Chapter 13. Memory and Learning

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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

Keyword: Alzheimers
Link ID: 28290 - Posted: 04.20.2022

Joan L. Luby, M.D., John N. Constantino, M.D., Deanna M. Barch, Ph.D. Numerous studies of children in the US across decades have shown striking correlations between poverty and less-than-optimal physical and mental health and developmental outcomes. Trauma, poor health care, inadequate nutrition, and increased exposures to psychosocial stress and environmental toxins—all of which have significant negative developmental impact—are likely to be involved. The effects of elevated stress on child-caregiver relationships appear to be particularly detrimental, unsurprising in that nurturing and supportive caregiver relationships are foundational for healthy development in early childhood. For adults whose job options are unconducive to their role as parents (such as working multiple jobs or night shift hours), or for whom family support is unavailable, or for those do not have the material resources they need, the resulting stress may result in sleep disruption, depression, and anxiety—all of which translate to poor developmental trajectories for their children. Other health and developmental risks often associated with poverty include lead and other pollutants in air and water, poor nutrition (often related to living in “food desert” areas where healthy foods such as fresh fruits and vegetables are scarce), neighborhood violence, and trauma. “Toxic stress” that exceeds a child’s ability to adapt can occur when the burden of stressful life experience overwhelms the brain’s regulatory capacity, or when the compensatory abilities of brain and body are compromised. A lack of cognitive stimulation (due to such factors as the absence of books and educational materials in the home, poor immersion in language, and a lack of after school or other enrichment activities) or disruption of sleep and circadian rhythms (by neighborhood noise or parents’ irregular work schedules) is likely to impact brain development and emotional and behavioral regulation when these systems are rapidly developing. © 2022 The Dana Foundation.

Keyword: Development of the Brain; Brain imaging
Link ID: 28288 - Posted: 04.16.2022

Kayt Sukel Each night, as you transition into deep sleep from wakefulness, your body undergoes a remarkable transformation. Your muscles relax. Your breathing slows. Your temperature and blood pressure drop. Even your brain activity changes, decelerating into slow, coordinated waves. Despite these remarkable physiological changes, scientists are now learning that the brain is far from idle during sleep. Rather, it remains hard at work, facilitating memory and learning while uncoupled from the external world. “For a long time, we believed that being awake all day depleted you and that sleep was what was required to restore and reinvigorate the whole body, including the brain,” says Robert Stickgold, a pioneering sleep researcher at Harvard Medical School. “It turns out that rest has very little to do with the function of sleep—rather, our brain is sorting and consolidating the information we learned during the day so we can better access it when it’s needed.” Anyone who has ever pulled an all-nighter knows the effect that sleep deprivation can have on cognitive function, including one’s ability to learn and retain new information. Yet, over the last few decades, neuroscientists across the globe have learned that sleep plays an integral role in memory—and it is a role that is highly conserved across the animal kingdom. To better understand how sleep helps us remember, these researchers have been working to characterize not only the physiological changes observed during sleep, but also the neural mechanisms underlying them. Nearly every animal on earth, from fruit flies to non-human primates, experiences some form of sleep, a naturally recurring state of altered consciousness and inhibited sensory activity. And while the exact amount of time spent in slumber, and the patterns of neural activity, differ from animal to animal, humans are no different. We need sleep to thrive. © 2022 The Dana Foundation.

Keyword: Sleep; Learning & Memory
Link ID: 28285 - Posted: 04.16.2022

by Peter Hess Two separate sets of neurons govern the social difficulties and repetitive behaviors associated with mutations in TSHZ3, a top autism candidate gene, according to a new mouse study. The results could help advance a circuit-level understanding of autism, says co-lead investigator Laurent Fasano, senior researcher at the French National Center for Scientific Research and Aix-Marseille University in Marseille, France. “Although we know that the results obtained with animal models will not necessarily be transposable to humans, we hope that our results will stimulate additional studies that will benefit autistic people.” In the new work, Fasano and his colleagues homed in on cortical projection neurons, which connect the cerebral cortex to other brain regions, and striatal cholinergic interneurons, which produce the chemical messenger acetylcholine in the striatum. Together, these cell types form part of the corticostriatal circuit, the dysfunction of which has been implicated in autism. “Whereas many studies have linked defective development and function of the corticostriatal pathway to autism, there is little evidence for an implication of striatal cholinergic interneurons,” says co-lead investigator Lydia Kerkerian-Le Goff, senior researcher at the French National Center for Scientific Research and Aix-Marseille University. Picking out specific cell types in the corticostriatal circuit and linking them to distinct autism-related behaviors is important, says Michael Ragozzino, professor of behavioral neuroscience at the University of Illinois Chicago, who was not involved in the study. The study’s results suggest that repetitive behaviors and social deficits, autism’s core traits, have different neurobiological roots, he says. “This may also suggest that different therapeutics may need to be developed to effectively treat both symptom domains.” © 2022 Simons Foundation

Keyword: Autism
Link ID: 28284 - Posted: 04.16.2022

Max Kozlov When neuroscientist Jakob Seidlitz took his 15-month-old son to the paediatrician for a check-up last week, he left feeling unsatisfied. There wasn’t anything wrong with his son — the youngster seemed to be developing at a typical pace, according to the height and weight charts the physician used. What Seidlitz felt was missing was an equivalent metric to gauge how his son’s brain was growing. “It is shocking how little biological information doctors have about this critical organ,” says Seidlitz, who is based at the University of Pennsylvania in Philadelphia. Soon, he might be able to change that. Working with colleagues, Seidlitz has amassed more than 120,000 brain scans — the largest collection of its kind — to create the first comprehensive growth charts for brain development. The charts show visually how human brains expand quickly early in life and then shrink slowly with age. The sheer magnitude of the study, published in Nature on 6 April1, has stunned neuroscientists, who have long had to contend with reproducibility issues in their research, in part because of small sample sizes. Magnetic resonance imaging (MRI) is expensive, meaning that scientists are often limited in the number of participants they can enrol in experiments. “The massive data set they assembled is extremely impressive and really sets a new standard for the field,” says Angela Laird, a cognitive neuroscientist at Florida International University in Miami. Even so, the authors caution that their database isn’t completely inclusive — they struggled to gather brain scans from all regions of the globe. The resulting charts, they say, are therefore just a first draft, and further tweaks would be needed to deploy them in clinical settings. If the charts are eventually rolled out to paediatricians, great care will be needed to ensure that they are not misinterpreted, says Hannah Tully, a paediatric neurologist at the University of Washington in Seattle. “A big brain is not necessarily a well-functioning brain,” she says. © 2022 Springer Nature Limited

Keyword: Development of the Brain; Brain imaging
Link ID: 28277 - Posted: 04.09.2022

By Lenny Bernstein Researchers have found variations in a small number of genes that appear to dramatically increase the likelihood of developing schizophrenia in some people. The interplay of a wide array of other genes is implicated for most people with schizophrenia, a severe brain disorder characterized by hallucinations, delusions and inability to function. But for some who possess mutations in the 10 genes identified in the new study, published Wednesday in the journal Nature, the likelihood of developing the disease can be 10, 20 and even 50 times greater. The discovery could one day lead to advances in diagnosis of, and therapy for, the disease, according to the lead author of the study, Tarjinder Singh, of the Broad Institute at MIT and Harvard, which led an effort that involved years of work by dozens of research institutions worldwide. “This is the biological clue that leads to better therapies,” Singh said in an interview. “But the key thing is, we haven’t had any meaningful clues for the longest time.” Ken Duckworth, chief medical officer for the National Alliance on Mental Illness, a nationwide advocacy group, said the study is an important development in the neuroscience that underlies schizophrenia. But he said it is difficult to predict how soon such basic research would pay off for people living with the disease. “This is a big step forward for science that may pay a long-term return for people with schizophrenia and the people who live with them,” Duckworth said. But, he said, “if this is a 17-inning game and they’ve gotten us from the first to the second inning, how does this help someone today?” Less than 1 percent of the U.S. population is believed to have schizophrenia, which is generally treated with an array of powerful antipsychotic medications. The disease reduces life expectancy by about 15 years, according to the new research. Scientists have long recognized a hereditary component to the disease, along with other factors such as environment. The work of isolating these genes could not have been accomplished even 10 or 15 years ago, Singh said, before the sequencing of the human genome and the spread of technology that allows such genetic detective work to be conducted in laboratories around the world. © 1996-2022 The Washington Post

Keyword: Schizophrenia; Genes & Behavior
Link ID: 28274 - Posted: 04.09.2022

By Jessica Contrera The carpet cleaner heaves his machine up the stairs, untangles its hoses and promises to dump the dirty water only in the approved toilet. Another day scrubbing rugs for less than $20 an hour. Another Washington area house with overflowing bookshelves and walls covered in travel mementos from places he would love to go one day. But this was not that day. “Tell me about this stain,” 46-year-old Vaughn Smith asks his clients. “Well,” says one of the homeowners, “Schroeder rubbed his bottom across it.” Vaughn knows just what to do about that, and the couple, Courtney Stamm and Kelly Widelska, know they can trust him to do it. They’d been hiring him for years, once watching him erase even a splattered Pepto Bismol stain. But this time when Vaughn called to confirm their January appointment, he quietly explained that there was something about himself that he’d never told them. That he rarely told anyone. And well, a reporter was writing a story about it. Could he please bring her along? Now as they listen to Vaughn discuss the porousness of wool, and the difference between Scotchgard and sanitizer, they can’t help but look at him differently. Once the stool stain is solved, Kelly just has to ask. “So, how many languages do you speak?” “Oh goodness,” Vaughn says. “Eight, fluently.” “Eight?” Kelly marvels. “Eight,” Vaughn confirms. English, Spanish, Bulgarian, Czech, Portuguese, Romanian, Russian and Slovak. “But if you go by like, different grades of how much conversation,” he explains, “I know about 25 more.” Vaughn glances at me. He is still underselling his abilities. By his count, it is actually 37 more languages, with at least 24 he speaks well enough to carry on lengthy conversations. He can read and write in eight alphabets and scripts. He can tell stories in Italian and Finnish and American Sign Language. He’s teaching himself Indigenous languages, from Mexico’s Nahuatl © 1996-2022 The Washington Post

Keyword: Language; Autism
Link ID: 28269 - Posted: 04.06.2022

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

Keyword: Alzheimers; Genes & Behavior
Link ID: 28267 - Posted: 04.06.2022

Elena Renken Even when it’s not apparent, cells in our tissues and organs are constantly on the move. In fact, the ability of cells to get where they need to go is essential to our health and survival. Skin cells migrate to heal wounds. Immune system cells migrate to fight infections. “Every day, you look at your body and it’s not changing much,” said Peter Devreotes, a professor of cell biology at the Johns Hopkins University School of Medicine. “But the cells within it are migrating constantly.” It starts from the earliest stages of life. When we are embryos just a few weeks old, a special population of “neural crest” cells in our back suddenly spreads through the body to become a wide range of essential tissues — bones, cartilage and nerves in the face, tendons, pigment cells in the skin, parts of the heart and more. But how do these cells know where to go? Studies long suggested that they were following chemical trails to their routes. Biologists traditionally saw these chemical gradients as simple and the cells as mere followers: Like dogs trotting toward the scent of food, the cells sensed the gradient and followed the stream of signals back to the source. Countless examples of this have been found among bacteria and other cells navigating through the wild, as well as inside larger organisms. When you nick your skin, for instance, the tissue around the cut releases a cloud of molecules that attract immune cells nearby. The immune cells crawl toward it and stave off infection. Yet scientists also came to understand that this system can’t sustain many of the migrations that unfold in the body. The structure of simple passive gradients is too fragile and too easily disrupted. Simple gradients like these don’t always reach far enough to guide cells’ lengthier journeys, and they may dissipate too quickly to maintain migrations that take longer. Raising the sensitivity of the cells might seem like a way to offset those problems, but then cells might often be too flooded with signals to sense where they come from. For a simple gradient to work, it has to be perfect, and nothing can go awry. But in reality, cells must find a way to navigate under all kinds of conditions. All Rights Reserved © 2022

Keyword: Development of the Brain
Link ID: 28261 - Posted: 03.30.2022

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

Keyword: Alzheimers; Learning & Memory
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.

Keyword: Alzheimers; Sleep
Link ID: 28256 - Posted: 03.30.2022

By Laura Sanders Like all writers, I spend large chunks of my time looking for words. When it comes to the ultracomplicated and mysterious brain, I need words that capture nuance and uncertainties. The right words confront and address hard questions about exactly what new scientific findings mean, and just as importantly, why they matter. The search for the right words is on my mind because of recent research on COVID-19 and the brain. As part of a large brain-scanning study, researchers found that infections of SARS-CoV-2, the virus that causes COVID-19, were linked with less gray matter, tissue that’s packed with the bodies of brain cells. The results, published March 7 in Nature, prompted headlines about COVID-19 causing brain damage and shrinkage. That coverage, in turn, prompted alarmed posts on social media, including mentions of early-onset dementia and brain rotting. As someone who has reported on brain research for more than a decade, I can say those alarming words are not the ones that I would choose here. The study is one of the first to look at structural changes in the brain before and after a SARS-CoV-2 infection. And the study is meticulous. It was done by an expert group of brain imaging researchers who have been doing this sort of research for a very long time. As part of the UK Biobank project, 785 participants underwent two MRI scans. Between those scans, 401 people had COVID-19 and 384 people did not. By comparing the before and after scans, researchers could spot changes in the people who had COVID-19 and compare those changes with people who didn’t get the infection. © Society for Science & the Public 2000–2022.

Keyword: Learning & Memory; Attention
Link ID: 28246 - Posted: 03.19.2022

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

Keyword: Alzheimers; 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

Keyword: Alzheimers; Learning & Memory
Link ID: 28243 - Posted: 03.19.2022

Yasemin Saplakoglu Imagine that while you are enjoying your morning bowl of Cheerios, a spider drops from the ceiling and plops into the milk. Years later, you still can’t get near a bowl of cereal without feeling overcome with disgust. Researchers have now directly observed what happens inside a brain learning that kind of emotionally charged response. In a new study published in January in the Proceedings of the National Academy of Sciences, a team at the University of Southern California was able to visualize memories forming in the brains of laboratory fish, imaging them under the microscope as they bloomed in beautiful fluorescent greens. From earlier work, they had expected the brain to encode the memory by slightly tweaking its neural architecture. Instead, the researchers were surprised to find a major overhaul in the connections. What they saw reinforces the view that memory is a complex phenomenon involving a hodgepodge of encoding pathways. But it further suggests that the type of memory may be critical to how the brain chooses to encode it — a conclusion that may hint at why some kinds of deeply conditioned traumatic responses are so persistent, and so hard to unlearn. “It may be that what we’re looking at is the equivalent of a solid-state drive” in the brain, said co-author Scott Fraser, a quantitative biologist at USC. While the brain records some types of memories in a volatile, easily erasable form, fear-ridden memories may be stored more robustly, which could help to explain why years later, some people can recall a memory as if reliving it, he said. Memory has frequently been studied in the cortex, which covers the top of the mammalian brain, and in the hippocampus at the base. But it’s been examined less often in deeper structures such as the amygdala, the brain’s fear regulation center. The amygdala is particularly responsible for associative memories, an important class of emotionally charged memories that link disparate things — like that spider in your cereal. While this type of memory is very common, how it forms is not well understood, partly because it occurs in a relatively inaccessible area of the brain. All Rights Reserved © 2022

Keyword: Learning & Memory; Brain imaging
Link ID: 28241 - Posted: 03.16.2022

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

Keyword: Alzheimers
Link ID: 28239 - Posted: 03.16.2022

By Pam Belluck Covid-19 may cause greater loss of gray matter and tissue damage in the brain than naturally occurs in people who have not been infected with the virus, a large new study found. The study, published Monday in the journal Nature, is believed to be the first involving people who underwent brain scans both before they contracted Covid and months after. Neurological experts who were not involved in the research said it was valuable and unique, but they cautioned that the implications of the changes were unclear and did not necessarily suggest that people might have lasting damage or that the changes might profoundly affect thinking, memory or other functions. The study, involving people aged 51 to 81, found shrinkage and tissue damage primarily in brain areas related to sense of smell; some of those areas are also involved in other brain functions, the researchers said. “To me, this is pretty convincing evidence that something changes in brains of this overall group of people with Covid,” said Dr. Serena Spudich, chief of neurological infections and global neurology at the Yale School of Medicine, who was not involved in the study. But, she cautioned: “To make a conclusion that this has some long-term clinical implications for the patients I think is a stretch. We don’t want to scare the public and have them think, ‘Oh, this is proof that everyone’s going to have brain damage and not be able to function.’” The study involved 785 participants in UK Biobank, a repository of medical and other data from about half a million people in Britain. The participants each underwent two brain scans roughly three years apart, plus some basic cognitive testing. In between their two scans, 401 participants tested positive for the coronavirus, all infected between March 2020 and April 2021. The other 384 participants formed a control group because they had not been infected with the coronavirus and had similar characteristics to the infected patients in areas like age, sex, medical history and socioeconomic status. With normal aging, people lose a tiny fraction of gray matter each year. For example, in regions related to memory, the typical annual loss is between 0.2 percent and 0.3 percent, the researchers said. © 2022 The New York Times Company

Keyword: Chemical Senses (Smell & Taste); Learning & Memory
Link ID: 28237 - Posted: 03.11.2022

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

Keyword: Alzheimers
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

Keyword: Alzheimers; ALS-Lou Gehrig's Disease
Link ID: 28225 - Posted: 03.02.2022

Dominique Potvin When we attached tiny, backpack-like tracking devices to five Australian magpies for a pilot study, we didn’t expect to discover an entirely new social behaviour rarely seen in birds. Our goal was to learn more about the movement and social dynamics of these highly intelligent birds, and to test these new, durable and reusable devices. Instead, the birds outsmarted us. As our new research paper explains, the magpies began showing evidence of cooperative “rescue” behaviour to help each other remove the tracker. While we’re familiar with magpies being intelligent and social creatures, this was the first instance we knew of that showed this type of seemingly altruistic behaviour: helping another member of the group without getting an immediate, tangible reward. As academic scientists, we’re accustomed to experiments going awry in one way or another. Expired substances, failing equipment, contaminated samples, an unplanned power outage—these can all set back months (or even years) of carefully planned research. For those of us who study animals, and especially behaviour, unpredictability is part of the job description. This is the reason we often require pilot studies. Our pilot study was one of the first of its kind—most trackers are too big to fit on medium to small birds, and those that do tend to have very limited capacity for data storage or battery life. They also tend to be single-use only. A novel aspect of our research was the design of the harness that held the tracker. We devised a method that didn’t require birds to be caught again to download precious data or reuse the small devices. © 1986–2022 The Scientist.

Keyword: Evolution; Learning & Memory
Link ID: 28218 - Posted: 02.26.2022