By Diana Kwon During an embryo's development, a piece of the still-growing brain branches off to form the retina, a sliver of tissue in the back of the eye. This makes the retina, which is composed of several layers of neurons, a piece of the central nervous system. As evidence builds that changes in the brain can manifest in this region, scientists are turning to retinas as a potential screening target for early signs of Alzheimer's, an incurable neurodegenerative disease that affects an estimated six million people in the U.S. alone. Initially clinicians could diagnose Alzheimer's only through brain autopsies after patients died. Since the early 2000s, however, research advances have made it possible to pinpoint signs of the disease—and to begin to investigate treatment—years before symptoms first appear. Today positron emission tomography (PET) brain imaging and tests of cerebrospinal fluid (CSF), the clear liquid surrounding the brain and spinal cord, aid Alzheimer's diagnosis at its early stages. “There have been tremendous improvements in our ability to detect early disease,” says Peter J. Snyder, a neuropsychologist and neuroscientist at the University of Rhode Island. But these diagnostic methods are not always readily available, and they can be expensive and invasive. PET imaging requires injecting a radioactive tracer molecule into the bloodstream, and spinal fluid must be extracted with a needle inserted between vertebrae in the back. “We need ways of funneling the right high-risk individuals into the diagnostic process with low-cost screening tools that are noninvasive and simple to administer,” Snyder says. The retina is a particularly attractive target, he adds, because it is closely related to brain tissue and can be examined noninvasively through the pupil, including with methods routinely used to check for eye diseases. © 2022 Scientific American,

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 7: Vision: From Eye to Brain
Link ID: 28442 - Posted: 08.24.2022

By Frances Stead Sellers A study published this week in the journal Lancet Psychiatry showed increased risks of some brain disorders two years after infection with the coronavirus, shedding new light on the long-term neurological and psychiatric aspects of the virus. The analysis, conducted by researchers at the University of Oxford and drawing on health records data from more than 1 million people around the world, found that while the risks of many common psychiatric disorders returned to normal within a couple of months, people remained at increased risk for dementia, epilepsy, psychosis and cognitive deficit (or brain fog) two years after contracting covid. Adults appeared to be at particular risk of lasting brain fog, a common complaint among coronavirus survivors. The study’s findings were a mix of good and bad news, said Paul Harrison, a professor of psychiatry at the University of Oxford and the senior author of the study. Among the reassuring aspects was the quick resolution of symptoms such as depression and anxiety. “I was surprised and relieved by how quickly the psychiatric sequelae subsided,” Harrison said. David Putrino, director of rehabilitation innovation at Mount Sinai Health System in New York, who has been studying the lasting impacts of the coronavirus since early in the pandemic, said the study revealed some very troubling outcomes. “It allows us to see without a doubt the emergence of significant neuropsychiatric sequelae in individuals that had covid and far more frequently than those who did not,” he said. Because it focused only on the neurological and psychiatric effects of the coronavirus, the study authors and others emphasized that it is not strictly long-covid research.

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: 28438 - Posted: 08.20.2022

By Lesley Evans Ogden Hana aced her memory test. After viewing the contents of three identical boxes arrayed in an arc on the back deck of her home, the 3-year-old Cavalier King Charles spaniel had to remember which box held a treat — a task she quickly learned after just a few trials. Hana is part of a pack that has grown to nearly 40,000 pet dogs enrolled in a citizen science initiative known as the Dog Aging Project, founded in 2014. Understanding the biology of aging in companion dogs is one of two main goals of the project, says cofounder and codirector Matt Kaeberlein, a pathologist at the University of Washington in Seattle who focuses on aging. “The other is to do something about it.” Through veterinary records, DNA samples, health questionnaires and cognitive tests like Hana’s treat-finding challenge, the initiative of the University of Washington and Texas A&M University will track many aspects of dogs’ lives over time. Smaller subsets of the dogs, including Hana, will participate in more focused studies and more extensive evaluations. From all of this, scientists hope to spot patterns and find links between lifestyles and health from puppyhood through the golden years. The effort joins that of an earlier one: the Family Dog Project, spearheaded in the 1990s at Eötvös Loránd University (ELTE) in Budapest to study “the behavioral and cognitive aspects of the dog-human relationship,” with tens of thousands of canines participating through the decades. The two projects have begun collaborating across continents, and the scientists hope that such a large combined group of dogs can help them tease out genetic and environmental factors that affect how long dogs live, and how much of that time is spent in good health. © 2022 Annual Reviews

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 28411 - Posted: 07.30.2022

ByCharles Piller In August 2021, Matthew Schrag, a neuroscientist and physician at Vanderbilt University, got a call that would plunge him into a maelstrom of possible scientific misconduct. A colleague wanted to connect him with an attorney investigating an experimental drug for Alzheimer’s disease called Simufilam. The drug’s developer, Cassava Sciences, claimed it improved cognition, partly by repairing a protein that can block sticky brain deposits of the protein amyloid beta (Aβ), a hallmark of Alzheimer’s. The attorney’s clients—two prominent neuroscientists who are also short sellers who profit if the company’s stock falls—believed some research related to Simufilam may have been “fraudulent,” according to a petition later filed on their behalf with the U.S. Food and Drug Administration (FDA). Schrag, 37, a softspoken, nonchalantly rumpled junior professor, had already gained some notoriety by publicly criticizing the controversial FDA approval of the anti-Aβ drug Aduhelm. His own research also contradicted some of Cassava’s claims. He feared volunteers in ongoing Simufilam trials faced risks of side effects with no chance of benefit. So he applied his technical and medical knowledge to interrogate published images about the drug and its underlying science—for which the attorney paid him $18,000. He identified apparently altered or duplicated images in dozens of journal articles. The attorney reported many of the discoveries in the FDA petition, and Schrag sent all of them to the National Institutes of Health (NIH), which had invested tens of millions of dollars in the work. (Cassava denies any misconduct [see sidebar, below].) But Schrag’s sleuthing drew him into a different episode of possible misconduct, leading to findings that threaten one of the most cited Alzheimer’s studies of this century and numerous related experiments. The first author of that influential study, published in Nature in 2006, was an ascending neuroscientist: Sylvain Lesné of the University of Minnesota (UMN), Twin Cities. His work underpins a key element of the dominant yet controversial amyloid hypothesis of Alzheimer’s, which holds that Aβ clumps, known as plaques, in brain tissue are a primary cause of the devastating illness, which afflicts tens of millions globally. In what looked like a smoking gun for the theory and a lead to possible therapies, Lesné and his colleagues discovered an Aβ subtype and seemed to prove it caused dementia in rats. If Schrag’s doubts are correct, Lesné’s findings were an elaborate mirage. © 2022 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: 28409 - Posted: 07.23.2022

By Paula Span Dementia cases are climbing along with an aging world population, and yet another much-anticipated Alzheimer’s medication, crenezumab, has proved ineffective in clinical trials — the latest of many disappointments. Public health experts and researchers argue that it is past time to turn our attention to a different approach — focusing on eliminating a dozen or so already known risk factors, like untreated high blood pressure, hearing loss and smoking, rather than on an exorbitantly priced, whiz-bang new drug. “It would be great if we had drugs that worked,” said Dr. Gill Livingston, a psychiatrist at University College London and chair of the Lancet Commission on Dementia Prevention, Intervention and Care. “But they’re not the only way forward.” Emphasizing modifiable risks — things we know how to change — represents “a drastic change in concept,” said Dr. Julio Rojas, a neurologist at the University of California, San Francisco. By focusing on behaviors and interventions that are already widely available and for which there is strong evidence, “we are changing how we understand the way dementia develops,” he said. The latest modifiable risk factor was identified in a study of vision impairment in the United States that was published recently in JAMA Neurology. Using data from the Health and Retirement Study, the researchers estimated that about 62 percent of current dementia cases could have been prevented across risk factors and that 1.8 percent — about 100,000 cases — could have been prevented through healthy vision. Though that’s a fairly small percentage, it represents a comparatively easy fix, said Dr. Joshua Ehrlich, an ophthalmologist and population health researcher at the University of Michigan and the study’s lead author. © 2022 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 7: Vision: From Eye to Brain
Link ID: 28388 - Posted: 07.05.2022

Viviane Callier The aging brains of people with Alzheimer’s, Parkinson’s and other neurodegenerative diseases are suffused with telltale aggregates of proteins in or around their neurons. How these protein clumps might be harming the neurons is often still unclear, but they are hallmarks of the conditions — and until now, they have been associated almost exclusively with elderly brains. But a recent study by a team of Stanford University researchers suggests that protein aggregation may be a universal phenomenon in aging cells and could be involved in many more diseases of aging than was suspected. Their discovery points to a new way of thinking about what goes wrong in cells as they age and, potentially, to new ways of staving off some consequences of the aging process. “This is widespread — it’s not just one specific tissue, it’s lots of different tissues,” said Della David, a researcher on aging at the Babraham Institute in Cambridge, England, who was not part of the study. The research also highlights that protein aggregation is tightly bound up with essential mechanisms that allow cells to regulate their physiologies with exquisite delicacy. Biologists will need to assess carefully, possibly on a case-by-case basis, whether protein aggregates represent a threat to cells or a defense they have created. The new work, which was posted to the biorxiv.org preprint server in March, is the first attempt to quantify how much protein aggregation occurs throughout the body during the natural aging of a vertebrate animal — in this case, a very short-lived fish. The study showed that protein aggregation probably contributes to the gradual deterioration of many tissues over time. The findings even offer a hint about why these aggregates are so much more obvious in the brain than in other tissues: It may be because brains have been evolving so rapidly.

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: 28385 - Posted: 06.30.2022

By Apoorva Mandavilli A small biotech company that trumpeted an exciting new treatment for Alzheimer’s disease is now under fire for irregularities in its research results, after several studies related to its work were retracted or questioned by scientific journals. The company, Cassava Sciences, based in Austin, Texas, announced last summer that its drug, simufilam, improved cognition in Alzheimer’s patients in a small clinical trial, describing it as the first such advance in treatment of the disease. Cassava later initiated a larger trial. The drug’s potential garnered enormous attention from investors. Alzheimer’s disease affects roughly six million Americans, a number that is expected to double by 2050, and an effective treatment would be lucrative. Cassava’s stock soared, by more than 1,500 percent at one point. The company was worth nearly $5 billion last summer. But many scientists have been deeply skeptical of the company’s claims, asserting that Cassava’s studies were flawed, its methods opaque and its results improbable. Families of some trial participants have said they see improvements. But critics noted that the trial reporting better cognition due to simufilam lacked a placebo group, and asserted that the Alzheimer’s patients were not followed long enough to confirm that any improvements in cognition were genuine. Some experts went further, accusing the company of manipulating its scientific results. In response to the allegations, in December The Journal of Neuroscience published “expressions of concern” regarding two brain studies authored by the company’s chief collaborator, Hoau-Yan Wang, a professor at the City University of New York. One was co-written by Lindsay H. Burns, chief scientist at Cassava. The journal editors also noted errors in the images accompanying the latter study. (An “expression of concern” indicates that the editors have reason to question the integrity and accuracy of a paper.) © 2022 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: 28290 - Posted: 04.20.2022

Hannah Devlin Science correspondent The largest genetic study of Alzheimer’s to date has provided compelling evidence linking the disease to disruption in the brain’s immune system. The study, using the genomes of 100,000 people with Alzheimer’s and 600,000 healthy people, identified 75 genes linked to an increased risk of the disease, including 42 that had not previously been implicated. The findings suggest degeneration in the brains of dementia patients could be spurred on by “over-aggressive” activity in the brain’s immune cells, called microglia. Prof Julie Williams, the director of the UK Dementia Research Institute at Cardiff University and a co-author of the study, said the findings could help reignite efforts to find an effective treatment. “This is an enormous clue to what’s going wrong,” she said. “Eight or nine years ago we weren’t working on the immune system. The genetics has refocused us.” The study, the largest of its kind to date, also allowed scientists to devise a genetic risk score that could predict which patients with cognitive impairment would, within three years of first showing symptoms, go on to develop Alzheimer’s. The score is not intended for clinical use at the moment, but could be used when recruiting people for clinical trials of drugs aimed at treating the disease in the earliest stages. Alzheimer’s disease is the most common cause of dementia, which affects more than 850,000 people in the UK. Despite the huge burden of the disease, there have been no new drugs for it in the past two decades, with the exception of Aducanumab, controversially licensed in the US but unavailable in Europe and the UK. Previous research has shown that while lifestyle factors such as smoking, exercise and diet influence Alzheimer’s risk, 60%-80% of the disease risk is based on genetics. However, Williams said, drug development was heavily influenced by the study of families with rare genetic mutations causing early onset Alzheimer’s. © 2022 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: 28267 - Posted: 04.06.2022

By Ariana Eunjung Cha People with “chemo brain” and covid brain fog could not seem more different: Those with “chemo brain” have a life-threatening disease for which they’ve taken toxic drugs or radiation. Many of those with covid brain fog, in contrast, describe themselves as previously healthy people who have had a relatively mild infection that felt like a cold. So when Stanford University neuroscientist Michelle Monje began studies on long covid, she was fascinated to find similar changes among patients in both groups, in specialized brain cells that serve as the organ’s surveillance and defense system. “It was really quite striking,” Monje said. In cancer patients undergoing treatment, a malfunction in those same cells, known as microglia, are believed to be a cause of the fuzzy thinking that many describe. Scientists have also theorized that in Alzheimer’s disease, these cells may be impeded, making it difficult for them to counteract the cellular wear and tear of aging. Monje’s project is part of a crucial and growing body of research that suggests similarities in the mechanisms of post-covid cognitive changes and other long-studied brain conditions, including “chemo brain,” Alzheimer’s and other post-viral syndromes following infections with influenza, Epstein-Barr, HIV or Ebola. “There is humongous overlap” between long covid and these other conditions, said Avindra Nath, intramural clinical director of the neurological disorders and stroke unit of the National Institutes of Health. Pre-covid, much of the medical research into brains (as well as other organs) was siloed by disease. But during the pandemic, as diverse scientists banded together to understand a complex, multi-organ disease, commonalities among the conditions began coming to light. © 1996-2022 The Washington Post

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: 28259 - Posted: 03.30.2022

Yue Leng Doctors often recommend “power naps” as a way to compensate for a poor night’s sleep and help keep alert until bedtime. But for older adults, extensive power naps could be an early sign of dementia. Research on how napping affects cognition in adults has had mixed results. Some studies on younger adults suggest that napping is beneficial to cognition, while others on older adults suggest it may be linked to cognitive impairment. However, many studies are based on just a single self-reported nap assessment. This methodology may not be accurate for people with cognitive impairment who may not be able to reliably report when or how long they napped. As an epidemiologist who studies sleep and neurodegeneration in older adults, I wanted to find out if changes in napping habits foreshadow other signs of cognitive decline. A study my colleagues and I recently published found that while napping does increase with age, excessive napping may foreshadow cognitive decline. Sleep may play a significant role in Alzheimer’s development. The link between daytime napping and dementia Sleep disturbance and daytime napping are known symptoms of mild to moderate Alzheimer’s disease and other forms of dementia in older adults. They often become more extreme as the disease progresses: Patients are increasingly less likely to fall asleep and more likely to wake up during the night and feel sleepy during the day. © 2010–2022, The Conversation US, Inc.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 10: Biological Rhythms and Sleep
Link ID: 28256 - Posted: 03.30.2022

Hannah Devlin Science corespondent Taking long naps could be a precursor of Alzheimer’s disease, according to a study that tracked the daytime sleeping habits of elderly people. The findings could help resolve the conflicting results of the effects of napping on cognition in older adults, with some previous studies highlighting the benefits of a siesta on mood, alertness and performance on mental tasks. The latest study suggests that an increase over time in naps was linked to a higher chance of developing mild cognitive impairment or Alzheimer’s. The scientists think it is more likely that excessive napping could be an early warning sign, rather than it causing mental decline. “It might be a signal of accelerated ageing,” said Dr Yue Leng, an assistant professor of psychiatry at the University of California San Francisco. “The main takeaway is if you didn’t used to take naps and you notice you’re starting to get more sleepy in the day, it might be a signal of declining cognitive health.” The scientists tracked more than 1,000 people, with an average age of 81, over several years. Each year, the participants wore a watch-like device to track mobility for up to 14 days. Each prolonged period of non-activity from 9am to 7pm was interpreted as a nap. The participants also underwent tests to evaluate cognition each year. At the start of the study 76% of participants had no cognitive impairment, 20% had mild cognitive impairment and 4% had Alzheimer’s disease. For participants who did not develop cognitive impairment, daily daytime napping increased by an average 11 minutes a year. The rate of increase doubled after a diagnosis of mild cognitive impairment to a total of 24 minutes and nearly tripled to a total of 68 minutes after a diagnosis of Alzheimer’s disease, according to the research published in the journal Alzheimer’s and dementia. © 2022 Guardian News & Media Limited

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 10: Biological Rhythms and Sleep
Link ID: 28244 - Posted: 03.19.2022

Jon Hamilton About 1 in 7 people age 60 or older have a brain condition that may be an early sign of Alzheimer's disease. The condition, called mild cognitive impairment, occupies a gray zone between normal aging of the brain and dementia. And most people know almost nothing about it. A national survey found that 82% of Americans are unfamiliar with the condition or know very little about it. More than half thought the symptoms sounded like "normal aging," according to the survey, which was part of a special report released this week by the Alzheimer's Association. "Mild cognitive impairment is often confused with normal aging because it is very subtle," says Maria Carrillo, chief science officer of the Alzheimer's Association. Symptoms include "forgetting people's names, forgetting perhaps that you've said something already, forgetting a story, forgetting words," she says. The condition, which affects about 10 million people in the U.S., is defined as changes in memory and thinking that are noticeable to the affected person and those around them but not serious enough to interfere with the individual's everyday activities. That makes it tricky to diagnose, says Dr. Pierre Tariot, director of the Banner Alzheimer's Institute in Phoenix. So after talking to a patient, Tariot often asks if he can speak with the person's spouse or a close family member. A patient's wife, for example, might notice that her husband is still managing to keep his appointments, Tariot says, but then she adds: "But a year ago, he had it all locked and loaded in his brain. And now, unless he writes it down 12 times and then asks me to double-check, he's not going to get there." © 2022 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: 28243 - Posted: 03.19.2022

By Linda Searing The more fit you are, the less likely you may be to develop Alzheimer’s disease — with those who are the most fit having a 33 percent lower risk for this dementia than the least fit, according to a report to be presented to the American Academy of Neurology at its annual meeting next month. FAQ: What to know about the omicron variant of the coronavirus D.C.-based researchers, from the Washington VA Medical Center and George Washington University, tested and tracked 649,605 veterans (average age 61) for nearly a decade. Based on their cardiorespiratory fitness, participants were divided into five categories, from lowest to highest fitness level. 10-minute exercising may slow progression to dementia for those with mild cognitive impairment The researchers found that, as fitness improved, people’s chances of developing the ailment decreased. Compared with the least-fit group, those slightly more fit had a 13 percent lower risk for Alzheimer’s; the middle group was 20 percent less likely to develop the disease; the next higher group was 26 percent less likely; with the odds reaching a 33 percent lower risk for those in the most-fit group. Alzheimer’s is the most common type of dementia. It is a progressive brain disorder that, over time, destroys memory and thinking skills and interferes with the ability to carry out daily tasks. About 6 million Americans 65 and older have Alzheimer’s. There are no proven ways to cure the disease. © 1996-2022 The Washington Post

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: 28239 - Posted: 03.16.2022

Alison Abbott Every two weeks, a nurse visits 43-year-old Marty Reiswig in Denver, Colorado, and injects him with an experimental drug called gantenerumab. Every month, Reiswig drives into town for a brain scan to make sure the drug has not caused any bleeds. And every year he flies to St Louis, Missouri, for four days of brain scans, spinal taps, blood analyses and exhaustive tests of his memory and reasoning capacity. Reiswig is fit and healthy and runs two local businesses. He goes through all of this because he has a rare genetic mutation that almost guarantees he will develop early-onset Alzheimer’s disease. He hopes that the international clinical trial he has been part of for nine years might prevent, or at least delay, the onset of symptoms that will otherwise arise in just a few years’ time. “I always do my best to give the researchers as much as I can — even if it turns out not to help me, it might help my children,” he says. The trial is one of several trying to understand whether treating the root cause of Alzheimer’s before symptoms start might be the best way to handle a disease that exacts such a large toll. The drugs under scrutiny are all antibodies that have been developed to target and clear amyloid-β proteins in the brain, which clog together into toxic masses called plaques (see ‘Antibodies against amyloid’). These drugs are of the same type as aducanumab, made by Biogen in Cambridge, Massachusetts, which was provisionally approved last year by the US Food and Drug Administration (FDA) for the treatment of mild Alzheimer’s, in large part owing to its ability to remove amyloid-β. And because such toxic proteins are a feature of several types of dementia, these antibody studies might also offer hints for how to treat the 55 million people around the world who have these conditions, says neurologist Paul Aisen at the University of Southern California in San Diego, who is a leader of the US Alzheimer’s Clinical Trials Consortium. Most dementias hit after 65 years of age; all have proved to be stubbornly incurable. Of more than 100 trials around the world, most are aiming to treat symptoms of the disease rather than its root cause. © 2022 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: 28236 - Posted: 03.11.2022

By Gina Kolata Dr. John Q. Trojanowski, a neuropathologist whose work was at the forefront of research on Alzheimer’s and other neurodegenerative diseases, died on Feb. 8 in a hospital in Philadelphia. He was 75. His wife and longtime collaborator, Virginia M.-Y. Lee, said the cause was complications of chronic spinal cord injuries. Dr. Trojanowski “was a giant in the field,” said Leslie Shaw, a professor with Dr. Trojanowski in the department of pathology and laboratory medicine at the University of Pennsylvania — adding that he meant that in two ways. At 6 feet 4 inches, Dr. Trojanowski towered over his colleagues. And, Dr. Shaw said, he was also a towering figure in his field, whose scientific contributions were “phenomenal” because they combined pathology and biochemistry to figure out what goes wrong, and why, when people get diseases as disparate as Alzheimer’s, Parkinson’s and A.L.S. The results can lead to improved diagnosis and potential treatments. Key to the work Dr. Trojanowski did with Dr. Lee was their establishment of a brain bank: stored brains from patients with diseases like Alzheimer’s and Parkinson’s, as well as from people without degenerative brain diseases. It allowed them to compare the brains of people with and without the conditions and ask what proteins were involved in the diseases and what brain regions were affected. Among their first quests was an attempt to solve the mystery of strange areas in the brains of people with Alzheimer’s. Known as tangles and first described by Alois Alzheimer himself at the turn of the 20th century, they look like twisted strands of spaghetti in dying nerve cells. In 1991, Dr. Trojanowski and Dr. Lee determined that the regions are made up of a malformed protein called tau, which causes the structure of nerve cells to collapse. At a time when most Alzheimer’s researchers and drug companies were focused on a different protein, amyloid, Dr. Trojanowski and Dr. Lee insisted that tau was equally important. They then discovered that it also played a central role in a rare group of degenerative dementias known as frontotemporal lobar degeneration. © 2022 The New York Times Company

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: 28225 - Posted: 03.02.2022

Ian Sample Science editor People who develop Alzheimer’s disease can experience sleep disturbances years before the condition takes hold, but whether one causes the other, or something more complex is afoot, has always proved hard for scientists to determine. Now, researchers in the US have shed light on the mystery, in work that raises hopes for new therapies, and how “good sleep hygiene” could help to tackle the disease and its symptoms. The findings show that humans’ 24-hour circadian clock controls the brain’s ability to mop up wayward proteins linked to Alzheimer’s disease. If the scientists are right, the work would explain, at least in part, how disruption to circadian rhythms and sleep disturbances might feed into the onset and progression of Alzheimer’s disease, and how preventing such disruption might stave off the condition. “Circadian disruption is correlated with Alzheimer’s diagnosis and it has been suggested that sleep disruptions could be an early warning sign of Alzheimer’s disease,” said Dr Jennifer Hurley, who led the research at Rensselaer Polytechnic Institute, in New York. Alzheimer’s takes hold when connections are lost between nerve cells in the brain. The disease is progressive and linked to abnormal plaques and tangles of proteins that steadily build up in the brain. The disease is the most common cause of dementia and affects more than half a million people in the UK, a figure that is set to rise. To keep the brain healthy, immune cells called microglia seek out and destroy troublesome proteins that threaten to accumulate in the brain. One type of protein targeted by the cells is called amyloid beta, a hallmark of Alzheimer’s. © 2022 Guardian News & Media Limited

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 10: Biological Rhythms and Sleep
Link ID: 28197 - Posted: 02.12.2022

By Elizabeth Landau My grandmother was in the advanced stages of Alzheimer’s disease when she died in 2007, not long after I graduated from journalism school. As a budding health reporter, I tried to learn everything I could about Alzheimer’s and wrote about new research on preventions and treatments that everyone wanted to believe had potential. It is demoralizing and infuriating to think about how, nearly 15 years later, no breakthrough cure or proven prevention strategy has panned out. But neurologist Sara Manning Peskin argues in “A Molecule Away from Madness: Tales of the Hijacked Brain” that we could be on the brink of a revolution in confronting diseases like this because scientists have a better handle on how molecules work in the brain. Molecular research has transformed our understanding and treatment of cancer in recent years, and now it is beginning to do the same for brain diseases. In fact, it has already been key to solving several mysteries of why seemingly healthy people appear to suddenly fall into a mental inferno. While the shadow of Alzheimer’s looms over the book, representing an intractable condition that Peskin routinely confronts in her clinical practice, “A Molecule Away from Madness” is a fascinating tour of different kinds of ways that the brain can lead to the breakdown of mental life. The book is organized according to how different molecules interact with our brains to wreak havoc — Peskin calls them “mutants, rebels, invaders, and evaders.” Some have helped scientists solve longstanding puzzles, while others, like the molecules associated with Alzheimer’s, continue to leave millions of people waiting for a cure.

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: 28196 - Posted: 02.12.2022

Bret Stetka It all started with genetic data. A gene here, a gene there. Eventually the story became clearer: If scientists are to one day find a cure for Alzheimer's disease, they should look to the immune system. Over the past couple decades, researchers have identified numerous genes involved in various immune system functions that may also contribute to Alzheimer's. Some of the prime suspects are genes that control humble little immune cells called microglia, now the focus of intense research in developing new Alzheimer's drugs. Microglia are amoeba-like cells that scour the brain for injuries and invaders. They help clear dead or impaired brain cells and literally gobble up invading microbes. Without them, we'd be in trouble. In a normal brain, a protein called beta-amyloid is cleared away through our lymphatic system by microglia as molecular junk. But sometimes it builds up. Certain gene mutations are one culprit in this toxic accumulation. Traumatic brain injury is another, and, perhaps, impaired microglial function. One thing everyone agrees on is that in people with Alzheimer's, too much amyloid accumulates between their brain cells and in the vessels that supply the brain with blood. Once amyloid begins to clog networks of neurons, it triggers the accumulation of another protein, called tau, inside of these brain cells. The presence of tau sends microglia and other immune mechanisms into overdrive, resulting in the inflammatory immune response that many experts believe ultimately saps brain vitality in Alzheimer's. To date, nearly a dozen genes involved in immune and microglial function have been tied to Alzheimer's. The first was CD33, identified in 2008. © 2022 npr

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: 28184 - Posted: 02.02.2022

By Jane E. Brody Many people aren’t overly concerned when an octogenarian occasionally forgets the best route to a favorite store, can’t remember a friend’s name or dents the car while trying to parallel park on a crowded city street. Even healthy brains work less efficiently with age, and memory, sensory perceptions and physical abilities become less reliable. But what if the person is not in their 80s but in their 30s, 40s or 50s and forgets the way home from their own street corner? That’s far more concerning. While most of the 5.3 million Americans who are living with Alzheimer’s disease or other forms of dementia are over 65, some 200,000 are younger than 65 and develop serious memory and thinking problems far earlier in life than expected. “Young-onset dementia is a particularly disheartening diagnosis because it affects individuals in the prime years,” Dr. David S. Knopman, a neurologist at the Mayo Clinic in Rochester, Minn., wrote in a July 2021 editorial in JAMA Neurology. Many of the afflicted are in their 40s and 50s, midcareer, hardly ready to retire and perhaps still raising a family. Dementia in a younger adult is especially traumatic and challenging for families to acknowledge, and many practicing physicians fail to recognize it or even suspect it may be an underlying cause of symptoms. “Complaints about brain fog in young patients are very common and are mostly benign,” Dr. Knopman told me. “It’s hard to know when they’re not attributable to stress, depression or anxiety or the result of normal aging. Even neurologists infrequently see patients with young-onset dementia.” Yet recent studies indicate that the problem is far more common than most doctors realize. Worldwide, as many as 3.9 million people younger than 65 may be affected, a Dutch analysis of 74 studies indicated. The study, published in JAMA Neurology in September, found that for every 100,000 people aged 30 to 64, 119 had early dementia. © 2022 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: 28161 - Posted: 01.19.2022

Mitch Leslie Medicine so far has nothing to offer that clearly prevents Alzheimer’s disease, although keeping your weight down, exercising regularly, and inheriting certain protective genes can lower your risk. Now, a study has identified another, unexpected source of protection: clonal hematopoiesis, a blood cell imbalance best known as a risk factor for cancer and heart disease. “Clonal hematopoiesis has been associated with so many bad outcomes that it is surprising that it is protective in this situation,” says cardiovascular biologist Kenneth Walsh of the University of Virginia, who wasn’t connected to the study, reported on 12 December at the American Society of Hematology meeting in Atlanta. But Walsh says the work is convincing and “will have to be reckoned with and explained.” He and other researchers caution that the discovery doesn’t offer any immediate opportunities for treating or preventing Alzheimer’s disease. Given the negative health effects of clonal hematopoiesis, inducing it in healthy people is a nonstarter. Still, the finding has a provocative implication: that cells from the bloodstream are restocking the brain’s immune cells, perhaps bolstering its ability to clear out toxic debris. Charles Darwin probably never imagined that natural selection unfolds in our bone marrow. But clonal hematopoiesis results from competition among the 50,000 to 200,000 stem cells that dwell there and divide to produce all our red and white blood cells. Over the years these stem cells accrue mutations, some of which result in a “fitter” cell whose progeny, known collectively as a clone, can soon outnumber their counterparts. In some people with clonal hematopoiesis, the offspring of a single mutated stem cell account for more than half of the blood cells in the body. © 2021 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: 28114 - Posted: 12.15.2021