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

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by Lauren Schenkman Autism is thought to arise during prenatal development, when the brain is spinning its web of excitatory and inhibitory neurons, the main signal-generating cell types in the cerebral cortex. Though this wiring process remains mysterious, one thing seemed certain after two decades of studies in mice: Although both neuron types arise from radial glia, excitatory neurons crop up in the developing cortex, whereas inhibitory neurons, also known as interneurons, originate outside of the cortex and then later migrate into it. Not so in the human brain, according to a study published in December in Nature. A team of researchers led by Tomasz Nowakowski, assistant professor of anatomy at the University of California, San Francisco, used a new viral barcoding method to trace the descendants of radial glial cells from the developing human cortex and found that these progenitor cells can give rise to both excitatory neurons and interneurons. “This is really a paradigm-shifting finding,” Nowakowski says. “It sets up a new framework for studying, understanding and interpreting experimental models of autism mutations.” Nowakowski spoke with Spectrum about the discovery’s implications for studying the origins of autism in the developing brain. Spectrum: Why did you investigate this topic? Tomasz Nowakowski: My lab and I are interested in understanding the early neurodevelopmental events that give rise to the incredible complexity of the human cerebral cortex. We know especially little about the early stages of human development, primarily because a lot of our knowledge comes from mouse models. As we’ve begun to realize over the past decade, the processes that underlie development of the brain in humans and mice can be quite different. © 2022 Simons Foundation

Keyword: Autism; Development of the Brain
Link ID: 28165 - Posted: 01.22.2022

By Jane E. Brody Many people aren’t overly concerned when an octogenarian occasionally forgets the best route to a favorite store, can’t remember a friend’s name or dents the car while trying to parallel park on a crowded city street. Even healthy brains work less efficiently with age, and memory, sensory perceptions and physical abilities become less reliable. But what if the person is not in their 80s but in their 30s, 40s or 50s and forgets the way home from their own street corner? That’s far more concerning. While most of the 5.3 million Americans who are living with Alzheimer’s disease or other forms of dementia are over 65, some 200,000 are younger than 65 and develop serious memory and thinking problems far earlier in life than expected. “Young-onset dementia is a particularly disheartening diagnosis because it affects individuals in the prime years,” Dr. David S. Knopman, a neurologist at the Mayo Clinic in Rochester, Minn., wrote in a July 2021 editorial in JAMA Neurology. Many of the afflicted are in their 40s and 50s, midcareer, hardly ready to retire and perhaps still raising a family. Dementia in a younger adult is especially traumatic and challenging for families to acknowledge, and many practicing physicians fail to recognize it or even suspect it may be an underlying cause of symptoms. “Complaints about brain fog in young patients are very common and are mostly benign,” Dr. Knopman told me. “It’s hard to know when they’re not attributable to stress, depression or anxiety or the result of normal aging. Even neurologists infrequently see patients with young-onset dementia.” Yet recent studies indicate that the problem is far more common than most doctors realize. Worldwide, as many as 3.9 million people younger than 65 may be affected, a Dutch analysis of 74 studies indicated. The study, published in JAMA Neurology in September, found that for every 100,000 people aged 30 to 64, 119 had early dementia. © 2022 The New York Times Company

Keyword: Alzheimers; Genes & Behavior
Link ID: 28161 - Posted: 01.19.2022

By Azeen Ghorayshi An upsurge in teenagers requesting hormones or surgeries to better align their bodies with their gender identities has ignited a debate among doctors over when to provide these treatments. An international group of experts focused on transgender health last month released a draft of new guidelines, the gold standard of the field that informs what insurers will reimburse for care. Many doctors and activists praised the 350-page document, which was updated for the first time in nearly a decade, for including transgender people in its drafting and for removing language requiring adults to have psychological assessments before getting access to hormone therapy. But the guidelines take a more cautious stance on teens. A new chapter dedicated to adolescents says that they must undergo mental health assessments and must have questioned their gender identity for “several years” before receiving drugs or surgeries. Experts in transgender health are divided on these adolescent recommendations, reflecting a fraught debate over how to weigh conflicting risks for young people, who typically can’t give full legal consent until they are 18 and who may be in emotional distress or more vulnerable to peer influence than adults are. Some of the drug regimens bring long-term risks, such as irreversible fertility loss. And in some cases, thought to be quite rare, transgender people later “detransition” to the gender they were assigned at birth. Given these risks, as well as the increasing number of adolescents seeking these treatments, some clinicians say that teens need more psychological assessment than adults do. “They absolutely have to be treated differently,” said Laura Edwards-Leeper, a child clinical psychologist in Beaverton, Ore., who works with transgender adolescents. Dr. Edwards-Leeper was one of seven authors of the new adolescent chapter, but the organization that publishes the guidelines, the World Professional Association for Transgender Health, did not authorize her to comment publicly on the draft’s proposed wording. © 2022 The New York Times Company

Keyword: Sexual Behavior; Hormones & Behavior
Link ID: 28156 - Posted: 01.15.2022

Melinda Wenner Moyer Like many paediatricians, Dani Dumitriu braced herself for the impact of the SARS-CoV-2 coronavirus when it first surged in her wards. She was relieved when most newborn babies at her hospital who had been exposed to COVID-19 seemed to do just fine. Knowledge of the effects of Zika and other viruses that can cause birth defects meant that doctors were looking out for problems. But hints of a more subtle and insidious trend followed close behind. Dumitriu and her team at the NewYork–Presbyterian Morgan Stanley Children’s Hospital in New York City had more than two years of data on infant development — since late 2017, they had been analysing the communication and motor skills of babies up to six months old. Dumitriu thought it would be interesting to compare the results from babies born before and during the pandemic. She asked her colleague Morgan Firestein, a postdoctoral researcher at Columbia University in New York City, to assess whether there were neurodevelopmental differences between the two groups. A few days later, Firestein called Dumitriu in a panic. “She was like, ‘We’re in a crisis, I don’t know what to do, because we not only have an effect of a pandemic, but it’s a significant one,’” Dumitriu recalled. She was up most of that night, poring over the data. The infants born during the pandemic scored lower, on average, on tests of gross motor, fine motor and communication skills compared with those born before it (both groups were assessed by their parents using an established questionnaire)1. It didn’t matter whether their birth parent had been infected with the virus or not; there seemed to be something about the environment of the pandemic itself. Dumitriu was stunned. “We were like, oh, my God,” she recalled. “We’re talking about hundreds of millions of babies.” Although children have generally fared well when infected with SARS-CoV-2, preliminary research suggests that pandemic-related stress during pregnancy could be negatively affecting fetal brain development in some children. Moreover, frazzled parents and carers might be interacting differently or less with their young children in ways that could affect a child’s physical and mental abilities.

Keyword: Development of the Brain; Learning & Memory
Link ID: 28152 - Posted: 01.12.2022

by Peter Hess Of all the brain chemistry that autism researchers study, few molecules have garnered as much attention as the so-called ‘social hormone,’ oxytocin. Some autistic children appear to have low blood levels of oxytocin, which has led several teams to test oxytocin delivered intranasally as an autism therapy. So far, though, such clinical trials have yielded inconsistent results. Here we explain what scientists know so far about oxytocin’s connection to autism. What does oxytocin do in the brain and body? Oxytocin serves multiple purposes, such as promoting trust between people, moderating our response to threats, and supporting lactation and mother-child bonding. The hormone is produced primarily in the hypothalamus, a brain region that mediates basic bodily functions, including hunger, thirst and body temperature. Oxytocin-producing neurons in the hypothalamus project into other parts of the brain, such as the nucleus accumbens, where the hormone regulates social-reward learning. In the brain’s sensory system, including the olfactory bulb, oxytocin seems to help balance excitatory and inhibitory signals, improving social-information processing, at least in rats. In the amygdala, oxytocin appears to help dull threat responses to negative social information and foster social recognition. The pituitary gland controls the release of oxytocin into the bloodstream. Blood oxytocin is crucial to start uterine muscle contractions during childbirth. It also supports lactation by facilitating the milk letdown reflex, stimulating the flow of milk into the nipple. © 2022 Simons Foundation

Keyword: Hormones & Behavior; Autism
Link ID: 28143 - Posted: 01.08.2022

by Anna Goshua A variety of traits, including developmental delay and intellectual disability, characterize people with mutations in the autism-linked gene MYT1L, according to a new study. The gene encodes a transcription factor important for cells that make myelin, which insulates nerve cells and is deficient in some forms of autism. The work, published 8 November in Human Genetics, represents the most detailed study of the traits associated with MYT1L mutations to date. “We wanted to gather more cases to bring a clearer clinical and molecular picture of the condition for lab scientists, clinicians and also for patients and families,” says study investigator Juliette Coursimault, a physician-researcher in the genetics department at Rouen University Hospital in France. She and her co-researchers described 62 people, whereas previous literature included only 12 cases. The new characterization will “benefit clinicians’ diagnosis and treatment strategies when a patient with MYT1L mutation arrives in their clinic,” says Brady Maher, a lead investigator at the Lieber Institute for Brain Development at Johns Hopkins University in Baltimore, Maryland, who was not part of the study. The researchers identified and reviewed data for 22 people with MYT1L mutations who had been described in the academic literature, and collected clinical and molecular data from an additional 40 people, aged 1 to 34 years old, with likely or confirmed pathogenic variants of MYT1L. They recruited the participants through Rouen University Hospital and data-sharing networks such as GeneMatcher, which connects clinicians and researchers. © 2021 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 28122 - Posted: 12.22.2021

Mir Jalil Razavi Weiying Dai The human brain has been called the most complex object in the known universe. And with good reason: It has around 86 billion neurons and several hundred thousand miles of axon fibers connecting them. Unsurprisingly, the process of brain folding that results in the brain’s characteristic bumps and grooves is also highly complex. Despite decades of speculation and research, the underlying mechanism behind this process remains poorly understood. As biomechanics and computer science researchers, we have spent several years studying the mechanics of brain folding and ways to visualize and map the brain, respectively. Figuring out this complexity may help researchers better diagnose and treat developmental brain disorders such as lissencephaly, or smooth brain, and epilepsy. Because many neurological disorders emerge at the early stages of development, understanding how brain folding works can provide useful insights into normal and pathological brain function. The mechanics of brain folding The brain is made of two layers. The outer layer, called the cerebral cortex, is composed of folded gray matter made up of small blood vessels and the spherical cell bodies of billions of neurons. The inner layer is composed of white matter, consisting mostly of the neurons’ elongated tails, called myelinated axons. When a story fascinates you, remember: Your donations make it possible Illustration of cross section of brain showing axonal pathways transitioning from gray matter into white matter. In recent years, researchers have shown that mechanics, or the forces that objects exert on one another, play an important role in the growth and folding of the brain. © 2010–2021, The Conversation US, Inc.

Keyword: Development of the Brain
Link ID: 28119 - Posted: 12.18.2021

Rafael Yuste Michael Levin In the middle of his landmark book On the Origin of Species, Darwin had a crisis of faith. In a bout of honesty, he wrote, “To suppose that the eye with all its inimitable contrivances for adjusting the focus to different distances, for admitting different amounts of light, and for the correction of spherical and chromatic aberration, could have been formed by natural selection, seems, I confess, absurd in the highest degree.” While scientists are still working out the details of how the eye evolved, we are also still stuck on the question of how intelligence emerges in biology. How can a biological system ever generate coherent and goal-oriented behavior from the bottom up when there is no external designer? In fact, intelligence—a purposeful response to available information, often anticipating the future—is not restricted to the minds of some privileged species. It is distributed throughout biology, at many different spatial and temporal scales. There are not just intelligent people, mammals, birds and cephalopods. Intelligent, purposeful problem-solving behavior can be found in parts of all living things: single cells and tissues, individual neurons and networks of neurons, viruses, ribosomes and RNA fragments, down to motor proteins and molecular networks. Arguably, understanding the origin of intelligence is the central problem in biology—one that is still wide open. In this piece, we argue that progress in developmental biology and neuroscience is now providing a promising path to show how the architecture of modular systems underlies evolutionary and organismal intelligence. © 2021 Scientific American

Keyword: Evolution; Development of the Brain
Link ID: 28118 - Posted: 12.18.2021

by Anna Goshua Researchers have identified hundreds of genes that may contribute to autism, but these genes can’t fully account for the condition’s traits. Studies from the past decade implicate an additional layer of ‘epigenetic’ complexity: chemical tags called methyl groups laid on top of a person’s genetic code. Enzymes that are mutated in some people with autism or related conditions attach the chemical tags to DNA. And that pattern of methyl marks across the genome can influence which genes are active or inactive at any given time. Much remains to be understood about this process, called DNA methylation. Here we describe how and when methylation happens and what researchers know about its relationship to autism. What is methylation? Methylation is the process by which enzymes called methyltransferases deposit methyl chemical groups onto DNA. The presence of these tags usually turns off nearby genes. The complete set of such modifications to the genome over a person’s lifetime is known as the methylome. Most methyl tags are deposited onto the DNA nucleotide called cytosine (C) whenever it occurs next to the nucleotide guanine (G). This CpG methylation begins during gestation and can change across the lifespan. Tags are also sometimes added to cytosines followed by other nucleotides, however. High levels of non-CpG methylation in the brain may be critical for neuron development. 2021 Simons Foundation

Keyword: Autism; Epigenetics
Link ID: 28115 - Posted: 12.15.2021

Mitch Leslie Medicine so far has nothing to offer that clearly prevents Alzheimer’s disease, although keeping your weight down, exercising regularly, and inheriting certain protective genes can lower your risk. Now, a study has identified another, unexpected source of protection: clonal hematopoiesis, a blood cell imbalance best known as a risk factor for cancer and heart disease. “Clonal hematopoiesis has been associated with so many bad outcomes that it is surprising that it is protective in this situation,” says cardiovascular biologist Kenneth Walsh of the University of Virginia, who wasn’t connected to the study, reported on 12 December at the American Society of Hematology meeting in Atlanta. But Walsh says the work is convincing and “will have to be reckoned with and explained.” He and other researchers caution that the discovery doesn’t offer any immediate opportunities for treating or preventing Alzheimer’s disease. Given the negative health effects of clonal hematopoiesis, inducing it in healthy people is a nonstarter. Still, the finding has a provocative implication: that cells from the bloodstream are restocking the brain’s immune cells, perhaps bolstering its ability to clear out toxic debris. Charles Darwin probably never imagined that natural selection unfolds in our bone marrow. But clonal hematopoiesis results from competition among the 50,000 to 200,000 stem cells that dwell there and divide to produce all our red and white blood cells. Over the years these stem cells accrue mutations, some of which result in a “fitter” cell whose progeny, known collectively as a clone, can soon outnumber their counterparts. In some people with clonal hematopoiesis, the offspring of a single mutated stem cell account for more than half of the blood cells in the body. © 2021 American Association for the Advancement of Science.

Keyword: Alzheimers
Link ID: 28114 - Posted: 12.15.2021

By Pam Belluck What if something in the blood of an athlete could boost the brainpower of someone who doesn’t or can’t exercise? Could a protein that gets amplified when people exercise help stave off symptoms of Alzheimer’s and other memory disorders? That’s the tantalizing prospect raised by a new study in which researchers injected sedentary mice with blood from mice that ran for miles on exercise wheels, and found that the sedentary mice then did better on tests of learning and memory. The study, published Wednesday in the journal Nature, also found that the type of brain inflammation involved in Alzheimer’s and other neurological disorders was reduced in sedentary mice after they received their athletic counterparts’ blood. “We’re seeing an increasing number of studies where proteins from outside the brain that are made when you exercise get into the brain and are helpful for improving brain health, or even improving cognition and disease,” said Rudolph Tanzi, a professor of neurology at Massachusetts General Hospital and Harvard Medical School. He led a 2018 study that found that exercise helped the brains of mice engineered to have a version of Alzheimer’s. The most promising outcome would be if exercise-generated proteins can become the basis for treatments, experts said. The study, led by researchers at Stanford School of Medicine, found that one protein — clusterin, produced in the liver and in heart muscle cells — seemed to account for most of the anti-inflammatory effects. But several experts noted that recent studies have found benefits from other proteins. They also said more needs to be learned about clusterin, which plays a role in many diseases, including cancer, and may have negative effects in early stages of Alzheimer’s before brain inflammation becomes dominant. © 2021 The New York Times Company

Keyword: Alzheimers; Hormones & Behavior
Link ID: 28108 - Posted: 12.11.2021

by Anna Goshua Mice that lack one copy of TBX1, a gene in the autism-linked 22q11.2 chromosomal region, produce too little myelin — the fatty insulation that surrounds neurons — and perform poorly on tasks that measure cognitive speed, according to a new study. The work, published 5 November in Molecular Psychiatry, may offer insight into the mechanisms that underlie impaired cognitive function in some people with a 22q11.2 deletion, and possibly other copy number variants (CNVs). “The myelin changes could potentially emerge as a common neuronal deficit that mediates cognitive changes among many CNV cases,” says lead investigator Noboru Hiroi, professor of pharmacology at the University of Texas Health Science Center at San Antonio. Neuronal axons — the projections that conduct nerve impulses — are coated with myelin, which serves to speed up electrical transmission. The brains of autistic people and several mouse models of autism have disruptions in myelin, previous research has shown. These connecting fibers are the “highways of the brain,” says Valerie Bolivar, research scientist at the New York State Department of Health’s Wadsworth Center in Albany. “If the highway doesn’t work, you can’t get your goods from one place to another as fast.” TBX1 encodes a protein that regulates the expression of other genes during brain development. Deleting one copy of TBX1 leads to social and communication deficits in mice, according to previous studies by Hiroi’s team. © 2021 Simons Foundation

Keyword: Autism; Glia
Link ID: 28103 - Posted: 12.08.2021

By Bob Goldstein On a cold, dry Tuesday in December, 1940, Rita Levi-Montalcini rode a train from the station near her home in Turin, Italy, for 80 miles to Milan to buy a microscope. Milan had not seen bombings for months. On her return to the Turin train station, two police officers stopped her and demanded to see inside the cake-sized box that she was carrying. With wartime food rationing, panettone cakes were only available illegally. The officers found her new microscope instead. They let her go. Just a week after her trip, British bombers hit Milan. Levi-Montalcini was a 31-year-old scientist who had been working at the University of Turin. Despite her father’s disapproval, she had trained in medicine, inspired by seeing a nanny succumb to cancer. In 1938, the Italian dictator Mussolini banned Jews from positions in universities. Levi-Montalcini was not raised in the Jewish religion, but her Jewish ancestry would have been evident from her surname. Mussolini’s ban had pushed Levi-Montalcini to leave Italy for Belgium in 1939, where she did research using fertilized chicken eggs as a source of material for her research topic: the developing nervous systems of vertebrate embryos. Levi-Montalcini also spent time with her older sister Nina, whose family was in Belgium as well. Rita wrote home to her mother of an “infinite desire to embrace you again,” but research at the university in Turin would have been impossible had she returned home. Her passion for research alternated with her frustration with challenges. When Hitler invaded Poland in September, launching war, her worst frustrations were realized. The “whole world was in danger,” Levi-Montalcini later wrote. In December 1939, she returned to Italy. © 2021 NautilusThink Inc,

Keyword: Apoptosis; Development of the Brain
Link ID: 28097 - Posted: 12.04.2021

By Gretchen Reynolds Staying physically active as we age substantially drops our risk of developing dementia during our lifetimes, and it doesn’t require prolonged exercise. Walking or moving about, rather than sitting, may be all it takes to help bolster the brain, and a new study of octogenarians from Chicago may help to explain why. The study, which tracked how often older people moved or sat and then looked deep inside their brains after they passed away, found that certain vital immune cells worked differently in the brains of older people who were active compared to their more sedentary peers. Physical activity seemed to influence their brain’s health, their thinking abilities and whether they experienced the memory loss of Alzheimer’s disease. The findings add to growing evidence that when we move our bodies, we change our minds, no matter how advanced our age. Already, plenty of scientific evidence indicates that physical activity bulks up our brains. Older, sedentary people who begin walking for about an hour most days, for instance, typically add volume to their hippocampus, the brain’s memory center, reducing or reversing the shrinkage that otherwise commonly occurs there over the years. Active people who are middle-aged or older also tend to perform better on tests of memory and thinking skills than people of the same age who rarely exercise, and are nearly half as likely eventually to be diagnosed with Alzheimer’s disease. Almost as heartening, active people who do develop dementia usually show their first symptoms years later than inactive people do. But precisely how movement remodels our brains is still mostly mysterious, although scientists have hints from animal experiments. When adult lab mice and rats run on wheels, for example, they goose production of hormones and neurochemicals that prompt the creation of new neurons, as well as synapses, blood vessels and other tissues that connect and nurture those young brain cells. © 2021 The New York Times Company

Keyword: Alzheimers
Link ID: 28094 - Posted: 12.01.2021

by Charles Q. Choi One injection of a potential new gene therapy for Angelman syndrome forestalls many of the neurodevelopmental condition’s key traits, according to early tests in mice. “While additional pharmacology and safety studies are needed, our viral vector can potentially provide transformative therapeutic relief with a single dose,” says lead investigator Benjamin Philpot, professor of neuroscience at the University of North Carolina at Chapel Hill. Angelman syndrome, which affects about one in 20,000 children, is associated with significant developmental delays and, often, autism. It arises from mutations or deletions in the maternal copy of the UBE3A gene, which encodes a protein that helps regulate the levels of other important proteins. There are no treatments specifically for Angelman syndrome, but several gene therapies are under development. One in clinical trials requires repeat injections in the spine and has shown serious side effects at high doses. These therapies all aim to restore UBE3A function in neurons. One challenge, though, is that neurons produce several variants, or ‘isoforms,’ of the UBE3A protein that vary slightly in length; in mice, for example, neurons make two isoforms in a ratio of about four short forms for every long one. In contrast to other gene therapies, the new one generates short and long forms of the UBE3A protein at nearly the same ratio as is seen in mouse neurons. Such proportions “may be important for therapeutic efficacy,” says Eric Levine, professor of neuroscience at the University of Connecticut in Farmington, who was not involved in this study. © 2021 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 28093 - Posted: 12.01.2021

To eavesdrop on a brain, one of the best tools neuroscientists have is the fMRI scan, which helps map blood flow, and therefore the spikes in oxygen that occur whenever a particular brain region is being used. It reveals a noisy world. Blood oxygen levels vary from moment to moment, but those spikes never totally flatten out. “Your brain, even resting, is not going to be completely silent,” says Poortata Lalwani, a PhD student in cognitive neuroscience at the University of Michigan. She imagines the brain, even at its most tranquil, as kind of like a tennis player waiting to return a serve: “He’s not going to be standing still. He’s going to be pacing a little bit, getting ready to hit the backhand.” Many fMRI studies filter out that noise to find the particular spikes researchers want to scrutinize. But for Lalwani, that noise is the most telling signal of all. To her, it’s a signal of cognitive flexibility. Young, healthy brains tend to have signals with a lot of variability in blood oxygen levels from moment to moment. Older ones vary less, at least in certain regions of the brain. About a decade ago, scientists first showed the link between low neural signal variability and the kind of cognitive decline that accompanies healthy aging, rather than specific dementias. A brain’s noisiness is a solid proxy for details that are more abstract, Lalwani says: “How efficient information transfer is, how well-connected the neural networks are, in general how well-functioning the underlying neural network is.” But why that change happens with age has been a mystery. So has the question of whether it’s reversible. © 2021 Condé Nast.

Keyword: Attention; Alzheimers
Link ID: 28091 - Posted: 11.24.2021

by Niko McCarty Growing numbers of autistic children are diagnosed with the condition before age 3, in the United States, and those diagnoses tend to precede the start of any interventions or developmental services, according to a new study based on parent surveys. Children traversing autism’s ‘diagnostic odyssey’ a decade ago were typically diagnosed years later, and only after they had begun receiving services. The analysis included data from 2,303 autistic children aged 2 to 17 years from the National Survey of Children’s Health, which asks parents questions about the children in their household. The selected participants, split into three groups based on their age, either had a plan for early intervention or had received special services to meet developmental needs. The oldest children, aged 12 to 17 at the time of the survey, had been diagnosed at about age 5 and a half years, on average. Their first intervention or developmental service occurred at around age 5. By contrast, the youngest cohort, aged 2 to 5, had been diagnosed at about age 2 and a half years and started their first intervention or developmental services at roughly the same age. The results are based on parent responses to a question — “How old was your child when a doctor or other health care provider first said they had autism?” — so the findings likely skew toward younger ages than if the researchers had used clinical diagnoses. Also, the study omitted children who did not already have a diagnosis, which might have pushed the average age older. Still, the findings suggest that the time between getting a diagnosis and accessing services is shrinking. © 2021 Simons Foundation

Keyword: Autism
Link ID: 28084 - Posted: 11.20.2021

Andrew Gregory Health editor Drinking coffee or tea may be linked with a lower risk of stroke and dementia, according to the largest study of its kind. Strokes cause 10% of deaths globally, while dementia is one of the world’s biggest health challenges – 130 million are expected to be living with it by 2050. In the research, 365,000 people aged between 50 and 74 were followed for more than a decade. At the start the participants, who were involved in the UK Biobank study, self-reported how much coffee and tea they drank. Over the research period, 5,079 of them developed dementia and 10,053 went on to have at least one stroke. Researchers found that people who drank two to three cups of coffee or three to five cups of tea a day, or a combination of four to six cups of coffee and tea, had the lowest risk of stroke or dementia. Those who drank two to three cups of coffee and two to three cups of tea daily had a 32% lower risk of stroke. These people had a 28% lower risk of dementia compared with those who did not drink tea or coffee. The research, by Yuan Zhang and colleagues from Tianjin Medical University, China, suggests drinking coffee alone or in combination with tea is also linked with lower risk of post-stroke dementia. Writing in the journal Plos Medicine, the authors said: “Our findings suggested that moderate consumption of coffee and tea separately or in combination were associated with lower risk of stroke and dementia.” © 2021 Guardian News & Media Limited

Keyword: Stroke; Drug Abuse
Link ID: 28082 - Posted: 11.20.2021

By Emily Willingham As with most decision points around pregnancy, cannabis use is a fraught subject. Researchers can’t assess it in randomized trials because dosing pregnant people with the psychoactive substance is unethical. The next best thing is studies with enough participants who use cannabis on their own, allowing for comparisons with those who do not. The findings of one such study, published on November 15 in the Proceedings of the National Academy of Sciences USA, highlight symptoms of increased anxiety, hyperactivity and aggression in children whose parents used cannabis during pregnancy. And its analysis of placental tissue points to changes in the activity of immunity-related genes. Today pregnant people “are being bombarded with a lot of ads to treat nausea and anxiety during pregnancy” with cannabis, says the paper’s senior author Yasmin Hurd, director of the Addiction Institute at Mount Sinai. “Our studies are about empowering them with knowledge and education so that they can make decisions.” The results are “very striking, very much a first,” says Daniele Piomelli, a professor and director of the Center for the Study of Cannabis at the University of California, Irvine, who was not involved in the work. Pregnancy studies in rodents and even in sheep, which have a placenta more like ours, have required cautious interpretations of findings that show effects on offspring behavior and function, he says. The new study is one of the first to tackle the question in people “in a systematic way,” Piomelli adds. © 2021 Scientific American

Keyword: ADHD; Drug Abuse
Link ID: 28078 - Posted: 11.17.2021

Asher Mullard When the US Food and Drug Administration (FDA) approved biotechnology firm Biogen’s drug for Alzheimer’s disease in June, regulators hoped to usher in a new era of treatment for the neurodegenerative condition. But the decision followed an independent advisory committee’s near-unanimous vote to reject the drug, called aducanumab — and instead divided the community. Some researchers think that the approval will bolster the development of drugs for treating brain disease, but others see it as a blemish on the FDA’s integrity and an obstacle to progress. Pharmaceutical company Eli Lilly in Indianapolis hopes that its antibody donanemab, which works in a similar way to aducanumab, will have a better reception. The firm plans to finish submitting its drug candidate for FDA approval in the next few months, paving the way for a decision in the second half of 2022. Meanwhile, Biogen, based in Cambridge, Massachusetts, and its partner Eisai, based in Tokyo, are racing to complete the submission of data for another competitor, lecanemab. The regulatory fate of these therapeutic hopefuls could foretell the future of Alzheimer’s and shape neurodegenerative drug development programmes for years. According to the ‘amyloid hypothesis’ of Alzheimer’s disease, the build-up of a protein called amyloid-β in the brain causes neurodegeneration. Aducanumab and its would-be competitors clear clumps of amyloid-β from the brain. But clinical trials have not meaningfully demonstrated that these therapeutics slow memory loss or cognitive decline. This is a particular point of contention for aducanumab, an antibody drug that is now on the market for around US$56,000 per year, despite prematurely halted phase III trials and the messy data set that was submitted for approval. © 2021 Springer Nature Limited

Keyword: Alzheimers
Link ID: 28077 - Posted: 11.17.2021