Chapter 13. Memory, Learning, and Development

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by Laura Dattaro Correcting a mutation in the autism gene SHANK3 in fetal mice lessens some autism-like behaviors after birth, according to a new study1. The work adds to evidence that gene therapy may help some people with SHANK3 mutations. In people, mutations in SHANK3 can lead to Phelan-McDermid syndrome, a condition that causes developmental delays and often autism. Up to 2 percent of people with autism have a mutation in SHANK32. “Our findings imply that early genetic correction of SHANK3 has the potential to provide therapeutic benefit for patients,” lead investigator Craig Powell, professor of neurobiology at the University of Alabama at Birmingham, wrote in an email. A 2016 study showed that correcting mutations in SHANK3 in both young and adult mice can decrease excessive grooming, which is thought to correspond to repetitive behaviors in people with autism. Last year, Powell and his team also showed that correcting SHANK3 mutations in adult mice eliminates some autism-like behaviors3. But the results were difficult to interpret. The team reversed the mutation using an enzyme called Cre-recombinase that could edit SHANK3 if the animals were given a drug called tamoxifen. Control mice in that study that did not receive tamoxifen but had the gene for Cre still showed behavior changes, raising the possibility that the enzyme affected their brains. © 2020 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 27270 - Posted: 05.29.2020

Diana Kwon What if you could boost your brain’s processing capabilities simply by sticking electrodes onto your head and flipping a switch? Berkeley, California–based neurotechnology company Humm has developed a device that it claims serves that purpose. Their “bioelectric memory patch” is designed to enhance working memory—the type of short-term memory required to temporarily hold and process information—by noninvasively stimulating the brain. In recent years, neurotechnology companies have unveiled direct-to-consumer (DTC) brain stimulation devices that promise a range of benefits, including enhancing athletic performance, increasing concentration, and reducing depression. Humm’s memory patch, which resembles a large, rectangular Band-Aid, is one such product. Users can stick the device to their forehead and toggle a switch to activate it. Electrodes within the patch generate transcranial alternating current stimulation (tACS), a method of noninvasively zapping the brain with oscillating waves of electricity. The company recommends 15 minutes of stimulation to give users up to “90 minutes of boosted learning” immediately after using the device. The product is set for public release in 2021. Over the last year or so, Humm has generated much excitement among investors, consumers, and some members of the scientific community. In addition to raising several million dollars in venture capital funding, the company has drawn interest both from academic research labs and from the United States military. According to Humm cofounder and CEO Iain McIntyre, the US Air Force has ordered approximately 1,000 patches to use in a study at their training academy that is set to start later this year. © 1986–2020 The Scientist

Keyword: Learning & Memory
Link ID: 27269 - Posted: 05.29.2020

A team of researchers has generated a developmental map of a key sound-sensing structure in the mouse inner ear. Scientists at the National Institute on Deafness and Other Communication Disorders (NIDCD), part of the National Institutes of Health, and their collaborators analyzed data from 30,000 cells from mouse cochlea, the snail-shaped structure of the inner ear. The results provide insights into the genetic programs that drive the formation of cells important for detecting sounds. The study also sheds light specifically on the underlying cause of hearing loss linked to Ehlers-Danlos syndrome and Loeys-Dietz syndrome. The study data is shared on a unique platform open to any researcher, creating an unprecedented resource that could catalyze future research on hearing loss. Led by Matthew W. Kelley, Ph.D., chief of the Section on Developmental Neuroscience at the NIDCD, the study appeared online in Nature Communications(link is external). The research team includes investigators at the University of Maryland School of Medicine, Baltimore; Decibel Therapeutics, Boston; and King’s College London. “Unlike many other types of cells in the body, the sensory cells that enable us to hear do not have the capacity to regenerate when they become damaged or diseased,” said NIDCD Director Debara L. Tucci, M.D., who is also an otolaryngology-head and neck surgeon. “By clarifying our understanding of how these cells are formed in the developing inner ear, this work is an important asset for scientists working on stem cell-based therapeutics that may treat or reverse some forms of inner ear hearing loss.”

Keyword: Hearing; Development of the Brain
Link ID: 27268 - Posted: 05.29.2020

Jef Akst The APOE ε4 gene variant that puts people at a greater risk of developing Alzheimer’s disease also has a link to COVID-19. According to a study published today (May 26) in The Journals of Gerontology, Series A, carrying two copies of the variant, often called APOE4, makes people twice as likely to develop a severe form of the disease, which is caused by the SARS-CoV-2 coronavirus currently spreading around the world. David Melzer of Exeter University and colleagues used genetic and health data on volunteers in the UK Biobank to look at the role of the APOE4 variant, which affects cholesterol transport and inflammation. Of some 383,000 people of European descent included in the study, more than 9,000 carried two copies. The researchers cross-referenced this list with people who tested positive for COVID-19 between March 16 and April 26—the assumption being that most such cases were severe because testing at the time was largely limited to hospital settings. The analysis suggested that the APOE4 homozygous genotype was linked to a doubled risk of severe disease, compared with people who had two copies of another variant called ε3. The result isn’t due to nursing home settings or to a greater likelihood of having a diagnosis of dementia, which none of the 37 people with two copies of APOE4 who tested positive for COVID-19 had. “It is pretty bulletproof—whatever associated disease we remove, the association is still there,” Melzer tells The Guardian. “So it looks as if it is the gene variant that is doing it.” © 1986–2020 The Scientist.

Keyword: Alzheimers; Genes & Behavior
Link ID: 27267 - Posted: 05.29.2020

R. Douglas Fields Discoveries that transcend boundaries are among the greatest delights of scientific research, but such leaps are often overlooked because they outstrip conventional thinking. Take, for example, a new discovery for treating dementia that defies received wisdom by combining two formerly unrelated areas of research: brain waves and the brain’s immune cells, called microglia. It’s an important finding, but it still requires the buy-in and understanding of researchers to achieve its true potential. The history of brain waves shows why. In 1887, Richard Caton announced his discovery of brain waves at a scientific meeting. “Read my paper on the electrical currents of the brain,” he wrote in his personal diary. “It was well received but not understood by most of the audience.” Even though Caton’s observations of brain waves were correct, his thinking was too unorthodox for others to take seriously. Faced with such a lack of interest, he abandoned his research and the discovery was forgotten for decades. Flash forward to October 2019. At a gathering of scientists that I helped organize at the annual meeting of the Society for Neuroscience in Chicago, I asked if anyone knew of recent research by neuroscientists at the Massachusetts Institute of Technology who had found a new way to treat Alzheimer’s disease by manipulating microglia and brain waves. No one replied. I understood: Scientists must specialize to succeed. Biologists studying microglia don’t tend to read papers about brain waves, and brain wave researchers are generally unaware of glial research. A study that bridges these two traditionally separate disciplines may fail to gain traction. But this study needed attention: Incredible as it may sound, the researchers improved the brains of animals with Alzheimer’s simply by using LED lights that flashed 40 times a second. Even sound played at this charmed frequency, 40 hertz, had a similar effect. All Rights Reserved © 2020

Keyword: Alzheimers; Glia
Link ID: 27264 - Posted: 05.28.2020

Peter Hess The relative contributions of genetic and environmental factors to autism and traits of the condition have held steady over multiple decades, according to a large twin study. Among tens of thousands of Swedish twins born over the span of 26 years, genetic factors have consistently had a larger impact on the occurrence of autism and autism traits than environmental factors have. The study suggests that genetics account for about 93 percent of the chance that a person has autism, and 61–73 percent of the odds she shows autism traits. The figures fall in line with previous work that shows genetics exert an outsized influence on autism odds. The findings also indicate that environmental factors are unlikely to explain the rise in autism prevalence. Otherwise, their contribution to autism among the twins would have also risen over time. “I think the relative consistency of the genetic and environmental factors underlying autism and autism traits is the most important aspect of this work,” says Mark Taylor, senior research specialist at the Karolinska Institutet in Stockholm, Sweden, who led the study. “Prior to our study, there had been no twin studies examining whether the genetic and environmental factors underlying autism had changed over time.” Family factors: The researchers analyzed data from two sources: 22,678 pairs of twins in the Swedish Twin Registry, who were born from 1982 to 2008; and 15,280 pairs of twins from the Child and Adolescent Twin Study in Sweden, born from 1992 to 2008. © 1986–2020 The Scientist.

Keyword: Autism; Genes & Behavior
Link ID: 27262 - Posted: 05.28.2020

by Peter Hess The relative contributions of genetic and environmental factors to autism and traits of the condition have held steady over multiple decades, according to a large twin study 1. Among tens of thousands of Swedish twins born over the span of 26 years, genetic factors have consistently had a larger impact on the occurrence of autism and autism traits than environmental factors have. The study suggests that genetics account for about 93 percent of the chance that a person has autism, and 61 to 73 percent of the odds she shows autism traits. The figures fall in line with previous work that shows genetics exert an outsized influence on autism odds. The findings also indicate that environmental factors are unlikely to explain the rise in autism prevalence. Otherwise, their contribution to autism among the twins would have also risen over time. “I think the relative consistency of the genetic and environmental factors underlying autism and autism traits is the most important aspect of this work,” says Mark Taylor, senior research specialist at the Karolinska Institutet in Stockholm, Sweden, who led the study. “Prior to our study, there had been no twin studies examining whether the genetic and environmental factors underlying autism had changed over time.” The researchers analyzed data from two sources: 22,678 pairs of twins in the Swedish Twin Registry, who were born from 1982 to 2008; and 15,280 pairs of twins from the Child and Adolescent Twin Study in Sweden, born from 1992 to 2008. © 2020 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 27256 - Posted: 05.20.2020

By Nicholas Bakalar Eating foods high in flavonoids — a group of nutrients found in many fruits and vegetables — may lower your risk for dementia, researchers report. The study, in the American Journal of Clinical Nutrition, looked at 2,801 men and women who were 50 and older and free of dementia at the start. Over an average of 20 years of follow-up, researchers gathered diet information at five periodic health examinations; during that time, 193 of the participants developed Alzheimer’s disease or other forms of dementia. Compared with those in the 15th percentile or lower for flavonoid intake, those in the 60th or higher had a 42 to 68 percent lower risk for dementia, depending on the type of flavonoid consumed. Intake of one type of flavonoid, anthocyanins, abundant in blueberries, strawberries and red wine, had the strongest association with lowered risk. Apples, pears, oranges, bananas and tea also contributed. The study controlled for many health and behavioral characteristics, including how strongly participants adhered to the government’s Dietary Guidelines for Americans, which in addition to fruits and vegetables emphasize whole grains, lean meats and other heart-healthy foods. The senior author, Paul F. Jacques, a scientist with the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, said that the amount consumed by those who benefited the most was not large. Their monthly average was about seven half-cup servings of strawberries or blueberries, eight apples or pears, and 17 cups of tea. “It doesn’t take much,” he said. “A couple of servings of berries a week, maybe an apple or two.” © 2020 The New York Times Company

Keyword: Alzheimers
Link ID: 27255 - Posted: 05.20.2020

Alejandra Manjarrez The brain is a master of forming patterns, even when it involves events occurring at different times. Take the phenomenon of trace fear conditioning—scientists can get an animal to notice the relationship between a neutral stimulus and an aversive stimulus separated by a temporal chasm (the trace) of a few or even tens of seconds. While it’s a well-established protocol in neuroscience and psychology labs, the mechanism for how the brain bridges the time gap between two related stimuli in order to associate them is “one of the most enigmatic and highly investigated” questions, says Columbia University neuroscientist Attila Losonczy. If the first stimulus is finished, the information about its presence and identity “should be somehow maintained through some neuronal mechanism,” he explains, so it can be associated with the second stimulus coming later. Losonczy and his colleagues have recently investigated how this might occur in a study published May 8 in Neuron. They measured the neural activity in the hippocampal CA1 region of the brain—known to be crucial for the formation of memories—of mice exposed to trace fear conditioning. The team found that associating the two events separated by time involved the activation of a subset of neurons that fired sparsely every time mice received the first stimulus and during the time gap that followed. The pattern emerged only after mice had learned to associate both stimuli. The study highlights “the important question of how we link memories across time,” says Denise Cai, a neuroscientist at the Icahn School of Medicine at Mount Sinai who was not involved in the work. Studying the basic mechanisms of temporal association is critical for understanding how it goes wrong in disorders such as post-traumatic stress disorder (PTSD) or Alzheimer’s disease, she says. © 1986–2020 The Scientist

Keyword: Learning & Memory; Stress
Link ID: 27254 - Posted: 05.18.2020

Sukanya Charuchandra Even for Darold Treffert, an expert in the study of savants who has met around 300 people with conditions such as autism who possess extraordinary mental abilities, Kim Peek stood out from the pack. Treffert first spoke with Peek on the phone in the 1980s. Peek asked Treffert for his date of birth and then proceeded to recount historical events that had taken place on that day and during that week, Treffert says. This display of recall left Treffert with no doubt that Peek was a savant. Peek’s abilities dazzled screenwriter Barry Morrow when the two men met in 1984 at a committee meeting of the Association for Retarded Citizens. Morrow went on to pen the script for the 1988 film Rain Man, basing Dustin Hoffman’s character on Peek. The concept of savant syndrome dates back to 1887, when physician J. Langdon Down coined the term “idiot savant” for persons who showed low IQ but superlative artistic, musical, mathematical, or other skills. (At the time, the word “idiot” denoted low IQ and was not considered insulting.) Nine months after Peek was born in 1951, a doctor told his family “that Kim was retarded, and they should put him in an institution and forget about him,” says Treffert. “Another doctor suggested a lobotomy, which fortunately they didn’t carry out.” Instead, his parents raised him at home in Utah where he raced through books, memorizing them. Despite his feats of memory and other abilities, such as performing impressive calculations in his head, Peek never learned to carry out many everyday tasks, such as dressing himself. MRIs would later reveal that Peek had abnormalities in the left hemisphere of his brain and was missing a corpus callosum, which controls communication between the two cerebral hemispheres. © 1986–2020 The Scientist

Keyword: Learning & Memory
Link ID: 27251 - Posted: 05.18.2020

By Rachel Love Nuwer The renowned biologist E.O. Wilson once quipped, “When you have seen one bird, you have not seen them all.” The diversity of the world’s 10,000-plus bird species is truly staggering, ranging from 2.5-inch-long hummingbirds that weigh as little as a dime, to 9-foot ostriches that can kick hard enough to kill a human. For decades, though, scientists generally thought of birds as conforming to a single set of rules: Females are drab and silent, while males are flashy and boisterous. Pairs are monogamous, and in the rare event of philandering, the male always initiates. Above all, this thinking posited that all birds are automatons, with pint-sized brains that constrain intelligence. Like many presumptions humans make about nature and other species, the truth turns out to be much more complex and fascinating than we ever imagined, according to science journalist Jennifer Ackerman in “The Bird Way: A New Look at How Birds Talk, Work, Play, Parent, and Think.” A new wave of research is not only dispelling old assumptions and showing that birds do not conform to sweeping generalizations, but also revealing that they are capable of nuanced, highly intelligent behaviors that we once believed to be uniquely human (or at least belonging solely to a few fellow mammals). Ackerman walks readers through the most extreme, surprising, and thought-provoking examples of recently uncovered bird behavior. She draws on hundreds of scientific studies and dozens of interviews and field visits with leading ornithologists to lay out the new revelations, from findings that choughs kidnap and enslave young from other groups (the only record of this disturbing act outside of humans and ants), to the discovery that palm cockatoos build their own musical instruments. The result is a book written for true nature and bird lovers — as well as those interested in the origins of intelligence, sociability, deception, altruism, innovation, language, and many of the other attributes at the heart of what we consider to be human.

Keyword: Intelligence; Evolution
Link ID: 27249 - Posted: 05.16.2020

Diana Kwon As Earth rotates around its axis, the organisms that inhabit its surface are exposed to daily cycles of darkness and light. In animals, light has a powerful influence on sleep, hormone release, and metabolism. Work by Takaomi Sakai, a neuroscientist at Tokyo Metropolitan University, and his team suggests that light may also be crucial for forming and maintaining long-term memories. The puzzle of how memories persist in the brain has long been of interest to Sakai. Researchers had previously demonstrated, in both rodents and flies, that the production of new proteins is necessary for maintaining long-term memories, but Sakai wondered how this process persisted over several days given cells’ molecular turnover. Maybe, he thought, an environmental stimulus, such as the light-dark cycles, periodically triggered protein production to enable memory formation and storage. Sakai and his colleagues conducted a series of experiments to see how constant darkness would affect the ability of Drosophila melanogaster to form long-term memories. Male flies exposed to light after interacting with an unreceptive female showed reduced courtship behaviors toward new female mates several days later, indicating they had remembered the initial rejection. Flies kept in constant darkness, however, continued their attempts to copulate. The team then probed the molecular mechanisms of these behaviors and discovered a pathway by which light activates cAMP response element-binding protein (CREB)—a transcription factor previously identified as important for forming long-term memories—within certain neurons found in the mushroom bodies, the memory center in fly brains. © 1986–2020 The Scientist.

Keyword: Learning & Memory; Biological Rhythms
Link ID: 27248 - Posted: 05.16.2020

By Ellen Ruppel Shell My first day in Mexico City was tough. The smog was so thick that I gasped for breath while climbing the stairs to my hotel room. I had braced for headaches from the high altitude and thin air, but I was not prepared for how dirty that air was or for the bloodshot eyes and burning lungs. Declared the world's most polluted metropolis by the United Nations in 1992, greater Mexico City has worked hard to clean up its act. To some degree it has: the city is rightfully proud of its miles of bike paths and lush parks. Yet a casual glance at the smudged horizon shows that those efforts are not enough. Most days the area has levels of airborne sooty particles that greatly exceed standards set by the World Health Organization, as well as elevated amounts of other pollutants. Clogged with more than 9.6 million vehicles and an estimated 50,000 smokestacks, Mexico City stews in a toxic brew known to corrode human lungs and hearts. Now many scientists agree that this pollution also damages the brain. In 2018 a study found lesions known to be hallmarks of Alzheimer's disease in the brains of Mexico City residents in their 30s and 40s—decades before signs of the disease normally can be detected—and tied this damage to exposure to the city's bad air. The researchers who did that work, who are from institutions in Mexico and the U.S., have also found early forms of this frightening damage in infants and young children. And Mexico City is not the only place where bad air has been linked to Alzheimer's. Just a few years ago a team of Harvard scientists released data from a large study of 10 million Medicare recipients ages 65 and older living in 50 different cities in the northeastern U.S. The researchers reported a strong correlation between exposure to specific air pollutants and a number of neurodegenerative disorders, including Alzheimer's. © 2020 Scientific American

Keyword: Alzheimers; Neurotoxins
Link ID: 27247 - Posted: 05.14.2020

Ashley Yeager Nearly seven years ago, Sheena Josselyn and her husband Paul Frankland were talking with their two-year-old daughter and started to wonder why she could easily remember what happened over the last day or two but couldn’t recall events that had happened a few months before. Josselyn and Frankland, both neuroscientists at the Hospital for Sick Children Research Institute in Toronto, suspected that maybe neurogenesis, the creation of new neurons, could be involved in this sort of forgetfulness. In humans and other mammals, neurogenesis happens in the hippocampus, a region of the brain involved in learning and memory, tying the generation of new neurons to the process of making memories. Josselyn and Frankland knew that in infancy, the brain makes a lot of new neurons, but that neurogenesis slows with age. Yet youngsters have more trouble making long-term memories than adults do, a notion that doesn’t quite jibe with the idea that the principal function of neurogenesis is memory formation. To test the connection between neurogenesis and forgetting, the researchers put mice in a box and shocked their feet with an electric current, then returned the animals to their home cages and either let them stay sedentary or had them run on a wheel, an activity that boosts neurogenesis. Six weeks later, the researchers put the mice back in the box where they had received the shocks. There, the sedentary mice froze in fear, anticipating a shock, but the mice that had run on a wheel didn’t show signs of anxiety. It was as if the wheel-running mice had forgotten they’d been shocked before. © 1986–2020 The Scientist.

Keyword: Learning & Memory; Glia
Link ID: 27245 - Posted: 05.14.2020

Amy Schleunes When Lilian Kloft stumbled across a 2015 study showing a connection between cannabis use and susceptibility to false memories, she found herself wondering about the legal implications of the results. The study had discovered that heavy users of cannabis were more likely than controls to form false memories—recollections of events that never occurred, for example, or warped memories of events that did—even when they were not at the moment “high.” This kind of false remembering can pose difficulties for people gathering reliable testimony in the event of a crime, says Kloft, a PhD student in psychopharmacology and forensic psychology at Maastricht University in the Netherlands. Consequently, the growing acceptance of cannabis worldwide raises questions not only about how the drug affects memory, but also about how law enforcement officials should conduct interviews with suspects, victims, and witnesses who may be under the influence or regular users of the drug. In order to further investigate the connection between cannabis and false memory formation, Kloft and collaborators recruited 64 volunteers for a series of experiments. Participants, who were occasional cannabis users, were given a vaporizer containing either cannabis or a hemp placebo and then told to inhale deeply and hold their breath for 10 seconds. After that, the researchers tested them in three different tasks designed to induce false memories. © 1986–2020 The Scientist.

Keyword: Drug Abuse; Learning & Memory
Link ID: 27244 - Posted: 05.12.2020

by Peter Hess Low levels of the hormone vasopressin in early infancy may presage an autism diagnosis in childhood, according to a new study1. Although preliminary, the results suggest that testing vasopressin levels — particularly in infants with high odds of having autism — could flag the condition in the first few months of life. Early identification would allow autistic children to start therapies far sooner than is currently possible, says co-lead investigator Karen Parker, associate professor of psychiatry and behavioral sciences at Stanford University in California. “By the time a child receives an autism diagnosis, they’re pretty far along the path of having these robust social impairments,” Parker says. Previous work has shown that autistic children have, on average, 66 percent less vasopressin in their cerebrospinal fluid than their neurotypical peers, and that low levels of vasopressin track with poor social skills. The new study found a similar trend in infants aged 3 months and younger. “The surprising thing is that this relationship extends to infancy,” before any observable autism traits have emerged, says Larry Young, chief of behavioral neuroscience and psychiatric disorders at Emory University in Atlanta, Georgia, who was not involved with the study. The results, if confirmed, suggest there is a direct biological connection between vasopressin release and autism, Young says. © 2020 Simons Foundation

Keyword: Autism; Hormones & Behavior
Link ID: 27243 - Posted: 05.12.2020

by Giorgia Guglielmi More than half of the genes expressed in the prefrontal cortex, a brain region that is implicated in autism, begin to change their expression patterns in late fetal development, according to a new study1. Previous studies have looked at how DNA variants can influence gene expression at specific developmental periods. This is the first to map their effects in a specific region over the full span of human brain development, says co-senior investigator Stephan Sanders, associate professor of psychiatry at the University of California, San Francisco. “If we ever really want to understand what autism is, understanding human fetal development of the brain is going to be absolutely critical,” Sanders says. Some of the changes in expression patterns vary depending on individual differences in neighboring DNA sequences, the study found. Some of that variation occurs in stretches of the genome linked to neurodevelopmental outcomes, such as how much schooling a person completes (a proxy for intelligence) or whether she develops schizophrenia. “This study creates a resource for trying to understand neurodevelopment and neuropsychiatric disorders,” Sanders says. Fetal expression: The researchers analyzed the prefrontal cortex of 176 postmortem brains from donors ranging in age from 6 weeks post-conception to 20 years. None had any known neuropsychiatric conditions or large-scale genetic anomalies. The team identified 23,782 genes expressed during brain development in the dorsolateral prefrontal cortex, a region implicated in many developmental conditions, including autism. © 2020 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 27239 - Posted: 05.08.2020

A small study funded by the National Institutes of Health suggests that sleep problems among children who have a sibling with autism spectrum disorder (ASD) may further raise the likelihood of an ASD diagnosis, compared to at-risk children who do not have difficulty sleeping. Previous research has shown that young children who have a sibling with ASD are at a higher risk for also being diagnosed with the condition. The study appears in The American Journal of Psychiatry. If confirmed by other studies, the findings may give clinicians a tool to identify sleep problems early and provide interventions to reduce their effects on the health and development of children with autism. The findings may also provide insights into the potential role of sleep problems in the development of ASD. The study was conducted by Annette M. Estes, Ph.D., of the University of Washington Autism Center in Seattle, and colleagues in the NIH Autism Centers of Excellence Infant Brain Imaging Study Network. NIH funding was provided by the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) and the National Institute of Mental Health. “The results are a promising lead,” said Alice Kau, Ph.D., of NICHD’s Intellectual and Developmental Disabilities Branch. “If confirmed by more in-depth studies, patterns of sleep disturbance in early life might be used to pinpoint increased risk for ASD among young children already at risk because they have a sibling with ASD.” The researchers analyzed data from a long-term study of children who do and do not have siblings with ASD. When the children were 6 and 12 months of age, parents were asked to respond to an infant temperament questionnaire that asks how much difficulty their child has falling asleep at bedtime and falling back to sleep after waking up during the night. At these time intervals, the children also received MRI scans to track their brain development. At 24 months, the children were assessed for ASD.

Keyword: Autism; Sleep
Link ID: 27238 - Posted: 05.08.2020

By Godfrey Pearlson Around the world, about 188 million people use marijuana every year. The drug has been legalized for recreational use in 11 U.S. states, and it may eventually become legal at the federal level. In a Gallup survey conducted last summer, 12 percent of American adults reported that they smoked marijuana, including 22 percent of 18- to 29-year-olds. Those are the stats. The consequences remain a mystery. As access to marijuana increases—and while acceptance of the drug grows and perception of its harmfulness diminishes—it is important to consider the potential for long-term ill effects, especially in users who start young. One of marijuana’s best-documented consequences is short-lived interference with memory. The substance makes it harder to get information into memory and, subsequently, to access it, with larger doses causing progressively more problems. Much less documented, however, is whether the drug has lasting effects on cognitive abilities. Finding the answer to that question is essential. Depending on the severity of any such effects and their persistence, marijuana use could have significant downstream impacts on education, employment, job performance and income. There are plausible reasons why the teenage brain may be especially vulnerable to the effects of marijuana use. Natural cannabinoids play an essential role in brain cell migration and development from fetal life onward. And adolescence is a crucial age for finalizing brain sculpting and white matter proliferation. The hippocampi, paired structures in the temporal lobe that are crucial in the formation of new memories, are studded with cannabinoid receptors. THC, the main ingredient behind marijuana’s “high,” acts on the brain’s cannabinoid receptors to mimic some of the effects of the body’s endogenous cannabinoids, such as anandamide. The compound’s effects are more persistent and nonphysiological, however. It may be throwing important natural processes out of balance. © 2020 Scientific American,

Keyword: Drug Abuse; Learning & Memory
Link ID: 27237 - Posted: 05.08.2020

Ashley Yeager In the spring of 2019, neuroscientist Heather Cameron set up a simple experiment. She and her colleagues put an adult rat in the middle of a plastic box with a water bottle at one end. They waited until the rat started drinking and then made a startling noise to see how the animal would respond. The team did this repeatedly with regular rats and with animals that were genetically altered so that they couldn’t make new neurons in their hippocampuses, a brain region involved in learning and memory. When the animals heard the noise, those that could make new hippocampal neurons immediately stopped slurping water and looked around, but the animals lacking hippocampal neurogenesis kept drinking. When the team ran the experiment without the water bottle, both sets of rats looked around right away to figure out where the sound was coming from. Rats that couldn’t make new neurons seemed to have trouble shifting their attention from one task to another, the researchers concluded. “It’s a very surprising result,” says Cameron, who works at the National Institute of Mental Health (NIMH) in Bethesda, Maryland. Researchers studying neurogenesis in the adult hippocampus typically conduct experiments in which animals have had extensive training in a task, such as in a water maze, or have experienced repetitive foot shocks, she explains. In her experiments, the rats were just drinking water. “It seemed like there would be no reason that the hippocampus should have any role,” she says. Yet in animals engineered to lack hippocampal neurogenesis, “the effects are pretty big.” The study joins a growing body of work that challenges the decades-old notion that the primary role of new neurons within the adult hippocampus is in learning and memory. More recently, experiments have tied neurogenesis to forgetting, one possible way to ensure the brain doesn’t become overloaded with information it doesn’t need, and to anxiety, depression, stress, and, as Cameron’s work suggests, attention. Now, neuro-scientists are rethinking the role that new neurons, and the hippocampus as a whole, play in the brain. © 1986–2020 The Scientist.

Keyword: Neurogenesis; Learning & Memory
Link ID: 27236 - Posted: 05.06.2020