Chapter 13. Memory and Learning

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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

by Laura Dattaro Some genomic areas that help determine cerebellar size are associated with autism, schizophrenia and bipolar disorder, according to a new study. But heritable genetic variants across the genome that also influence cerebellar size are not. The cerebellum sits at the base of the skull, below and behind the much larger cerebrum. It coordinates movement and may also play roles in social cognition and autism, according to previous research. The new work analyzed genetic information and structural brain scans from more than 33,000 people in the UK Biobank, a biomedical and genetic database of adults aged 40 to 69 living in the United Kingdom. A total of 33 genetic sequence variants, known as single nucleotide polymorphisms (SNPs), were associated with differences in cerebellar volume. Only one SNP overlapped with those linked to autism, but the association should be explored further in other cohorts, says lead investigator Richard Anney, senior lecturer in bioinformatics at Cardiff University in Wales. “There’s lots of caveats to say why it might be worth following up on,” Anney says. “But from this data alone, it’s not telling us there’s a major link between [autism] and cerebellar volume.” So far, cognitive neuroscientists have largely ignored the cerebellum, says Jesse Gomez, assistant professor of neuroscience at Princeton University, who was not involved in the work. The new study represents a first step in better understanding genetic influences on the brain region and its role in neurodevelopmental conditions, he says. “It’s a fun paper,” Gomez says. “It’s the beginning of what’s an exciting revolution in the field.” Of the 33 inherited variants Anney’s team found, 5 had not previously been significantly associated with cerebellar volume. They estimated that the 33 variants account for about 50 percent of the differences in cerebellar volume seen across participants. © 2022 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 28215 - Posted: 02.23.2022

by Angie Voyles Askham Mice chemically coaxed to produce high levels of an autism-linked gut molecule have anxiety-like behavior and unusual patterns of brain connectivity, according to a study published today in Nature. The findings present a direct mechanism by which the gut could send signals to the brain and alter development, the researchers say. “It’s a true mechanistic paper, [like] the field has been asking for,” says Jane Foster, professor of psychiatry and behavioral neurosciences at McMaster University in Hamilton, Canada, who was not involved in the study. Although it’s not clear that this exact signaling pathway is happening in people, she says, “this is the sort of work that’s going to get us that answer.” The molecule, 4-ethylphenol (4EP), is produced by gut microbes in mice and people. An enzyme in the colon and liver converts 4EP to 4-ethylphenyl sulfate (4EPS), which then circulates in the blood. Mice exposed to a maternal immune response in the womb have atypically high blood levels of 4EPS, as do some autistic people, previous research shows. And injecting mice with the molecule increases behaviors indicative of anxiety. But it wasn’t clear how the molecule could contribute to those traits. In the new work, researchers show that 4EPS can enter the brain and that its presence is associated with altered brain connectivity and a decrease in myelin — the insulation around axons that helps conduct electrical signals. Boosting the function of myelin-producing cells, the team found, eases the animals’ anxiety. “This is one of the first — maybe, arguably, the first — demonstrations of a specific microbe molecule that has such a profound impact on a complex behavior,” says lead researcher Sarkis Mazmanian, professor of microbiology at the California Institute of Technology in Pasadena. “How it’s doing it, we still need to understand.” without the engineered enzymes, they showed increased anxiety-like behaviors, © 2022 Simons Foundation

Keyword: Development of the Brain; Neuroimmunology
Link ID: 28205 - Posted: 02.16.2022

By Linda Searing Health-care workers and others who are exposed on the job to formaldehyde, even in low amounts, face a 17 percent increased likelihood of developing memory and thinking problems later on, according to research published in the journal Neurology. The finding adds cognitive impairment to already established health risks associated with formaldehyde. As the level of exposure increases, those risks range from eye, nose and throat irritation to skin rashes and breathing problems. At high levels of exposure, the chemical is considered a carcinogen, linked to leukemia and some types of nose and throat cancer. A strong-smelling gas, formaldehyde is used in making building materials and plastics and often as a component of disinfectants and preservatives. Materials containing formaldehyde can release it into the air as a vapor that can be inhaled, which is the main way people are exposed to it. The study, which included data from more than 75,000 people, found that the majority of those exposed were workers in the health-care sector — nurses, caregivers, medical technicians and those working in labs and funeral homes. Other study participants who had been exposed to formaldehyde included workers in textile, chemistry and metal industries; carpenters; and cleaners. At highest risk were those whose work had exposed them to formaldehyde for 22 years or more, giving them a 21 percent higher risk for cognitive problems than those who had not been exposed. Using a battery of standardized tests, the researchers found that formaldehyde exposure created higher risk for every type of cognitive function that was tested, including memory, attention, reasoning, word recall and other thinking skills.

Keyword: Learning & Memory; Neurotoxins
Link ID: 28203 - Posted: 02.16.2022

Jordana Cepelewicz We often think of memory as a rerun of the past — a mental duplication of events and sensations that we’ve experienced. In the brain, that would be akin to the same patterns of neural activity getting expressed again: Remembering a person’s face, for instance, might activate the same neural patterns as the ones for seeing their face. And indeed, in some memory processes, something like this does occur. But in recent years, researchers have repeatedly found subtle yet significant differences between visual and memory representations, with the latter showing up consistently in slightly different locations in the brain. Scientists weren’t sure what to make of this transformation: What function did it serve, and what did it mean for the nature of memory itself? Now, they may have found an answer — in research focused on language rather than memory. A team of neuroscientists created a semantic map of the brain that showed in remarkable detail which areas of the cortex respond to linguistic information about a wide range of concepts, from faces and places to social relationships and weather phenomena. When they compared that map to one they made showing where the brain represents categories of visual information, they observed meaningful differences between the patterns. And those differences looked exactly like the ones reported in the studies on vision and memory. The finding, published last October in Nature Neuroscience, suggests that in many cases, a memory isn’t a facsimile of past perceptions that gets replayed. Instead, it is more like a reconstruction of the original experience, based on its semantic content. All Rights Reserved © 2022

Keyword: Learning & Memory; Language
Link ID: 28202 - Posted: 02.12.2022

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

Keyword: Alzheimers; 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.

Keyword: Alzheimers
Link ID: 28196 - Posted: 02.12.2022

By Pallab Ghosh A paralysed man with a severed spinal cord has been able to walk again, thanks to an implant developed by a team of Swiss researchers. It is the first time someone who has had a complete cut to their spinal cord has been able to walk freely. The same technology has improved the health of another paralysed patient to the extent that he has been able to become a father. The research has been published in the journal Nature Medicine. Michel Roccati was paralysed after a motorbike accident five years ago. His spinal cord was completely severed - and he has no feeling at all in his legs. But he can now walk - because of an electrical implant that has been surgically attached to his spine. Someone this injured has never been able to walk like this before. The researchers stress that it isn't a cure for spinal injury and that the technology is still too complicated to be used in everyday life, but hail it nonetheless as a major step to improving quality of life. I met Michel at the lab where the implant was created. He told me that the technology "is a gift to me". "I stand up, walk where I want to, I can walk the stairs - it's almost a normal life." It was not the technology alone that drove Michel's recovery. The young Italian has a steely resolve. He told me that from the moment of his accident, he was determined to make as much progress as he could. "I used to box, run and do fitness training in the gym. But after the accident, I could not do the things that I loved to do, but I did not let my mood go down. I never stopped my rehabilitation. I wanted to solve this problem." The speed of Michel's recovery amazed the neurosurgeon who inserted the implant and expertly attached electrodes to individual nerve fibres, Prof Jocelyne Bloch at Lausanne University Hospital "I was extremely surprised," she told me. "Michel is absolutely incredible. He should be able to use this technology to progress and be better and better." © 2022 BBC.

Keyword: Robotics; Regeneration
Link ID: 28194 - Posted: 02.09.2022

By Laura Sanders A tussle with COVID-19 can leave people’s brains fuzzy. SARS-CoV-2, the virus behind COVID-19, doesn’t usually make it into the brain directly. But the immune system’s response to even mild cases can affect the brain, new preliminary studies suggest. These reverberating effects may lead to fatigue, trouble thinking, difficulty remembering and even pain, months after the infection is gone. It’s not a new idea. Immune systems gone awry have been implicated in cognitive problems that come with other viral infections such as HIV and influenza, with disorders such as myalgic encephalomyelitis/chronic fatigue syndrome, or ME/CFS, and even from the damaging effects of chemotherapy. What’s different with COVID-19 is the scope of the problem. Millions of people have been infected, says neurologist Avindra Nath of the National Institutes of Health in Bethesda, Md. “We are now faced with a public health crisis,” he says. Sign up for e-mail updates on the latest coronavirus news and research To figure out ways to treat people for the fuzzy thinking, headaches and fatigue that hang around after a bout with COVID-19, scientists are racing to figure out what’s causing these symptoms (SN: 4/27/21). Cognitive neurologist Joanna Hellmuth at the University of California, San Francisco had a head start. As someone who had studied the effects of HIV on the brain, she quickly noted similarities in the neurological symptoms of HIV and COVID-19. The infections paint “the same exact clinical picture,” she says. HIV-related cognitive symptoms have been linked to immune activation in the body, including the brain. “Maybe the same thing is happening in COVID,” Hellmuth says. © Society for Science & the Public 2000–2022.

Keyword: Neuroimmunology; Learning & Memory
Link ID: 28189 - Posted: 02.05.2022

Anastasia Brodovskaya Jaideep Kapur Epilepsy is a disease marked by recurrent seizures, or sudden periods of abnormal, excessive or synchronous neuronal activity in the brain. One in 26 people in the U.S. will develop epilepsy at some point in their life. While people with mild seizures might experience a brief loss of awareness and muscle twitches, more severe seizures could last for several minutes and lead to injury from falling down and losing control of their limbs. Many people with epilepsy also experience memory problems. Patients often experience retrograde amnesia, where they cannot remember what happened immediately before their seizure. Electroconvulsive therapy, a form of treatment for major depression that intentionally triggers small seizures, can also cause retrograde amnesia. So why do seizures often cause memory loss? We are neurology researchers who study the mechanisms behind how seizures affect the brain. Our brain-mapping study found that seizures affect the same circuits of the brain responsible for memory formation. Understand new developments in science, health and technology, each week One of the earliest descriptions of seizures was written on a Babylonian tablet over 3,000 years ago. Seizures can be caused by a number of factors, ranging from abnormalities in brain structure and genetic mutations to infections and autoimmune conditions. Often, the root cause of a seizure isn’t known. The most common type of epilepsy involves seizures that originate in the brain region located behind the ears, the temporal lobe. Some patients with temporal lobe epilepsy experience retrograde amnesia and are unable to recall events immediately before their seizure. © 2010–2022, The Conversation US, Inc.

Keyword: Epilepsy; Learning & Memory
Link ID: 28187 - Posted: 02.05.2022

by Holly Barker New software uses machine-learning to automatically detect and quantify gait and posture from videos of mice moving around their cage. The tool could accelerate research on how autism-linked mutations or drug treatments affect motor skills, says lead researcher Vivek Kumar, associate professor of mammalian genetics at The Jackson Laboratory in Bar Harbor, Maine. Most efforts to analyze motor behavior involve placing a mouse on a treadmill or training it to walk through a maze. These assays are a simple way of testing speed, but they restrict the animals’ movement and force mice to walk in an unnatural way. The algorithm processes footage from an overhead camera and tracks 12 key points on a mouse’s body as it freely explores its surroundings. As the animal wanders, the software detects the position of its limbs and other body parts, automatically generating data on its gait and posture. The researchers described their method in January in Cell Reports. Kumar’s group trained the software by feeding it about 8,000 video frames that had been manually annotated to tag key points on the animal’s body, such as the nose, ears and tip of the tail. They repeated the process with a variety of different strains to teach the algorithm to recognize mice of all shapes and sizes. The trained software learned to read the rodent’s pose, which was further analyzed to extract more detailed information, such as the speed and length of each stride and the width of the mouse’s stance. © 2022 Simons Foundation

Keyword: Autism; Movement Disorders
Link ID: 28186 - Posted: 02.05.2022