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By Gretchen Reynolds When we start to lift weights, our muscles do not strengthen and change at first, but our nervous systems do, according to a fascinating new study in animals of the cellular effects of resistance training. The study, which involved monkeys performing the equivalent of multiple one-armed pull-ups, suggests that strength training is more physiologically intricate than most of us might have imagined and that our conception of what constitutes strength might be too narrow. Those of us who join a gym — or, because of the current pandemic restrictions and concerns, take up body-weight training at home — may feel some initial disappointment when our muscles do not rapidly bulge with added bulk. In fact, certain people, including some women and most preadolescent children, add little obvious muscle mass, no matter how long they lift. But almost everyone who starts weight training soon becomes able to generate more muscular force, meaning they can push, pull and raise more weight than before, even though their muscles may not look any larger and stronger. Scientists have known for some time that these early increases in strength must involve changes in the connections between the brain and muscles. The process appears to involve particular bundles of neurons and nerve fibers that carry commands from the brain’s motor cortex, which controls muscular contractions, to the spinal cord and, from there, to the muscles. If those commands become swifter and more forceful, the muscles on the receiving end should respond with mightier contractions. Functionally, they would be stronger. © 2020 The New York Times Company

Keyword: Movement Disorders; Learning & Memory
Link ID: 27343 - Posted: 07.02.2020

Jason Bruck Human actions have taken a steep toll on whales and dolphins. Some studies estimate that small whale abundance, which includes dolphins, has fallen 87% since 1980 and thousands of whales die from rope entanglement annually. But humans also cause less obvious harm. Researchers have found changes in the stress levels, reproductive health and respiratory health of these animals, but this valuable data is extremely hard to collect. To better understand how people influence the overall health of dolphins, my colleagues and I at Oklahoma State University’s Unmanned Systems Research Institute are developing a drone to collect samples from the spray that comes from their blowholes. Using these samples, we will learn more about these animals’ health, which can aid in their conservation. Today, researchers wanting to measure wild dolphins’ health primarily use remote biopsy darting – where researchers use a small dart to collect a sample of tissue – or handle the animals in order to collect samples. These methods don’t physically harm the animals, but despite precautions, they can be disruptive and stressful for dolphins. Additionally, this process is challenging, time-consuming and expensive. My current research focus is on dolphin perception – how they see, hear and sense the world. Using my experience, I am part of a team building a drone specifically designed to be an improvement over current sampling methods, both for dolphins and the researchers. Our goal is to develop a quiet drone that can fly into a dolphin’s blind spot and collect samples from the mucus that is mixed with water and air sprayed out of a dolphin’s blowhole when they exhale a breath. This is called the blow. Dolphins would experience less stress and teams could collect more samples at less expense. © 2010–2020, The Conversation US, Inc.

Keyword: Learning & Memory; Evolution
Link ID: 27342 - Posted: 07.02.2020

By Lisa Sanders, M.D. The early-morning light wakened the middle-aged man early on a Saturday morning in 2003. He felt his 51-year-old wife move behind him and turned to see her whole body jerking erratically. He was a physician, a psychiatrist, and knew immediately that she was having a seizure. He grabbed his phone and dialed 911. His healthy, active wife had never had a seizure before. But this was only the most recent strange episode his wife had been through over the past 18 months. A year and a half earlier, the man returned to his suburban Pittsburgh home after a day of seeing patients and found his wife sitting in the kitchen, her hair soaking wet. He asked if she had just taken a shower. No, she answered vaguely, without offering anything more. Before he could ask her why she was so sweaty, their teenage son voiced his own observations. Earlier that day, the boy reported, “She wasn’t making any sense.” That wasn’t like her. Weeks later, his daughter reported that when she arrived home from school, she heard a banging sound in a room in the attic. She found her mother under a futon bed, trying to sit up and hitting her head on the wooden slats underneath. Her mother said she was looking for something, but she was obviously confused. The daughter helped her mother up and brought her some juice, which seemed to help. With both episodes, the children reported that their mother didn’t seem upset or distressed. The woman, who had trained as a psychiatrist before giving up her practice to stay with the kids, had no recollection of these odd events. The Problem Is Sugar Her husband persuaded her to see her primary-care doctor. Upon hearing about these strange spells, the physician said she suspected that her patient was having episodes of hypoglycemia. Very low blood sugar sends the body into a panicked mode of profuse sweating, shaking, weakness and, in severe cases, confusion. She referred her to a local endocrinologist. © 2020 The New York Times Company

Keyword: Epilepsy
Link ID: 27341 - Posted: 07.02.2020

By Veronique Greenwood Planarians have unusual talents, to say the least. If you slice one of the tiny flatworms in half, the halves will grow back, giving you two identical worms. Cut a flatworm’s head in two, and it will grow two heads. Cut an eye off a flatworm — it will grow back. Stick an eye on a flatworm that lacks eyes — it’ll take root. Pieces as small as one-279th of a flatworm will turn into new, whole flatworms, given the time. This process of regeneration has fascinated scientists for more than 200 years, prompting myriad zany, if somewhat macabre, experiments to understand how it is possible for a complex organism to rebuild itself from scratch, over and over and over again. In a paper published Friday in Science, researchers revealed a tantalizing glimpse into how the worms’ nervous systems manage this feat. Specialized cells, the scientists report, point the way for neurons stretching from newly grown eyes to the brain of the worm, helping them connect correctly. The research suggests that cellular guides hidden throughout the planarian body may make it possible for the worm’s newly grown neurons to retrace their steps. Gathering these and other insights from the study of flatworms may someday help scientists interested in helping humans regenerate injured neurons. María Lucila Scimone, a researcher at M.I.T.’s Whitehead Institute for Biomedical Research, first noticed these cells while studying Schmidtea mediterranea, a planarian common to bodies of freshwater in Southern Europe and North Africa. During another experiment, she noted that they were expressing a gene involved in regeneration. The team looked more closely and realized that some of the regeneration-related cells were positioned at key branching points in the network of nerves between the worms’ eyes and their brains. When the researchers transplanted an eye from one animal to another, the neurons growing from the new eye always grew toward these cells. When the nerve cells reached their target, they kept growing along the route that would take them to the brain. Removing those cells meant the neurons got lost and did not reach the brain. © 2020 The New York Times Company

Keyword: Development of the Brain; Regeneration
Link ID: 27340 - Posted: 07.01.2020

By Arianne Cohen1 minute Read You know all those studies about brain activity? The ones that reveal thought patterns and feelings as a person performs a task? There’s a problem: The measurement they’re based on is inaccurate, according to a study out of Duke University that is rocking the field. Functional MRI machines (fMRIs) are excellent at determining the brain structures involved in a task. For example, a study asking 50 people to count or remember names while undergoing an fMRI scan would accurately identify which parts of the brain are active during the task. Brain scans showing functional MRI mapping for three tasks across two different days. Warm colors show the high consistency of activation levels across a group of people. Cool colors represent how poorly unique patterns of activity can be reliably measured in individuals. View image larger here. [Image: Annchen Knodt/Duke University] The trouble is that when the same person is asked to do the same tasks weeks or months apart, the results vary wildly. This is likely because fMRIs don’t actually measure brain activity directly: They measure blood flow to regions of the brain, which is used as a proxy for brain activity because neurons in those regions are presumably more active. Blood flow levels, apparently, change. “The correlation between one scan and a second is not even fair, it’s poor,” says lead author Ahmad Hariri, a professor of neuroscience and psychology at Duke University. The researchers reexamined 56 peer-reviewed, published papers that conducted 90 fMRI experiments, some by leaders in the field, and also looked at the results of so-called “test/retest” fMRIs, where 65 subjects were asked to do the same tasks months apart. They found that of seven measures of brain function, none had consistent readings.

Keyword: Brain imaging
Link ID: 27339 - Posted: 07.01.2020

By Courtney Linder Perception is certainly not always reality. Some people might think this image is a rabbit, for example, while others see it as a raven: But what if your brain just stopped recognizing numbers one day? That's precisely the basis for a recent Johns Hopkins University study about a man with a rare brain anomaly that prevents him from seeing certain numbers. Instead, the man told doctors, he sees squiggles that look like spaghetti, like in this video: And it's not just a matter of perception for him—not an optical illusion, nor something a Rorschach test could psychoanalyze away. It's actually proof that our brains can processes the world around us, and yet we could have no awareness of those sights. "We present neurophysiological evidence of complex cognitive processing in the absence of awareness, raising questions about the conditions necessary for visual awareness," the scientists note in a new paper published in the journal Proceedings of the National Academy of Sciences. RFS—the name researchers use to refer to the man in the study—has been diagnosed with a rare degenerative brain disease that has led to extensive atrophy in his cortex and basal ganglia. Atrophy is basically a loss of neurons and connective tissue, so you can think of it as the brain shrinking, in a sense. The cortex is the gray matter in your brain that controls things like attention, perception, awareness, and consciousness, while the basal ganglia are responsible for motor learning, executive functions, and emotional behaviors. ©2020 Hearst Magazine Media, Inc.

Keyword: Attention; Vision
Link ID: 27338 - Posted: 07.01.2020

The Human Brain Project (HBP) has announced the start of its final phase as an EU-funded FET Flagship. The European Commission has signed a grant agreement to fund the HBP with 150 million Euros from now until 2023. Over the next three years, the project will narrow its focus to advance three core scientific areas – brain networks, their role in consciousness, and artificial neural nets – while expanding its innovative EBRAINS infrastructure. EBRAINS offers the most comprehensive atlas and database on the human brain, directly coupled with powerful computing and simulation tools, to research communities around neuroscience, medicine and technology. Currently transitioning into a sustainable infrastructure, EBRAINS will remain available to the scientific community, as a lasting contribution of the HBP to global scientific progress. Supercomputers, Big Data Analytics, Simulation, Robots and AI have all become new additions to the “toolbox” of modern neuroscience – a development strongly pushed forward by the HBP and its EBRAINS infrastructure. Started in 2013 as a FET Flagship project, the HBP is the largest brain science project in Europe. Now entering the final phase of its ten-year lifespan, the project is proud to present its scientific workplan and transformative technological offerings for brain research and brain-inspired research and development. HBP’s scientific activities in the new phase focus on three topics: networks that are studied across different spatial and temporal scales, their significance for consciousness and disorders of consciousness, and the development of artificial neural networks and neurorobotics.

Keyword: Brain imaging
Link ID: 27337 - Posted: 07.01.2020

By Pam Belluck Kim Victory was paralyzed on a bed and being burned alive. Just in time, someone rescued her, but suddenly, she was turned into an ice sculpture on a fancy cruise ship buffet. Next, she was a subject of an experiment in a lab in Japan. Then she was being attacked by cats. Nightmarish visions like these plagued Ms. Victory during her hospitalization this spring for severe respiratory failure caused by the coronavirus. They made her so agitated that one night, she pulled out her ventilator breathing tube; another time, she fell off a chair and landed on the floor of the intensive care unit. “It was so real, and I was so scared,” said Ms. Victory, 31, now back home in Franklin, Tenn. To a startling degree, many coronavirus patients are reporting similar experiences. Called hospital delirium, the phenomenon has previously been seen mostly in a subset of older patients, some of whom already had dementia, and in recent years, hospitals adopted measures to reduce it. “All of that has been erased by Covid,” said Dr. E. Wesley Ely, co-director of the Critical Illness, Brain Dysfunction and Survivorship Center at Vanderbilt University and the Nashville Veteran’s Administration Hospital, whose team developed guidelines for hospitals to minimize delirium. Now, the condition is bedeviling coronavirus patients of all ages with no previous cognitive impairment. Reports from hospitals and researchers suggest that about two-thirds to three-quarters of coronavirus patients in I.C.U.’s have experienced it in various ways. Some have “hyperactive delirium,” paranoid hallucinations and agitation; some have “hypoactive delirium,” internalized visions and confusion that cause patients to become withdrawn and incommunicative; and some have both. © 2020 The New York Times Company

Keyword: Schizophrenia
Link ID: 27336 - Posted: 06.29.2020

By Melinda Wenner Moyer For three months, Chelsea Alionar has struggled with fevers, headaches, dizziness and a brain fog so intense it feels like early dementia. She came down with the worst headache of her life on March 9, then lost her sense of taste and smell. She eventually tested positive for the coronavirus. But her symptoms have been stranger, and lasted longer, than most. “I tell the same stories repeatedly; I forget words I know,” she told me. Her fingers and toes have been numb, her vision blurry and her fatigue severe. The 37-year-old is a one of the more than 4,000 members of a Facebook support group for Covid survivors who have been ill for more than 80 days. The more we learn about the coronavirus, the more we realize it’s not just a respiratory infection. The virus can ravage many of the body’s major organ systems, including the brain and central nervous system. Among patients hospitalized for Covid-19 in Wuhan, China, more than a third experienced nervous system symptoms, including seizures and impaired consciousness. Earlier this month, French researchers reported that 84 percent of Covid patients who had been admitted to the I.C.U. experienced neurological problems, and that 33 percent continued to act confused and disoriented when they were discharged. According to Dr. Mady Hornig, a psychiatrist and epidemiologist at the Columbia University Mailman School of Public Health, the possibility that neurological issues “will persist and create disability, or difficulties, for individuals downstream is really looking more and more likely.” Infections have long been implicated in neurological diseases. Syphilis and H.I.V. can induce dementia. Zika is known to invade developing brains and limit their growth, while untreated Lyme disease can cause nerve pain, facial palsy and spinal cord inflammation. One man with SARS developed delirium that progressed into coma, and was found to have the virus in his brain tissue after his death. © 2020 The New York Times Company

Keyword: Alzheimers; Learning & Memory
Link ID: 27335 - Posted: 06.29.2020

By William Schwalbe More than three years ago, I came down with a mysterious illness I thought might be a flu, but turned out to be something entirely different. My blizzard of symptoms began innocuously in November 2016 with terribly cold feet. So cold that even when I got under the covers with a hot water bottle between them, and they were warm to the touch, they still felt like painful ice-blocks. At other times, I had the equally unpleasant sensation that my feet and shins were burning or already burnt. A few weeks later, I started to experience intense throbbing pain in all my toes, as if someone had seconds before stomped on them with heavy boots, which made walking or standing difficult. Often my legs were so heavy that I could barely move them. Occasionally, my feet turned bright red. And every few hours came shooting pains, electric shocks that traveled up my legs. In my 55 years on earth, I’d never felt pain like that — except when a dentist drilled without Novocain. All the symptoms increased at night, so sleep became elusive. I wound up sticking my feet outside the covers because even a sheet brushing against them proved too painful to bear. Before long, the same panoply of pains had moved to my hands and then arms — and occasionally my face and stomach. Heat made the symptoms worse; cold and damp made them much worse. But often these pains flared for no discernible reason. Totally unrelated, or so I thought, were other things that began to go wrong with me over the next few months: I often found myself pouring with sweat from my forehead, but became unable to sweat on my legs and arms; I lost all the hair on my lower legs; I was increasingly faint and dizzy, with my heart racing whenever I changed position or had a shower; and I was experiencing a fatigue and bone-pain so profound that every few hours I needed to stop whatever I was doing and lie down on the floor. © 1996-2020 The Washington Post

Keyword: Pain & Touch
Link ID: 27334 - Posted: 06.29.2020

By Richard Sandomir Dr. William Dement, whose introduction to the mysteries of slumber as a postgraduate student in the 1950s led him to become an eminent researcher of sleep disorders and to preach the benefits of a good night’s sleep, died on June 17 in Stanford, Calif. He was 91. His son, Nick, a physician, said the cause was complications of a heart procedure. Dr. Dement spent his working life as a popular professor in the department of psychiatry at Stanford University, where he started what is believed to be the world’s first successful sleep disorders clinic. He taught a class on sleep and dreams that drew as many as 1,200 students. When he awakened dozing students with spritzes from a water gun, Dr. Dement gave them extra credit if they recovered and shouted, “Drowsiness is red alert!” — his rallying cry to make sleep deprivation a public health priority. Drowsiness was the last step before falling asleep, he often said. Sleep deprivation put people at a higher risk of an accident on the road, diminished their productivity, increased the likelihood of their making mistakes, made them irritable and actually hurt their ability to fall asleep. “Bill Dement was an evangelist about sleep,” Dr. Rafael Pelayo, a Stanford psychiatry professor who succeeded Dr. Dement in leading the sleep class, said in a phone interview. “He felt that not enough people knew about sleep disorders, and he thought of his students as multipliers who would tell the world about them.” Dr. Dement’s expertise led to his appointment as chairman of a federal commission on sleep disorders. The commission reported in 1992 that 40 million Americans had undiagnosed, untreated, mistreated or chronic sleep problems — findings that led Congress to establish the National Center on Sleep Disorders Research, within the National Institutes of Health, in 1993. When Dr. Dement testified on Capitol Hill five years later about the sleep center’s progress, he said he was pleased with its research but disappointed that the government had not sounded loud enough alarms about the serious, sometimes fatal, consequences of unhealthful sleep. © 2020 The New York Times Company

Keyword: Sleep
Link ID: 27333 - Posted: 06.29.2020

By Bruce Bower An aptitude for mentally stringing together related items, often cited as a hallmark of human language, may have deep roots in primate evolution, a new study suggests. In lab experiments, monkeys demonstrated an ability akin to embedding phrases within other phrases, scientists report June 26 in Science Advances. Many linguists regard this skill, known as recursion, as fundamental to grammar (SN: 12/4/05) and thus peculiar to people. But “this work shows that the capacity to represent recursive sequences is present in an animal that will never learn language,” says Stephen Ferrigno, a Harvard University psychologist. Recursion allows one to elaborate a sentence such as “This pandemic is awful” into “This pandemic, which has put so many people out of work, is awful, not to mention a health risk.” Ferrigno and colleagues tested recursion in both monkeys and humans. Ten U.S. adults recognized recursive symbol sequences on a nonverbal task and quickly applied that knowledge to novel sequences of items. To a lesser but still substantial extent, so did 50 U.S. preschoolers and 37 adult Tsimane’ villagers from Bolivia, who had no schooling in math or reading. Those results imply that an ability to grasp recursion must emerge early in life and doesn’t require formal education. Three rhesus monkeys lacked humans’ ease on the task. But after receiving extra training, two of those monkeys displayed recursive learning, Ferrigno’s group says. One of the two animals ended up, on average, more likely to form novel recursive sequences than about three-quarters of the preschoolers and roughly half of the Bolivian villagers. © Society for Science & the Public 2000–2020.

Keyword: Language; Evolution
Link ID: 27332 - Posted: 06.27.2020

Jon Hamilton A research effort based at the Allen Institute in Seattle, Wash., will tap leading scientists from several institutions to dive even deeper into brain genetics and physiology. The aim: Find clues to the earliest beginnings of Alzheimer's. Allen Institute Three research institutions in Seattle have joined forces to study how Alzheimer's disease takes root in the brain. The consortium will create a new research center at the Allen Institute for Brain Science to study tissue from brains donated by people who died with Alzheimer's. UW Medicine and the Kaiser Permanente Washington Health Research Group are also part of the effort, which will be funded by a five-year $40.5 million grant from the National Institute on Aging, a part of the National Institutes of Health. The project, with its emphasis on basic research, represents part of a global do-over for the Alzheimer's field, which has weathered a series of failed attempts to develop a drug that could slow or stop the disease. "The premise of this project here is that we need to take a step back," says Ed Lein, a senior scientist at the Allen Institute and the center's lead investigator. That's a marked change from a decade ago, when there was great excitement about experimental drugs that could scrub away the sticky brain plaques thought to cause Alzheimer's. Studies have shown that the drugs do their job, removing a toxic protein called amyloid-beta from the brain. But they don't help patients avoid memory loss or cognitive problems. © 2020 npr

Keyword: Alzheimers
Link ID: 27331 - Posted: 06.27.2020

By Laura Sanders COVID-19 cases described by U.K. doctors offer a sharper view of the illness’s possible effects on the brain. Strokes, confusion and psychosis were found among a group of 125 people hospitalized with infections of SARS-CoV-2, the coronavirus behind the pandemic. The results, described June 25 in Lancet Psychiatry, come from a group of severely sick people, so they can’t answer how common these types of neurological symptoms may be in a more general population. Still, these details bring scientists closer to better understanding COVID-19. Brain-related symptoms of COVID-19 patients can slip through the cracks. “These relatively rare but incredibly severe complications get missed, like needles in a haystack,” says Benedict Michael, a neurologist at the University of Liverpool in England. So he and his colleagues designed a survey to uncover these symptoms. Sign up for e-mail updates on the latest coronavirus news and research In April, neurologists, stroke physicians, psychiatrists and other doctors across the United Kingdom entered COVID-19 patient details to a centralized database as part of the survey. Targeting these scientific specialties meant that the patients included were likely to have brain-related symptoms. Of the 125 patients described fully, 77 experienced an interruption of blood flow in the brain, most often caused by a blood clot in the brain. Blood clots are a well-known and pernicious COVID-19 complication (SN: 6/23/20), and strokes have been seen in younger people with COVID-19. About a third of the 125 patients had a shift in mental state, including confusion, personality change or depression. Eighteen of 37 patients with altered mental states were younger than 60. So far, it’s unclear exactly how SARS-CoV-2 causes these symptoms. © Society for Science & the Public 2000–2020.

Keyword: Stroke
Link ID: 27330 - Posted: 06.27.2020

By Abigail Zuger, M.D. Do I dare to eat a Cheeto? I do not; I can’t even let one into the house. The same goes for its delectably plump twin, the Cheez Doodle; its tasty rotund cousin, the Cheez Ball; and its heavenly brother by another mother, that sandwich of two Cheezy crackers glued together with peanut butter. I dare not even walk down the supermarket aisle where this neon orange family lives, for while others may succumb to chocolate or pastry, my Waterloo is this cheesy goodness — let’s call it Cheez. One Cheez Doodle would lead to a bag, then to more bags, and then to the certain catastrophe of a larger, sicker me. I know these delicacies are terrible for a person’s health. How exactly do I know that? It’s not because I’m a medical professional, that’s for sure; there were zero discussions of Cheez in our pre- or post-graduate training. I know because I just know, is all. Overprocessed chemical-laden stuff is bad for you; it’s pure malevolent junk. Everyone knows that. George Zaidan, an MIT-trained chemist of contrarian bent, knows it too. That is, he knows it to be piously reiterated received wisdom, and thus legitimate fodder for dissection, examination, refutation, and cheerfully self-indulgent obscenity-laden riffs. Further, he has chosen this junk food truth as an excellent starting point for “Ingredients: The Strange Chemistry of What We Put in Us and On Us,” an entertaining and enlightening jaunt around the perimeters of exactly what we can ever hope science can teach us about stuff that is good and bad for us. And it all begins with a single Cheeto, the putative first brick on the winding golden road to nutritional hell.

Keyword: Obesity
Link ID: 27329 - Posted: 06.27.2020

By Jack J. Lee For some bottlenose dolphins, finding a meal may be about who you know. Dolphins often learn how to hunt from their mothers. But when it comes to at least one foraging trick, Indo-Pacific bottlenose dolphins in Western Australia’s Shark Bay pick up the behavior from their peers, researchers argue in a report published online June 25 in Current Biology. While previous studies have suggested that dolphins learn from peers, this study is the first to quantify the importance of social networks over other factors, says Sonja Wild, a behavioral ecologist at the University of Konstanz in Germany. Cetaceans — dolphins, whales and porpoises — are known for using clever strategies to round up meals. Humpback whales (Megaptera novaeangliae) off Alaska sometimes use their fins and circular bubble nets to catch fish (SN: 10/15/19). At Shark Bay, Indo-Pacific bottlenose dolphins (Tursiops aduncus) use sea sponges to protect their beaks while rooting for food on the seafloor, a strategy the animals learn from their mothers (SN: 6/8/05). These Shark Bay dolphins also use a more unusual tool-based foraging method called shelling. A dolphin will trap underwater prey in a large sea snail shell, poke its beak into the shell’s opening, lift the shell above the water’s surface and shake the contents into its mouth. © Society for Science & the Public 2000–2020.

Keyword: Learning & Memory; Evolution
Link ID: 27328 - Posted: 06.26.2020

Hemant Khanna In recent months, even as our attention has been focused on the coronavirus outbreak, there have been a slew of scientific breakthroughs in treating diseases that cause blindness. Researchers at U.S.-based Editas Medicine and Ireland-based Allergan have administered CRISPR for the first time to a person with a genetic disease. This landmark treatment uses the CRISPR approach to a specific mutation in a gene linked to childhood blindness. The mutation affects the functioning of the light-sensing compartment of the eye, called the retina, and leads to loss of the light-sensing cells. According to the World Health Organization, at least 2.2 billion people in the world have some form of visual impairment. In the United States, approximately 200,000 people suffer from inherited forms of retinal disease for which there is no cure. But things have started to change for good. We can now see light at the end of the tunnel. I am an ophthalmology and visual sciences researcher, and am particularly interested in these advances because my laboratory is focusing on designing new and improved gene therapy approaches to treat inherited forms of blindness. The eye as a testing ground for CRISPR Gene therapy involves inserting the correct copy of a gene into cells that have a mistake in the genetic sequence of that gene, recovering the normal function of the protein in the cell. The eye is an ideal organ for testing new therapeutic approaches, including CRISPR. That is because the eye is the most exposed part of our brain and thus is easily accessible. © 2010–2020, The Conversation US, Inc.

Keyword: Vision
Link ID: 27327 - Posted: 06.26.2020

Nicola Davis People living with inflammatory bowel disease (IBD) have more than twice the risk of developing dementia, researchers have revealed in the latest study to link gut health to neurological diseases. A growing body of research suggests changes in the gastrointestinal tract may affect the brain through two-way communication known as the gut-brain axis. Scientists have previously found signs that the abnormally folded proteins involved in Parkinson’s disease may arise in the gut and travel to the brain via the vagus nerve, while changes to the microbial community in the gut – the gut microbiome – have been linked with conditions ranging from mental health problems to motor neurone disease and Parkinson’s disease. In addition, previous work has shown people with IBD have a higher risk of Parkinson’s disease. Researchers now say they have found that people with IBD – inflammatory conditions including ulcerative colitis and Crohn’s disease, which have symptoms including stomach pain and bloody stools – have a greater chance of developing dementia than those without, and tend to be diagnosed with dementia several years earlier. “The findings suggest that there may be a connection between IBD and neurocognitive decline,” said Dr Bing Zhang, first author of the research from the University of California San Francisco. While the study does not prove IBD causes dementia, Zhang and his colleagues outlined a number of ways the two may be linked, noting chronic inflammation has been suggested to trigger processes involved in Alzheimer’s disease, and blood clots and stroke – features involved in vascular dementia. © 2020 Guardian News & Media Limited or its affiliated companies.

Keyword: Alzheimers; Neuroimmunology
Link ID: 27326 - Posted: 06.26.2020

by Peter Hess / Inherited mutations in a gene called ACTL6B lead to autism, epilepsy and intellectual disability, according to a new study1. The mutations are recessive, which means that they lead to autism only if a person inherits them in both copies of the gene — one from each parent, who are silent carriers. Most other mutations implicated in autism are spontaneous, or ‘de novo,’ mutations, which are not inherited. The study suggests that recessive mutations in ACTL6B could be a relatively common cause of autism, says co-lead researcher Joseph Gleeson, professor of neurosciences and pediatrics at the University of California, San Diego. ACTL6B helps to control the expression of other genes in brain cells by encoding part of a protein complex called BAF. This complex tightens and loosens chromatin, the bundle of DNA and protein crammed inside a cell’s nucleus, during transcription. Scientists have linked autism to mutations in many other chromatin regulation genes — including several that encode other parts of the BAF complex. ACTL6B mutations have previously been associated with neurodevelopmental conditions, but the new study makes a strong case that they are tied to autism, says Gaia Novarino, professor of neuroscience at the Institute of Science and Technology in Klosterneuburg, Austria, who was not involved in the study. The work also provides a comprehensive look at how mutations in ACTL6B affect the brains of people, mice and flies, and suggests that the gene plays a common role across species. © 2020 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 27325 - Posted: 06.26.2020

Ruth Williams Turning off just one factor in the brain’s astrocyte cells is sufficient to convert them into neurons in live mice, according to a paper published in Nature today (June 24) and one this spring by another research team in Cell. By flipping this cellular identity switch, researchers have, to some extent, been able to reverse the neuron loss and motor deficits caused by a Parkinson’s-like illness. Not everyone is entirely convinced by the claims. “I think this is very exciting work,” says Pennsylvania State University’s Gong Chen of the Nature paper. It reaffirms that “using the brain’s internal glial cells to regenerate new neurons is a really new avenue for the treatment of brain disorders,” he continues. Chen, who is also based at Jinan University and is the chief scientific officer for NeuExcell—a company developing astrocyte-to-neuron conversion therapies—has performed such conversions in the living mouse brain by a different method but was not involved in the new study. In Parkinson’s disease, dopaminergic neurons within the brain’s substantia nigra—a region in the midbrain involved in movement and reward—gradually die. This results in a deterioration of motor control, characterized by tremors and other types of dyskinesia, with other faculties such as cognition and mood sometimes affected too, especially at later stages of the disease. While treatments to boost diminishing dopamine levels, such as the drug levodopa, can ameliorate symptoms, none can stop the underlying disease process that relentlessly eats away at the patient’s neurological functions and quality of life. © 1986–2020 The Scientist.

Keyword: Parkinsons; Glia
Link ID: 27324 - Posted: 06.26.2020