Chapter 13. Memory and Learning

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Heidi Ledford Severe COVID-19 is linked to changes in the brain that mirror those seen in old age, according to an analysis of dozens of post-mortem brain samples1. The analysis revealed brain changes in gene activity that were more extensive in people who had severe SARS-CoV-2 infections than in uninfected people who had been in an intensive care unit (ICU) or had been put on ventilators to assist their breathing — treatments used in many people with serious COVID-19. The study, published on 5 December in Nature Aging, joins a bevy of publications cataloguing the effects of COVID-19 on the brain. “It opens a plethora of questions that are important, not only for understanding the disease, but to prepare society for what the consequences of the pandemic might be,” says neuropathologist Marianna Bugiani at Amsterdam University Medical Centers. “And these consequences might not be clear for years.” Maria Mavrikaki, a neurobiologist at the Beth Israel Deaconess Medical Center in Boston, Massachusetts, embarked on the study about two years ago, after seeing a preprint, later published as a paper2, that described cognitive decline after COVID-19. She decided to follow up to see whether she could find changes in the brain that might trigger the effects. She and her colleagues studied samples taken from the frontal cortex — a region of the brain closely tied to cognition — of 21 people who had severe COVID-19 when they died and one person with an asymptomatic SARS-CoV-2 infection at death. The team compared these with samples from 22 people with no known history of SARS-CoV-2 infection. Another control group comprised nine people who had no known history of infection but had spent time on a ventilator or in an ICU — interventions that can cause serious side effects. The team found that genes associated with inflammation and stress were more active in the brains of people who had had severe COVID-19 than in the brains of people in the control group. Conversely, genes linked to cognition and the formation of connections between brain cells were less active. © 2022 Springer Nature Limited

Keyword: Development of the Brain; Brain imaging
Link ID: 28584 - Posted: 12.06.2022

Nicola Davis Science correspondent The brains of teenagers who lived through Covid lockdowns show signs of premature ageing, research suggests. The researchers compared MRI scans of 81 teens in the US taken before the pandemic, between November 2016 and November 2019, with those of 82 teens collected between October 2020 and March 2022, during the pandemic but after lockdowns were lifted. After matching 64 participants in each group for factors including age and sex, the team found that physical changes in the brain that occurred during adolescence – such as thinning of the cortex and growth of the hippocampus and the amygdala – were greater in the post-lockdown group than in the pre-pandemic group, suggesting such processes had sped up. In other words, their brains had aged faster. “Brain age difference was about three years – we hadn’t expected that large an increase given that the lockdown was less than a year [long],” said Ian Gotlib, a professor of psychology at Stanford University and first author of the study. Writing in the journal Biological Psychiatry: Global Open Science, the team report that the participants – a representative sample of adolescents in the Bay Area in California – originally agreed to take part in a study looking at the impact of early life stress on mental health across puberty. As a result, participants were also assessed for symptoms of depression and anxiety. The post-lockdown group self-reported greater mental health difficulties, including more severe symptoms of anxiety, depression and internalising problems. © 2022 Guardian News & Media

Keyword: Stress; Development of the Brain
Link ID: 28578 - Posted: 12.03.2022

By Gina Kolata In a bold attempt to stop the progress of some cases of Alzheimer’s disease, a group of researchers is trying something new — injecting a protective gene into patients’ brains. The trial involved just five patients with a particular genetic risk for Alzheimer’s. They received a very low dose of the gene therapy — a test of safety, which the treatment passed. But the preliminary results, announced Friday during the Clinical Trials on Alzheimer’s Disease conference, showed that proteins from the added gene appeared in the patients’ spinal fluid, and levels in the brain of two markers of Alzheimer’s disease, tau and amyloid, fell. Those findings were promising enough to advance the clinical trial into its next phase. Treatment of another five patients at a higher dose is underway, and the work, initially funded by the nonprofit Alzheimer’s Drug Discovery Foundation, is supported by Lexeo Therapeutics, a fledgling company founded by Dr. Ronald Crystal, who is also chairman of the department of genetic medicine at Weill Cornell Medicine in New York. The hope is to get a stronger response, eventually leading to a treatment that might slow the disease in whom it has started or, even better, protect people at high risk who have no symptoms. “It’s a very provocative, very intriguing approach,” said Dr. Eliezer Masliah, director of the neuroscience division at the National Institute on Aging. Participants in the study are among the approximately 2 percent of people who have inherited a pair of copies of a gene, APOE4, which markedly increases their risk of Alzheimer’s. For the study subjects, the first symptoms of Alzheimer’s had already emerged — their genetic risk had played out, and they had few options. There is no treatment that is directed specifically at APOE4-driven Alzheimer’s, nor is one on the near horizon. © 2022 The New York Times Company

Keyword: Alzheimers; Genes & Behavior
Link ID: 28575 - Posted: 12.03.2022

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 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 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 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

Linda Geddes Science correspondent Lead exposure during childhood may lead to reduced cognitive abilities in later life, meaning people experience symptoms of dementia sooner, data suggest. The study, one of the first to investigate the decades-long consequences of lead poisoning, suggests countries could face an explosion of people seeking support for dementia as individuals who were exposed to high lead levels during early life progress into old age. “In the US, and I would imagine the UK, the prime years when children were exposed to the most lead was in the 1960s and 70s. That’s when the most leaded gasoline was getting used, lead paint was still common, and municipal water systems hadn’t done much to clean up their lead,” said Prof John Robert Warren at the University of Minnesota in Minneapolis, who was involved in the research. “Those children who are now in their 40s, 50s and early 60s, will soon be entering the time of life when cognitive impairment and dementia are really common. So there’s this coming wave, potentially, of problems for the people who were most exposed.” Although scientists have long known that children and adults who are exposed to lead have poorer cognitive and educational outcomes, few studies have investigated the longer-term consequences. Warren and his colleagues combined data from the US-based longitudinal Health and Retirement Study (HRS), which has followed the brain health of thousands of adults over several decades, with census records to pinpoint where 1,089 of these individuals lived as children. They also mapped the locations of towns and cities that used lead pipes and had acidic or alkaline water – a proxy for high lead exposure. The research, published in Science Advances, revealed that people who lived in cities with lead-contaminated water as children had worse baseline cognitive functioning – a measure of their ability to learn, process information, and reason – at age 72, compared with those who did not. The difference was equivalent to being roughly eight years older. © 2022 Guardian News & Media Limited

Keyword: Neurotoxins; Alzheimers
Link ID: 28550 - Posted: 11.13.2022

Emma Marris For the first time, octopuses have been spotted throwing things — at each other1. Octopuses are known for their solitary nature, but in Jervis Bay, Australia, the gloomy octopus (Octopus tetricus) lives at very high densities. A team of cephalopod researchers decided to film the creatures with underwater cameras to see whether — and how — they interact. Once the researchers pulled the cameras out of the water, they sat down to watch more than 20 hours of footage. “I call it octopus TV,” laughs co-author David Scheel, a behavioural ecologist at Alaska Pacific University in Anchorage. One behaviour stood out: instances in which the eight-limbed creatures gathered shells, silt or algae with their arms — and then hurled them away, propelling them with water jetted from their siphon. And although some of the time it seemed that they were just throwing away debris or food leftovers, it did sometimes appear that they were throwing things at each other. The team found clues that the octopuses were deliberately targeting one another. Throws that made contact with another octopus were relatively strong and often occurred when the thrower was displaying a uniform dark or medium body colour. Another clue: sometimes the octopuses on the receiving end ducked. Throws that made octo-contact were also more likely to be accomplished with a specific set of arms, and the projectile was more likely to be silt. “We weren’t able to try and assess what the reasons might be,” Scheel cautions. But throwing, he says, “might help these animals deal with the fact that there are so many octopuses around”. In other words, it is probably social. © 2022 Springer Nature Limited

Keyword: Evolution; Learning & Memory
Link ID: 28549 - Posted: 11.13.2022

Laurel Wamsley Perhaps the real law of the jungle is that it's good to have friends — especially those who know where to find the the free food. Case in point: It turns out chimpanzees and gorillas can be pals, evidently with advantages for all. That finding is from a new paper in the journal iScience that analyzes social interactions between the primate species over two decades at the Nouabalé-Ndoki Park in the Republic of Congo. Over that 20-year period, researchers saw gorillas follow the sound of chimps to a canopy full of ripe figs, and then co-feed at the same tree. They witnessed young individuals of both species playing and wrestling with each other – interactions that can foster their development. And when bands of the two species encountered each other, researchers saw gorillas and chimps scan the others and then approach the ones they knew. They even saw chimpanzees beating their chests – a behavior associated with gorillas. Researchers had theorized that associations between the species could perhaps be to avoid predators such as leopards or snakes. But the apes' behavior didn't show that to be a major factor in their interactions. "Predation is certainly a threat in this region, as we have cases in which chimpanzees have been killed by leopards," Washington University primatologist Crickette Sanz, who led the research, said in a news release. "However, the number of chimpanzees in daily subgroups remains relatively small, and gorillas within groups venture far from the silverback who is thought to be a protector from predation." Instead, better foraging seemed to be a key upside for both species – sometimes eating at the same tree, sometimes dining nearby on different foods. Not every interaction was warm and friendly. "Interspecific aggression was bidirectional and most frequently consisted of threats," the study notes – but it never rose to the level of lethal aggression that has occurred between chimps and gorillas in Gabon. © 2022 npr

Keyword: Evolution; Learning & Memory
Link ID: 28548 - Posted: 11.13.2022

by David Dobbs For 40 years, Leo Kanner and Hans Asperger have dominated virtually every story about the ‘pioneers of autism research.’ These two men published in 1943 and 1944, respectively, what were long accepted as the first descriptions of, as Kanner’s seminal paper claimed, ”children whose condition differs … markedly and uniquely from anything reported so far.” Both papers are absorbing, touching and authoritative. Both describe young people whose challenges defied the known diagnoses of the time but clearly fall into what we now call autism. And both offered a new diagnostic category for such people. Kanner’s 1943 paper, ”Autistic Disturbances of Affective Contact,” drew almost immediate attention. Within a year, he renamed the condition these children shared, dubbing it ‘early infantile autism,’ which soon became known as ‘autism’ or ‘Kanner’s syndrome.’ His articulation of the condition, based on observations of 11 children he and his associates treated in his Baltimore, Maryland, clinic, remained the standard well into the 1980s and involved three elements: Autism was a condition marked by: (1) emergence early in childhood, (2) deficits in communication and social interaction, and (3) restricted or repetitive behaviors and a desire for sameness. Even today, these three elements anchor the official diagnostic criteria in the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders, as well as the widely used International Classification of Diseases and Related Health Problems. Asperger’s 1944 paper, which presented case studies on four children he and his colleagues had seen in his clinic in Vienna, Austria, made its impact far more slowly. In fact, because Asperger published in German (and in a German journal in the middle of a war that had essentially halted transatlantic scholarly exchange), the paper went largely unnoticed outside Europe for decades. Asperger’s descriptions resembled Kanner’s in many ways, although he outlined a wider apparent range of intelligence and capabilities than Kanner did, with some of his study participants reaching prominence in their fields. Asperger coined the diagnostic term ‘autistic psychopathy.’ © 2022 Simons Foundation

Keyword: Autism
Link ID: 28544 - Posted: 11.09.2022

Jon Hamilton An idea that has propelled Alzheimer's research for more than 30 years is approaching its day of reckoning. Scientists are launching a study designed to make or break the hypothesis that Alzheimer's is caused by a sticky substance called beta-amyloid. The study will give an experimental anti-amyloid drug to people as young as 18 who have gene mutations that often cause Alzheimer's to appear in their 30s or 40s. The study comes after several experimental drugs have failed to prevent declines in memory and thinking even though they succeeded in removing amyloid from the brains of patients in the early stages of Alzheimer's. Those failures have eroded support for the idea that amyloid is responsible for a cascade of events that eventually lead to the death of brain cells. "Many of us think of that as the ultimate test of the amyloid hypothesis," says Dr. Randall Bateman, a professor of neurology at Washington University School of Medicine in St. Louis."If that doesn't work, nothing will work." The new experiment, called the DIAN-TU primary Prevention Trial, is scheduled to begin enrolling patients by the end of the year. The amyloid hypothesis can be traced to Dr. Alois Alzheimer, a pathologist who first described the disease that would bear his name in 1906. Alzheimer was working at a psychiatric clinic in Munich, where he had the chance to conduct an autopsy on a woman who died at 50 after experiencing memory loss, disorientation, and hallucinations. He observed that the woman's brain had an "unusual disease of the cerebral cortex," including "senile plaque" usually seen in much older people. © 2022 npr

Keyword: Alzheimers
Link ID: 28534 - Posted: 11.02.2022

By Erika Check Hayden Weeks after Valeria Schenkel took an experimental drug named after her, the daily seizures that had afflicted her from birth became less frequent. But the drug caused fluid to build up in her brain, and a year later, she died at age 3. The drug was given to only one other child, and she experienced the same side effect and nearly died last year. The drug contained snippets of genetic material tailor-made to turn off the mutated gene causing the extremely rare form of epilepsy that these children were born with. A handful of researchers and nonprofit organizations have raised millions of dollars to make these treatments, known as antisense drugs, for at least 19 children and adults with severe diseases that are too rare to garner interest from pharmaceutical companies. The treatments have helped some of these patients, raising hopes that the personalized approach might one day save thousands of lives. But the brain side effect, known as hydrocephalus, reported on Sunday at the American Neurological Association meeting in Chicago, is a blow for the niche medical field that has made rapid progress over the past five years. Hydrocephalus happens when too much fluid fills cavities in the brain, increasing pressure on brain tissue and risking lethal damage if untreated. “I think it’s worth saying: No question that encountering hydrocephalus has been a setback, sobering and important,” said Dr. Timothy Yu, the neurologist and genetics researcher at Boston Children’s Hospital who developed the drug, known as valeriasen. But traditional drug companies, he added, are not helping patients with thousands of rare, untreatable and rapidly progressing diseases that cause death and severe disabilities. Personalized genetic treatments may be their only hope. “We have to learn as much as we can from each and every one, because they’re just so incredibly valuable in every sense,” Dr. Yu said. Scientists first imagined creating “antisense oligonucleotide” drugs — pieces of custom-made DNA or RNA designed to correct for genetic errors in cells — in the 1960s. But it took decades to make stable and effective versions of such drugs. © 2022 The New York Times Company

Keyword: Epilepsy; Development of the Brain
Link ID: 28529 - Posted: 10.28.2022

Nina Lakhani The mystery behind the astronomical rise in neurological disorders like Parkinson’s disease and Alzheimer’s could be caused by exposure to environmental toxins that are omnipresent yet poorly understood, leading doctors warn. At a conference on Sunday, the country’s leading neurologists and neuroscientists will highlight recent research efforts to fill the gaping scientific hole in understanding of the role environmental toxins – air pollution, pesticides, microplastics, forever chemicals and more – play in increasingly common diseases like dementias and childhood developmental disorders. Humans may encounter a staggering 80,000 or more toxic chemicals as they work, play, sleep and learn – so many that it is almost impossible to determine their individual effects on a person, let alone how they may interact or the cumulative impacts on the nervous system over a lifespan. Some contact with environmental toxins is inevitable given the proliferation of plastics and chemical pollutants, as well as America’s hands off regulatory approach, but exposure is unequal. In the US, communities of color, Indigenous people and low income families are far more likely to be exposed to a myriad of pollutants through unsafe housing and water, manufacturing and agricultural jobs, and proximity to roads and polluting industrial plants, among other hazards. It’s likely genetic makeup plays a role in how susceptible people are to the pathological effects of different chemicals, but research has shown higher rates of cancers and respiratory disease in environmentally burdened communities. © 2022 Guardian News & Media Limited

Keyword: Alzheimers; Parkinsons
Link ID: 28526 - Posted: 10.26.2022