimer’s in a control group. The treatments are not a cure, but the first to physically alter the course of the disease rather than just addressing its symptoms, the FDA said. The video player is currently playing an ad. Indianapolis-based Eli Lilly reported the success of its trial a year ago, and subsequently applied for the FDA authorization that was announced today. Experts at the time said it “could be the beginning of the end of Alzheimer’s disease”, which affects almost 7 million people, mostly older Americans, according to the Alzheimer’s Association. “Kisunla demonstrated very meaningful results for people with early symptomatic Alzheimer’s disease, who urgently need effective treatment options,” Anne White, executive vice-president of Eli Lilly said on Tuesday, referring to donanemab by the brand name it will be sold under. © 2024 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: 29374 - Posted: 07.03.2024