Chapter 7. Life-Span Development of the Brain and Behavior

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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

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

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

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

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

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 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

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

Keyword: Alzheimers; Neuroimmunology
Link ID: 28184 - Posted: 02.02.2022

by Laura Dattaro Early in her first postdoctoral position, Hollis Cline first showed her hallmark flair for creative problem-solving. Cline, who goes by Holly, and her adviser, neuroscientist Martha Constantine-Paton, wanted to study the brain’s ‘topographical maps’ — internal representations of sensory input from the external world. These maps are thought to shape a person’s ability to process sensory information — filtering that can go awry in autism and other neurodevelopmental conditions. No one knew just how these maps formed or what could potentially disrupt them. Cline and Constantine-Paton, who was then at Yale University and is now emerita professor of brain and cognitive sciences at the Massachusetts Institute of Technology, weren’t sure how to find out. But as a first step, the pair decided to take the plunge with an unusual animal model: the frog — specifically, a spotted greenish-brown species called Rana pipiens, or the northern leopard frog. The amphibians spend two to three months as tadpoles, a span during which their brains change rapidly and visibly — unlike in mammals, which undergo similar stages of development inside of the mother’s body. These traits made it possible for Cline and Constantine-Paton to introduce changes and repeatedly watch their effects in real time. “That’s an extended period when you can actually have access to the developing brain,” Cline says. The unorthodox approach paid off. Cline, 66, now professor of neuroscience at the Scripps Research Institute in La Jolla, California, worked out that a receptor for the neurotransmitter glutamate, which had been shown to be important for learning and memory, also mediated how visual experiences influence the developing topographical map. She later created a novel live imaging technique to visualize frog neurons’ development over time and, sticking with frogs over the ensuing decades, went on to make fundamental discoveries about how sensory experiences shape brain development and sensory processing. © 2022 Simons Foundation

Keyword: Development of the Brain; Autism
Link ID: 28179 - Posted: 02.02.2022

By Meeri Kim Kellie Carr and her 13-year-old son, Daniel, sat in the waiting room of a pediatric neurology clinic for yet another doctor’s appointment in 2012. For years, she struggled to find out what was causing his weakened right side. It wasn’t an obvious deficit, by any means, and anyone not paying close attention would see a normal, healthy teenage boy. At that point, no one had any idea that Daniel had suffered a massive stroke as a newborn and lost large parts of his brain as a result. “It was the largest stroke I’d ever seen in a child who hadn’t died or suffered extreme physical and mental disability,” said Nico Dosenbach, the pediatric neurologist at Washington University School of Medicine in St. Louis who finally diagnosed him using a magnetic resonance imaging (MRI) scan. "If I saw the MRI first, I would have assumed this kid's probably in a wheelchair, has a feeding tube and might be on a ventilator," Dosenbach said. "Because normally, when a child is missing that much brain, it's bad." But Daniel — as an active, athletic young man who did fine in school — defied all logic. Before the discovery of the stroke, his mother had noticed some odd mannerisms, such as zipping up his coat or eating a burger using only his left hand. When engaged, his right hand often served as club-like support instead of a dexterous appendage with fingers. Daniel excelled as a left-handed pitcher in competitive baseball, but his coach found it unusual that he would always switch the glove to his left hand when catching the ball. Medical professionals tried to help — first his pediatrician, followed by an orthopedic doctor who sent him to physical therapy — but no one could figure out the root cause. They tried constraint-induced movement therapy, which forces patients to use the weaker arm by immobilizing the other in a cast, but Daniel soon rebelled and broke himself free. © 1996-2022 The Washington Post

Keyword: Development of the Brain; Stroke
Link ID: 28174 - Posted: 01.26.2022

By Jason DeParle WASHINGTON — A study that provided poor mothers with cash stipends for the first year of their children’s lives appears to have changed the babies’ brain activity in ways associated with stronger cognitive development, a finding with potential implications for safety net policy. The differences were modest — researchers likened them in statistical magnitude to moving to the 75th position in a line of 100 from the 81st — and it remains to be seen if changes in brain patterns will translate to higher skills, as other research offers reason to expect. Still, evidence that a single year of subsidies could alter something as profound as brain functioning highlights the role that money may play in child development and comes as President Biden is pushing for a much larger program of subsidies for families with children. “This is a big scientific finding,” said Martha J. Farah, a neuroscientist at the University of Pennsylvania, who conducted a review of the study for the Proceedings of the National Academy of Sciences, where it was published on Monday. “It’s proof that just giving the families more money, even a modest amount of more money, leads to better brain development.” Another researcher, Charles A. Nelson III of Harvard, reacted more cautiously, noting the full effect of the payments — $333 a month — would not be clear until the children took cognitive tests. While the brain patterns documented in the study are often associated with higher cognitive skills, he said, that is not always the case. © 2022 The New York Times Company

Keyword: Development of the Brain; Learning & Memory
Link ID: 28172 - Posted: 01.26.2022