By Kevin Hartnett A mouse is running on a treadmill embedded in a virtual reality corridor. In its mind’s eye, it sees itself scurrying down a tunnel with a distinctive pattern of lights ahead. Through training, the mouse has learned that if it stops at the lights and holds that position for 1.5 seconds, it will receive a reward — a small drink of water. Then it can rush to another set of lights to receive another reward. This setup is the basis for research published in July in Cell Reports by the neuroscientists Elie Adam, Taylor Johns and Mriganka Sur of the Massachusetts Institute of Technology. It explores a simple question: How does the brain — in mice, humans and other mammals — work quickly enough to stop us on a dime? The new work reveals that the brain is not wired to transmit a sharp “stop” command in the most direct or intuitive way. Instead, it employs a more complicated signaling system based on principles of calculus. This arrangement may sound overly complicated, but it’s a surprisingly clever way to control behaviors that need to be more precise than the commands from the brain can be. Control over the simple mechanics of walking or running is fairly easy to describe: The mesencephalic locomotor region (MLR) of the brain sends signals to neurons in the spinal cord, which send inhibitory or excitatory impulses to motor neurons governing muscles in the leg: Stop. Go. Stop. Go. Each signal is a spike of electrical activity generated by the sets of neurons firing. The story gets more complex, however, when goals are introduced, such as when a tennis player wants to run to an exact spot on the court or a thirsty mouse eyes a refreshing prize in the distance. Biologists have understood for a long time that goals take shape in the brain’s cerebral cortex. How does the brain translate a goal (stop running there so you get a reward) into a precisely timed signal that tells the MLR to hit the brakes? Simons Foundation, All Rights Reserved © 2022

Keyword: Movement Disorders
Link ID: 28573 - Posted: 11.30.2022

By Pam Belluck The hotly anticipated results of a clinical trial of an experimental Alzheimer’s drug suggest that the treatment slowed cognitive decline somewhat for people in the early stages of the disease but also caused some patients to experience brain swelling or brain bleeding. The new data, released Tuesday evening, offered the first detailed look at the effects of the drug, lecanemab, and comes two months after its manufacturers, Eisai and Biogen, stoked excitement by announcing that the drug had shown positive results. Alzheimer’s experts said the new information showed reason for both optimism and caution. “The benefit is real; so too are the risks,” said Dr. Jason Karlawish, a co-director of the University of Pennsylvania’s Penn Memory Center, who was not involved in the research. A report of the findings published in the New England Journal of Medicine said that over 18 months, lecanemab “resulted in moderately less decline on measures of cognition and function,” compared with patients receiving a placebo. Still, the study of nearly 1,800 patients with mild symptoms, which was funded by the companies and co-written by scientists at Eisai, concluded that “longer trials are warranted to determine the efficacy and safety of lecanemab in early Alzheimer’s disease.” The companies’ initial announcement in September had sent their stock prices soaring because the field of Alzheimer’s drug development has been marked by years of failures. © 2022 The New York Times Company

Keyword: Alzheimers
Link ID: 28572 - Posted: 11.30.2022

Cephalopods like octopuses, squids and cuttlefish are highly intelligent animals with complex nervous systems. In “Science Advances”, a team led by Nikolaus Rajewsky of the Max Delbrück Center has now shown that their evolution is linked to a dramatic expansion of their microRNA repertoire. If we go far enough back in evolutionary history, we encounter the last known common ancestor of humans and cephalopods: a primitive wormlike animal with minimal intelligence and simple eyespots. Later, the animal kingdom can be divided into two groups of organisms – those with backbones and those without. While vertebrates, particularly primates and other mammals, went on to develop large and complex brains with diverse cognitive abilities, invertebrates did not. With one exception: the cephalopods. Scientists have long wondered why such a complex nervous system was only able to develop in these mollusks. Now, an international team led by researchers from the Max Delbrück Center and Dartmouth College in the United States has put forth a possible reason. In a paper published in “Science Advances”, they explain that octopuses possess a massively expanded repertoire of microRNAs (miRNAs) in their neural tissue – reflecting similar developments that occurred in vertebrates. “So, this is what connects us to the octopus!” says Professor Nikolaus Rajewsky, Scientific Director of the Berlin Institute for Medical Systems Biology of the Max Delbrück Center (MDC-BIMSB), head of the Systems Biology of Gene Regulatory Elements Lab, and the paper’s last author. He explains that this finding probably means miRNAs play a fundamental role in the development of complex brains.

Keyword: Evolution; Epigenetics
Link ID: 28571 - Posted: 11.30.2022

By Sidney Perkowitz In 2019, Edward Chang, a neurosurgeon at the University of California, San Francisco, opened the skull of a 36-year-old man, nicknamed “Pancho,” and placed a thin sheet of electrodes on the surface of his brain.1 The electrodes gather electrical signals from the motor neurons that control the movement of the mouth, larynx, and other body parts to produce speech. A small port, implanted on top of Pancho’s head, relayed the brain signals to a computer. This “brain-computer interface,” or BCI, solved an intractable medical problem. In 2003, Pancho, a field worker in California’s vineyards, was involved in a car crash. Days after undergoing surgery, he suffered a brainstem stroke, reported the New York Times Magazine.2 The stroke robbed Poncho of the power of speech. He could communicate only by laboriously spelling out words one letter at a time with a pointing device. After training with the computer outfitted with deep-learning algorithms that interpreted his brain activity, Pancho could think the words that he wanted to say, and they would appear on the computer screen. Scientists called the results “groundbreaking”; Pancho called them “life-changing.” The clinical success of BCIs (there are other stories to go along with Pancho’s) appear to vindicate the futurists who claim that BCIs may soon enhance the brains of healthy people. Most famously, Ray Kurzweil, author of The Singularity Is Near, has asserted that exponentially rapid developments in neuroscience, bioscience, nanotechnology, and computation will coalesce and allow us to transcend the limitations of our bodies and brains. A major part of this huge shift will be the rise of artificial intelligences that are far more capable than human brains. It is an inevitability of human evolution, Kurzweil thinks, that the two kinds of intelligence will merge to form powerful hybrid brains, which will define the future of humanity. This, he predicted, would happen by 2045. While futuristic scenarios like Kurzweil’s are exciting to ponder, they are brought back down to Earth by the technological capabilities of brain-computer hybrids as they exist today. BCIs are impressive, but the path from helping stroke victims to giving people superpowers is neither direct nor inevitable. © 2022 NautilusThink Inc,

Keyword: Brain imaging; Robotics
Link ID: 28570 - Posted: 11.30.2022

By Gary Stix  Many people with bipolar disorder have a strong attraction to marijuana. A 2019 review of 53 studies found that almost a quarter of a combined sample of 51,756 individuals with the condition used cannabis or had a problematic pattern of consumption (cannabis use disorder), compared with 2 to 7 percent in the general population—and an earlier study placed usage estimates still higher. Cannabis and bipolar disorder do not go particularly well together. Consumption may increase manic and psychotic symptoms, and there may be a greater risk of suicide. But can the allure of cannabis be explained as a mere form of substance misuse? Why are people with bipolar disorder so attracted to marijuana? Could they be getting any possible benefit from it? Alannah Miranda of the University of California, San Diego, is a postdoctoral scholar working with U.C.S.D. psychiatry professors William Perry and Arpi Minassian to explore these questions. Miranda presented her and her colleagues’ unpublished work at this year’s giant Society for Neuroscience conference, which attracted more than 24,000 people earlier this month. She talked to Scientific American about what she discovered in this continuing study, which has been funded by the National Institute on Drug Abuse. [An edited transcript of the interview follows.] Tell me about what you’re studying. I’m researching the effects of cannabis on cognition in people with bipolar disorder. People with bipolar disorder report that it’s helping alleviate some of their symptoms in terms of issues related to memory, attention, focus and anxiety. © 2022 Scientific American,

Keyword: Schizophrenia; Drug Abuse
Link ID: 28569 - Posted: 11.30.2022

By Lisa Mulcahy If you’ve ever had your vision “white out” (or “gray out”), you’ve probably felt a little unnerved by the experience. “You’ll see a bright light, and your vision will go pale,” says Teri K. Geist, an optometrist and trustee of the American Optometry Association. As disconcerting as they are, vision whiteouts are usually benign. Making sure, though, means talking with a physician or optometrist. Before you do, here are some things to consider. If you have recurrent whiteouts, counting their duration in real time can help get you the correct diagnosis. Note any specific details the whiteouts appear to have in common. Do they happen right after you stand up from a chair, for example? Most often, whiteouts occur when a person is ready to pass out because of a sudden drop in blood pressure. About 1 in 3 people will faint at some point in their lives. “Fainting can be benign when it’s related to a sudden stress,” says Sarah Thornton, a neuro-ophthalmologist at Wills Eye Hospital in Philadelphia. “Standing up too fast, overexerting, becoming dehydrated or taking certain medications can also lead to hypotension — low blood pressure — and potentially, a whiteout.” A less common risk: “Whiteouts can occur with changes in G force,” says Geist, for instance, in a car accident or on a roller coaster. A whiteout caused by physical stress or exertion will clear within just a few minutes. Although fainting is usually benign, always tell your doctor if you’ve fainted — occasionally, whiteouts and fainting are tied to something serious. “An underlying heart condition, such as aortic stenosis, could cause fainting symptoms, including whiteout,” says Dean M. Cestari, a neuro-ophthalmologist at Mass General Brigham Mass Eye and Ear in Boston and associate professor of ophthalmology at Harvard Medical School. Other such conditions can include arrhythmias, heart failure and atrial fibrillation.

Keyword: Vision
Link ID: 28568 - Posted: 11.30.2022

By Sandra G. Boodman The first time it happened, Erin Bousquet was a high school freshman who had been diagnosed with strep throat, a common infection in her family. After three days on an antibiotic, she wasn’t getting better, so the 14-year-old was prescribed a second drug. A day or two later, Kristen Bousquet noticed worrisome changes in her oldest child. Erin seemed “lethargic and out of it,” her mother recalled. She was irritable, her pupils looked dilated, and much of what she said made no sense. Most alarming was Erin’s newfound ability to sleep for up to 20 hours at a time. “It was quite scary,” Kristen recalled. “At first we thought she was joking.” That bizarre episode, which occurred in September 2017, has been followed by 11 more, each lasting an average of 10 days. Between episodes, Erin’s behavior is normal. For 2 1/2 years she and her parents, who live in Lincoln, Neb., consulted pediatric neurologists, a neurosurgeon, an obstetrician-gynecologist and other specialists in a largely fruitless search to identify the condition that drastically alters her personality and temporarily shuts down her life two or three times a year. The diagnosis, made in March 2020, was an enormous relief. But it has required the Bousquets to cope with continued uncertainty because so little is known about Erin’s disorder. “The hardest thing for me are the things I’ve missed out on,” said Erin, a 19-year-old sophomore at the University of Nebraska at Lincoln. They include a high school basketball championship, her 18th birthday, a family Christmas trip to Colorado and the start of her sophomore year of college. Erin slept through them all. Because her symptoms — disorientation and prolonged sleep — can be signs of a serious, even life-threatening, illness, the staff at the urgent care clinic where Erin had been treated for strep told her mother to take her to an emergency room. A test for infectious mononucleosis, a contagious virus common among adolescents and young adults that causes profound fatigue was negative and a quick neurological exam was normal. Erin was sent home.

Keyword: Sleep
Link ID: 28567 - Posted: 11.23.2022

By Ingrid Wickelgren  Science has largely neglected pregnancy’s effect on the brain, even though it involves dramatic surges in steroid hormones, which are known to alter the organ. A decade ago neuroscientist Elseline Hoekzema, then a young postdoctoral fellow thinking about having her first child, and two of her female colleagues set out to bridge the knowledge gap. “There’s this enormous event involving such strong hormone changes,” says Hoekzema, now at Amsterdam University Medical Center. “It’s really weird that so little was known about this.” Their initial study, published in 2016, revealed for the first time that pregnancy produced significant structural changes in a woman’s brain that endured for at least two years after birth. Now in a new seven-year study, Hoekzema and her colleagues have seen the same structural changes in different women and have shown that pregnancy also alters the function of a key brain network involved in self-reflection. According to the work, which appeared on Nov. 22 in Nature Communications, the brain changes correlate with a mother’s enhanced bonding with her baby. The findings were derived from examining the female participants’ physiology and using questionnaires to assess their behavior and mental state. And for the first time in humans, the researchers found strong evidence that female hormones are behind it all. The biggest changes occur in a brain network that is active when the brain is idling—that is, when it is not engaged in any particular task—suggesting that pregnancy alters the organ’s baseline state. “[The researchers] are seeing these functional connectivity changes even at rest,” says Jodi Pawluski, a neuroscientist at the University of Rennes 1 in France, who studies the maternal brain and perinatal mental illness but was not involved in the study. “That speaks to the significance of this stage in a birthing person’s life and how it really is transformative in the brain.”

Keyword: Hormones & Behavior; Sexual Behavior
Link ID: 28566 - Posted: 11.23.2022

By Elizabeth Preston Ryan Grant was in his 20s and serving in the military when he learned that the numbness and tingling in his hands and feet, as well as his unshakeable fatigue, were symptoms of multiple sclerosis. Like nearly a million other people with MS in the United States, Grant had been feeling his immune system attack his central nervous system. The insulation around his nerves was crumbling, weakening the signals between his brain and body. The disease can have a wide range of symptoms and outcomes. Now 43, Grant has lost the ability to walk, and he has moved into a veterans’ home in Oregon, so that his wife and children don’t have to be his caretakers. He’s all too familiar with the course of the illness and can name risk factors he did and didn’t share with other MS patients, three-quarters of whom are female. But until recently, he hadn’t heard that many scientists now believe the most important factor behind MS is a virus.  For decades, researchers suspected that Epstein-Barr virus, a common childhood infection, is linked to multiple sclerosis. In January, the journal Science pushed that connection into headlines when it published the results of a two-decade study of people who, like Grant, have served in the military. The study’s researchers concluded that EBV infection is “the leading cause” of MS.  Bruce Bebo, executive vice president of research at the nonprofit National Multiple Sclerosis Society, which helped fund the study, said he believes the findings fall just short of proving causation. They do, however, provide “probably the strongest evidence to date of that link between EBV and MS,” he said. Epstein-Barr virus has infected about 95 percent of adults. Yet only a tiny fraction of them will develop multiple sclerosis. Other factors are also known to affect a person’s MS risk, including genetics, low vitamin D, smoking, and childhood obesity. If this virus that infects nearly everyone on Earth causes multiple sclerosis, it does so in concert with other actors in a choreography that scientists don’t yet understand.

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 28565 - Posted: 11.23.2022

By Virginia Hughes CRANSTON, R.I. — Audrey Pirri, 16, had been terrified of vomiting since she was a toddler. She worried every time she shared a meal with family or friends, restricting herself to “safe” foods like pretzels and salad that wouldn’t upset her stomach, if she ate at all. She was afraid to ride in the car with her brother, who often got carsick. She fretted for hours about an upcoming visit to a carnival or stadium — anywhere with lots of people and their germs. But on a Tuesday evening in August, in her first intensive session of a treatment called exposure therapy, Audrey was determined to confront one of the most potent triggers of her fear: a set of rainbow polka dot sheets. For eight years she had avoided touching the sheets, ever since the morning when she woke up with a stomach bug and vomited on them. Now, surrounded by her parents, a psychologist and a coach in her pale pink bedroom, she pulled the stiff linens from her dresser, gingerly slid them over the mattress and sat down on top. “You ready to repeat after me?” said Abbe Garcia, the psychologist. “I guess,” Audrey replied softly. “‘I am going to sleep on these sheets tonight,’” Dr. Garcia began. Audrey repeated the phrase. “‘And I might throw up,’” Dr. Garcia said. Audrey paused for several long seconds, her feet twitching and eyes welling with tears, as she imagined herself vomiting. She inhaled deeply and hurried out the words: “And I might throw up.” One in 11 American children has an anxiety disorder, and that figure has been growing steadily for the past two decades. The social isolation, family stress and relentless news of tragedy during the pandemic have only exacerbated the problem. But Audrey is one of the relatively few children to have tried exposure therapy. The decades-old treatment, which is considered a gold-standard approach for tackling anxiety, phobias and obsessive-compulsive disorder, encourages patients to intentionally face the objects or situations that cause them the most distress. A type of cognitive behavioral therapy, exposure often works within months and has minimal side effects. But financial barriers and a lack of providers have kept the treatment out of reach for many. © 2022 The New York Times Company

Keyword: Stress; Learning & Memory
Link ID: 28564 - Posted: 11.23.2022

By Diana Kwon Crows are some of the smartest creatures in the animal kingdom. They are capable of making rule-guided decisions and of creating and using tools. They also appear to show an innate sense of what numbers are. Researchers now report that these clever birds are able to understand recursion—the process of embedding structures in other, similar structures—which was long thought to be a uniquely human ability. Recursion is a key feature of language. It enables us to build elaborate sentences from simple ones. Take the sentence “The mouse the cat chased ran.” Here the clause “the cat chased” is enclosed within the clause “the mouse ran.” For decades, psychologists thought that recursion was a trait of humans alone. Some considered it the key feature that set human language apart from other forms of communication between animals. But questions about that assumption persisted. “There’s always been interest in whether or not nonhuman animals can also grasp recursive sequences,” says Diana Liao, a postdoctoral researcher at the lab of Andreas Nieder, a professor of animal physiology at the University of Tübingen in Germany. In a study of monkeys and human adults and children published in 2020, a group of researchers reported that the ability to produce recursive sequences may not actually be unique to our species after all. Both humans and monkeys were shown a display with two pairs of bracket symbols that appeared in a random order. The subjects were trained to touch them in the order of a “center-embedded” recursive sequence such as { ( ) } or ( { } ). After giving the right answer, humans received verbal feedback, and monkeys were given a small amount of food or juice as a reward. Afterward the researchers presented their subjects with a completely new set of brackets and observed how often they arranged them in a recursive manner. Two of the three monkeys in the experiment generated recursive sequences more often than nonrecursive sequences such as { ( } ), although they needed an additional training session to do so. One of the animals generated recursive sequences in around half of the trials. Three- to four-year-old children, by comparison, formed recursive sequences in approximately 40 percent of the trials. © 2022 Scientific American,

Keyword: Evolution; Learning & Memory
Link ID: 28563 - Posted: 11.23.2022

Ian Sample Science editor At the end of November, thousands of researchers from around the world will descend on San Francisco for the annual Clinical Trials on Alzheimer’s Disease meeting. The conference is a mainstay of the dementia research calendar, the place where the latest progress – and all too often, setbacks – in the quest for Alzheimer’s treatments are made public for the first time. This year’s meeting is poised to be a landmark event. After more than a century of research into Alzheimer’s, scientists expect to hear details of the first treatment that can unambiguously alter the course of the disease. Until now, nothing has reversed, halted or even slowed the grim deterioration of patients’ brains. Given that dementia and Alzheimer’s are the No 1 killer in the UK, and the seventh largest killer worldwide, there is talk of a historic moment. The optimism comes from a press statement released in September from Eisai, a Japanese pharmaceutical firm, and Biogen, a US biotech. It gave top-line results from a major clinical trial of an antibody treatment, lecanemab, given to nearly 2,000 people with early Alzheimer’s disease. The therapy slowed cognitive decline, the statement said, raising hopes that a drug might finally apply the brakes to Alzheimer’s and provide “a clinically meaningful impact on cognition and function”. The announcement was greeted, broadly, with delight and relief from researchers who have endured failure after failure in the long search for Alzheimer’s drugs. But even the most enthusiastic conceded that significant questions remained. With only a press release to go on, it was hard to be sure the claims stood up. The answer will come on 29 November when researchers leading the trial, named Clarity AD, present their results at the San Francisco meeting. © 2022 Guardian News & Media Limited

Keyword: Alzheimers
Link ID: 28562 - Posted: 11.23.2022

By Ken Belson SHICKLEY, Neb. — Chris Eitzmann seemed to excel at everything until he didn’t. He parlayed a Harvard football captaincy into an invite in 2000 to Patriots training camp. After bouncing around the N.F.L., Eitzmann retired from pro football in 2002, got an M.B.A. from Dartmouth and worked at several big financial firms in Boston, where he and his wife, Mikaela, had four children. By 2015, however, Chris began a descent that has become familiar to former football players afflicted with C.T.E., or chronic traumatic encephalopathy, the degenerative brain disease associated with repeated blows to the head. Chris had loved mountain biking, running and lifting weights, but he quit exercising and drank to excess. After a move to Mikaela’s family farm back in their home state of Nebraska two years later, Chris’s behavior became more alarming. He would disappear for long stretches of the day and neglect his work. His drinking got worse, and she said he would sometimes drive drunk. In December 2021, Chris Eitzmann was found dead in his Boston apartment of alcohol poisoning at 44. Almost a year later, doctors at Boston University found that he had C.T.E., a disease that can still only be diagnosed posthumously. Mikaela said that knowing whether her husband had the disease while he was alive would have markedly changed the final years of his life. “If he had known that it really was something, and not just this endless vacuum of not knowing, if he had an idea that he could have grabbed on to, that clarity and understanding would have been so valuable,” she said. Without treatment options, a C.T.E. diagnosis could provide only clarity for former players such as Eitzmann who have reason to believe they may be affected. But it could eventually help current players make risk assessments about when to give up tackle football and help former players seek treatment. © 2022 The New York Times Company

Keyword: Brain Injury/Concussion
Link ID: 28561 - Posted: 11.19.2022

By Laurie McGinley Few illnesses instill as much fear as Alzheimer’s, a fatal neurodegenerative disease that destroys memory and identity. The dread is compounded by the uncertainty that often surrounds the diagnosis of the most common form of dementia. Brain autopsies remain the only way to know for sure whether someone had the disease, which the Centers for Disease Control and Prevention estimates affects 6.5 million people in the United States. Over the past several years, sophisticated tests such as spinal taps and specialized PET scans have become available — but they are invasive and costly and not routinely used. As a result, Alzheimer’s is frequently misdiagnosed, especially in the early stages. Other illnesses, including depression, can have similar symptoms and require other treatments. But simple blood tests designed to help doctors diagnose Alzheimer’s now are on the market. More are on the way. The tests are seen as an important scientific advance, but have ignited debate about how and when they should be used. Some experts say much more research is needed before the new tests can be widely deployed, especially in primary-care settings. Others say there already is sufficient information on the accuracy of some tests. All agree that no single test is perfect and physicians still should perform a complete clinical assessment. Widespread use of the tests may be some time off in the future — after insurance coverage improves and even more accurate next-generation tests become available. For now, none is covered by Medicare, and private insurance coverage is patchy. In the past few years, scientific and technological advances have made it possible to detect in the blood tiny fragments of brain proteins implicated in Alzheimer’s. That has prompted experts in academia and industry to develop blood tests for the disease. Some of the tests detect a sticky protein called amyloid beta, while others look for another protein called tau. Some search for both or other markers of disease. The abnormal accretions of amyloid plaques and tau tangles are the defining characteristics of Alzheimer’s. washingtonpost.com © 1996-2022

Keyword: Alzheimers
Link ID: 28560 - Posted: 11.19.2022

Researchers at the National Institutes of Health have successfully identified differences in gene activity in the brains of people with attention deficit hyperactivity disorder (ADHD). The study, led by scientists at the National Human Genome Research Institute (NHGRI), part of NIH, found that individuals diagnosed with ADHD had differences in genes that code for known chemicals that brain cells use to communicate. The results of the findings, published in Molecular Psychiatry(link is external), show how genomic differences might contribute to symptoms. To date, this is the first study to use postmortem human brain tissue to investigate ADHD. Other approaches to studying mental health conditions include non-invasively scanning the brain, which allows researchers to examine the structure and activation of brain areas. However, these studies lack information at the level of genes and how they might influence cell function and give rise to symptoms. The researchers used a genomic technique called RNA sequencing to probe how specific genes are turned on or off, also known as gene expression. They studied two connected brain regions associated with ADHD: the caudate and the frontal cortex. These regions are known to be critical in controlling a person’s attention. Previous research found differences in the structure and activity of these brain regions in individuals with ADHD. As one of the most common mental health conditions, ADHD affects about 1 in 10 children in the United States. Diagnosis often occurs during childhood, and symptoms may persist into adulthood. Individuals with ADHD may be hyperactive and have difficulty concentrating and controlling impulses, which may affect their ability to complete daily tasks and their ability to focus at school or work. With technological advances, researchers have been able to identify genes associated with ADHD, but they had not been able to determine how genomic differences in these genes act in the brain to contribute to symptoms until now.

Keyword: ADHD; Genes & Behavior
Link ID: 28559 - Posted: 11.19.2022

By Elie Dolgin, No gene variant is a bigger risk factor for Alzheimer’s disease than one called APOE4. But exactly how the gene spurs brain damage has been a mystery. A study has now linked APOE4 with faulty cholesterol processing in the brain, which in turn leads to defects in the insulating sheaths that surround nerve fibres and facilitate their electrical activity. Preliminary results hint that these changes could cause memory and learning deficits. And the work suggests that drugs that restore the brain’s cholesterol processing could treat the disease. “This fits in with the picture that cholesterol needs to be in the right place,” says Gregory Thatcher, a chemical biologist at the University of Arizona in Tucson. Inheriting a single copy of APOE4 raises the risk of developing Alzheimer’s around 3-fold; having two copies boosts the chances 8- to 12-fold. Interactions between the protein encoded by APOE4 and sticky plaques of amyloid—a substance tied to brain cell death—in the brain partially explain the connection. But those interactions are not the whole story. As neuroscientist Li-Huei Tsai at the Massachusetts Institute of Technology (MIT) in Cambridge and her colleagues report today in Nature, APOE4 triggers insulation-making brain cells known as oligodendrocytes to accumulate the fatty molecule cholesterol—a type of lipid—in all the wrong places. This interferes with the cells’ ability to cover nerve fibres in a protective wrapper made of a lipid-rich material called myelin. Electrical signalling in the brain then slows, and cognition usually suffers. Tsai’s team had previously linked lipid changes to malfunctions in other cell types, including some that offer structural support to neurons and others that provide immune protection for the brain. The latest findings add oligodendrocytes and their essential myelin function to the mix. © 2022 Scientific American

Keyword: Alzheimers; Genes & Behavior
Link ID: 28558 - Posted: 11.19.2022

By Joanna Thompson Two recent papers have shown that during a critical early period of brain development, the gut’s microbiome — the assortment of bacteria that grow within in it — helps to mold a brain system that’s important for social skills later in life. Scientists found this influence in fish, but molecular and neurological evidence plausibly suggests that some form of it could also occur in mammals, including humans. In a paper published in early November in PLOS Biology, researchers found that zebra fish who grew up lacking a gut microbiome were far less social than their peers with colonized colons, and the structure of their brains reflected the difference. In a related article in BMC Genomics in late September, they described molecular characteristics of the neurons affected by the gut bacteria. Equivalents of those neurons appear in rodents, and scientists can now look for them in other species, including humans. In recent decades, scientists have come to understand that the gut and the brain have powerful mutual influences. Certain types of intestinal ulcers, for example, have been linked to worsening symptoms in people with Parkinson’s disease. And clinicians have long known that gastrointestinal disorders are more common in people who also have neurodevelopmental disorders, such as ADHD and autism spectrum disorder. “Not only does the brain have an impact on the gut, but the gut can also profoundly affect the brain,” said Kara Margolis, a pediatric gastroenterologist at New York University’s Langone Health, who was not involved in the new research. How these anatomically separate organs exert their effects, however, is far less clear. Philip Washbourne, a molecular biologist at the University of Oregon and one of the principal co-authors of the new studies, has been studying genes implicated in autism and the development of social behaviors for over two decades. But he and his lab were looking for a new model organism, one that displayed social behavior but was quicker and easier to breed than their go-to, mice. “Can we do this in fish?” he recalls thinking, and then: “Let’s get really quantitative about it and see if we can measure how friendly the fish get.” All Rights Reserved © 2022

Keyword: Sexual Behavior; Obesity
Link ID: 28557 - Posted: 11.16.2022

By Laura Sanders SAN DIEGO — Scientists have devised ways to “read” words directly from brains. Brain implants can translate internal speech into external signals, permitting communication from people with paralysis or other diseases that steal their ability to talk or type. New results from two studies, presented November 13 at the annual meeting of the Society for Neuroscience, “provide additional evidence of the extraordinary potential” that brain implants have for restoring lost communication, says neuroscientist and neurocritical care physician Leigh Hochberg. Some people who need help communicating can currently use devices that require small movements, such as eye gaze changes. Those tasks aren’t possible for everyone. So the new studies targeted internal speech, which requires a person to do nothing more than think. “Our device predicts internal speech directly, allowing the patient to just focus on saying a word inside their head and transform it into text,” says Sarah Wandelt, a neuroscientist at Caltech. Internal speech “could be much simpler and more intuitive than requiring the patient to spell out words or mouth them.” Neural signals associated with words are detected by electrodes implanted in the brain. The signals can then be translated into text, which can be made audible by computer programs that generate speech. That approach is “really exciting, and reinforces the power of bringing together fundamental neuroscience, neuroengineering and machine learning approaches for the restoration of communication and mobility,” says Hochberg, of Massachusetts General Hospital and Harvard Medical School in Boston, and Brown University in Providence, R.I. © Society for Science & the Public 2000–2022.

Keyword: Brain imaging; Language
Link ID: 28556 - Posted: 11.16.2022

By Megan Twohey and Christina Jewett The medical guidance was direct. Eleven-year-old Emma Basques had identified as a girl since toddlerhood. Now, as she worried about male puberty starting, a Phoenix pediatrician advised: Take a drug to stop it. At 13, Jacy Chavira felt increasingly uncomfortable with her maturing body and was beginning to believe she was a boy. Use the drug, her endocrinologist in Southern California recommended, and puberty would be suspended. An 11-year-old in New York with deepening depression expressed a desire to no longer be a girl. A therapist told the family the drug was the preteen’s best option, and a local doctor agreed. “‘Puberty blockers really help kids like this,’” the child’s mother recalled the therapist saying. “It was presented as a tourniquet that would stop the hemorrhaging.” As the number of adolescents who identify as transgender grows, drugs known as puberty blockers have become the first line of intervention for the youngest ones seeking medical treatment. Their use is typically framed as a safe — and reversible — way to buy time to weigh a medical transition and avoid the anguish of growing into a body that feels wrong. Transgender adolescents suffer from disproportionately high rates of depression and other mental health issues. Studies show that the drugs have eased some patients’ gender dysphoria — a distress over the mismatch of their birth sex and gender identity. “Anxiety drains away,” said Dr. Norman Spack, who pioneered the use of puberty blockers for trans youth in the United States and is one of many physicians who believe the drugs can be lifesaving. “You can see these kids being so relieved.” But as an increasing number of adolescents identify as transgender — in the United States, an estimated 300,000 ages 13 to 17 and an untold number who are younger — concerns are growing among some medical professionals about the consequences of the drugs, a New York Times examination found. The questions are fueling government reviews in Europe, prompting a push for more research and leading some prominent specialists to reconsider at what age to prescribe them and for how long. A small number of doctors won’t recommend them at all. © 2022 The New York Times Company

Keyword: Sexual Behavior; Hormones & Behavior
Link ID: 28555 - Posted: 11.16.2022

By Laurie McGinley An experimental Alzheimer’s drug designed to slow cognitive decline failed to meet the goals of two closely watched clinical trials, a discouraging development that underscores the challenges of developing treatments for the memory-robbing disease. Genentech, a division of health-care giant Roche, said in a news release Monday that the treatment, called gantenerumab, slowed the pace of decline in patients with early-stage disease but not enough to be statistically significant. The therapy was tested in identical late-stage trials, each with 1,000 participants. Half received placebos and half got the treatment. The studies lasted 27 months. The drug, a monoclonal antibody, is designed to remove from the brain clumps of an abnormal version of a protein called amyloid beta, a hallmark of the disease. The company said Monday that the treatment removed less amyloid beta than expected. Some scientists have thought for years that amyloid-busting medicines could slow the fatal neurodegenerative disease, but there have been multiple failures, and just a few encouraging signs, involving amyloid-busting drugs. “So many of our families have been directly affected by Alzheimer’s, so this news is very disappointing to deliver,” Levi Garraway, Roche’s chief medical officer and head of global product development, said in a statement. He said the company looks forward to sharing more information about the results “as we continue to search for new treatments for this complex disease.” Genentech said that 25 percent of the patients who received gantenerumab experienced a side effect that can cause brain swelling and bleeding but that most did not have symptoms and few needed to stop taking the drug. The company said it planned to present more data from the trials at an Alzheimer’s conference this month. The company assessed the drug by measuring trial participants’ performance on an 18-point measure of memory and cognition, called the Clinical Dementia Rating scale — Sum of Boxes. The news on gantenerumab is a disappointment for patients, physicians and researchers desperate for effective treatments for a disease that affects 6.5 million Americans.

Keyword: Alzheimers
Link ID: 28554 - Posted: 11.16.2022