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

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By Carl Zimmer Sign up for Science Times Get stories that capture the wonders of nature, the cosmos and the human body. Get it sent to your inbox. For half a billion years or so, our ancestors sprouted tails. As fish, they used their tails to swim through the Cambrian seas. Much later, when they evolved into primates, their tails helped them stay balanced as they raced from branch to branch through Eocene jungles. But then, roughly 25 million years ago, the tails disappeared. Charles Darwin first recognized this change in our ancient anatomy. But how and why it happened has remained a mystery. Now a team of scientists in New York say they have pinpointed the genetic mutation that may have erased our tails. When the scientists made this genetic tweak in mice, the animals didn’t grow tails, according to a new study that was posted online last week. This dramatic anatomical change had a profound impact on our evolution. Our ancestors’ tail muscles evolved into a hammock-like mesh across the pelvis. When the ancestors of humans stood up and walked on two legs a few million years ago, that muscular hammock was ready to support the weight of upright organs. Although it’s impossible to definitively prove that this mutation lopped off our ancestors’ tails, “it’s as close to a smoking gun as one could hope for,” said Cedric Feschotte, a geneticist at Cornell who was not involved in the study. Darwin shocked his Victorian audiences by claiming that we descended from primates with tails. He noted that while humans and apes lack a visible tail, they share a tiny set of vertebrae that extend beyond the pelvis — a structure known as the coccyx. “I cannot doubt that it is a rudimentary tail,” he wrote. © 2021 The New York Times Company

Keyword: Evolution; Genes & Behavior
Link ID: 28001 - Posted: 09.22.2021

by Giorgia Guglielmi Severe infections during early childhood are linked to autism — at least in some boys, a new study in mice and people suggests. The findings were published today in Science Advances. Researchers analyzed the health records of millions of children in the United States and found that boys diagnosed with autism are more likely than non-autistic boys to have had an infection requiring medical attention between age 1 and a half and 4. The study also showed that provoking a strong immune response in newborn mice with only one copy of TSC2, a gene tied to autism, leads to social memory problems in adult male rodents. In people, mutations in TSC2 cause tuberous sclerosis, a condition characterized by non-cancerous tumors and skin growths. About half of all people with tuberous sclerosis also have autism. “If the TSC2 mutation was sufficient to cause autism, then everyone with that mutation would have autism — but they don’t,” says senior investigator Alcino Silva, director of the Integrative Center for Learning and Memory at the University of California, Los Angeles. A child’s chances of having autism rise with severe infections in the child or his mother, previous studies show, but not all children who contract serious infections go on to be diagnosed with autism. The new study is the first to examine the relationship between immune activation and a specific genetic variant tied to autism, Silva says. The findings suggest that genetics and severe infection represent a ‘two-hit’ scenario for autism. © 2021 Simons Foundation

Keyword: Autism; Development of the Brain
Link ID: 27996 - Posted: 09.18.2021

Emma Yasinski Some genetic risk factors for alcohol use disorder overlap with those for neurodegenerative diseases like Alzheimer’s, scientists reported in Nature Communications on August 20. The study, which relied on a combination of genetic, transcriptomic, and epigenetic data, also offers insight into the molecular commonalities among these disorders, and their connections to immune disfunction. “By meshing findings from genome wide association studies . . . with gene expression in brain and other tissues, this new study has prioritized genes likely to harbor regulatory variants influencing risk of Alcohol Use Disorder,” writes David Goldman, a neurogenetics researcher at the National Institute on Alcohol Abuse and Alcoholism (NIAAA), in an email to The Scientist. “Several of these genes are also associated with neurodegenerative disorders—an intriguing connection because of alcohol’s ability to prematurely age the brain.” Over the past several years, researchers have published a handful of massive genome-wide association studies (GWAS) studies identifying loci—regions of the genome that can contain 10 or more individual genes—that likely influence a person’s risk of developing an alcohol use disorder (AUD). In a study published two years ago, Manav Kapoor, a neuroscientist and geneticist at the Icahn School of Medicine at Mount Sinai and first author on the new paper, and his team found evidence that the immune system might be overactive in people with AUD, but the finding left him with more questions. The first was whether excessive drinking directly causes immune dysfunction, or if instead some people’s genetic makeup puts them at risk for both simultaneously. The second was which of the dozen or so genes at each previous GWAS-identified locus actually influences drinking behaviors. Lastly, he wanted to know if there is a genetic difference between people who consume higher numbers of alcoholic beverages per week but are not diagnosed with AUD and those who have received the diagnosis. © 1986–2021 The Scientist.

Keyword: Alzheimers; Genes & Behavior
Link ID: 27995 - Posted: 09.18.2021

by Rachel Zamzow The X chromosome holds stronger-than-expected genetic sway over the structure of several brain regions, a new study finds. The X-linked genes that may underlie this oversized influence have ties to autism and intellectual disability. “There were already hints that the X chromosome was likely to be conspicuous, with how involved it is with the brain,” says lead investigator Armin Raznahan, chief of the section on developmental neurogenomics at the U.S. National Institute of Mental Health. Many X chromosome genes — including those at the root of several autism-related conditions, such as fragile X syndrome and Rett syndrome — are expressed in the brain, for example. But the new findings suggest that the X chromosome, despite containing only 5 percent of the human genome, has a privileged role in shaping the brain — one that may be particularly relevant to developmental conditions. What’s more, this influence may be stronger in men than in women, the study shows. “What they’re showing is X is fundamentally different,” says David Glahn, professor of psychology at Harvard University, who was not involved in the new study. “It’s off the scale.” Research over the past decade has linked genetic variation to shifts in brain features, such as overall size or patterns of connectivity between regions, Glahn says. But “the X chromosome and the Y chromosome are fundamentally understudied,” because including them requires extra analytical legwork, he says. © 2021 Simons Foundation

Keyword: Development of the Brain; Genes & Behavior
Link ID: 27992 - Posted: 09.15.2021

Andrew Gregory Health editor Millions of people with eye conditions including age-related macular degeneration, cataracts and diabetes-related eye disease have an increased risk of developing dementia, new research shows. Vision impairment can be one of the first signs of the disease, which is predicted to affect more than 130 million people worldwide by 2050. Previous research has suggested there could be a link between eye conditions that cause vision impairment, and cognitive impairment. However, the incidence of these conditions increases with age, as do systemic conditions such as diabetes, high blood pressure, heart disease, depression and stroke, which are all accepted risk factors for dementia. That meant it was unclear whether eye conditions were linked with a higher incidence of dementia independently of systemic conditions. Now researchers have found that age-related macular degeneration, cataracts and diabetes-related eye disease are independently associated with increased risk of dementia, according to a new study published in the British Journal of Ophthalmology. The research examined data from 12,364 British adults aged 55 to 73, who were taking part in the UK Biobank study. They were assessed in 2006 and again in 2010 with their health information tracked until early 2021. More than 2,300 cases of dementia were documented, according to the international team of experts led by academics from the Guangdong Eye Institute in China. After assessing health data, researchers found those with age-related macular degeneration had a 26% increased risk of developing dementia. Those with cataracts had an 11% increased risk and people with diabetes-related eye disease had a 61% heightened risk. Glaucoma was not linked to a significant increase in risk. © 2021 Guardian News & Media Limited

Keyword: Alzheimers; Vision
Link ID: 27990 - Posted: 09.15.2021

Jon Hamilton The visual impairment known as "lazy eye" can be treated in kids by covering their other eye with a patch. Scientists may have found a way to treat adults with the condition using a pufferfish toxin. MARY LOUISE KELLY, HOST: Children who develop the visual impairment often called lazy eye can be treated by covering their other eye with a patch. Now researchers think they have found a way to treat adults using a toxin found in deadly puffer fish. The approach has only been tried in animals so far, but NPR's Jon Hamilton reports the results are encouraging. JON HAMILTON, BYLINE: A lazy eye isn't really lazy. The term refers to amblyopia, a medical condition that occurs when the brain starts ignoring the signals from one eye. Existing treatments restrict use of the strong eye in order to force the brain to pay attention to the weak one. But Mark Bear, a neuroscientist at MIT, says that approach has limits. MARK BEAR: There are a very significant number of adults with amblyopia where the treatment either didn't work or it was initiated too late. HAMILTON: After a critical period that ends at about age 10, the connections between eye and brain become less malleable. They lose what scientists call plasticity. So for several decades, Bear and a team of researchers have been trying to answer a question. BEAR: How can we rejuvenate these connections? How can they be brought back online? HAMILTON: To find out, Bear's team studied adults with amblyopia who lost their strong eye to a disease or an injury. © 2021 npr

Keyword: Vision; Development of the Brain
Link ID: 27989 - Posted: 09.15.2021

James M. Gaines Young macaques given the popular antidepressant fluoxetine for two years had lower levels of certain fatty acids and other lipids in their brains than ones not given the drug, finds a recent study (July 28) in International Journal of Molecular Sciences. The findings may help explain why younger people sometimes experience adverse side effects when taking the drug. Fluoxetine, often sold under the brand name Prozac, is a prescription medication that can be given to adults as well as children as young as 7 or 8 years old. But there’s not good literature on the long-term impact of fluoxetine and other psychoactive drugs that we use to treat adult symptoms in the young brain, says Bita Moghaddam, a behavioral neuroscientist at Oregon Health & Science University who was not involved in the study, “so [it] was really nice to see that there is this level of focus.” While genes and neurotransmitters may get the lion’s share of the attention in neuroscience research, brains are mostly made of up fats and other lipids. But lipids, it turns out, can be hard to study. So, when University of California Davis brain scientist Mari Golub and her colleagues wanted to know what was going on with the fats in the brains of the monkeys they were studying, they reached out to the brain lab at the Skoltech Institute of Science and Technology in Moscow where Anna Tkachev—the lead author on the new paper—works. “We happen to specialize in lipids in particular,” says Tkachev. For years, Golub and her colleagues had been using macaques to investigate the effects of fluoxetine. The antidepressant can be an effective treatment for maladies such as depression and obsessive-compulsive disorder. However, some studies suggest that the drug can occasionally cause serious, long-term side effects, and perhaps counter-intuitively for an antidepressant, it’s been linked to an increased risk of suicidal thinking and behavior, particularly in young people. © 1986–2021 The Scientist.

Keyword: Depression; Development of the Brain
Link ID: 27988 - Posted: 09.13.2021

By Carolyn Wilke Babies may laugh like some apes a few months after birth before transitioning to chuckling more like human adults, a new study finds. Laughter links humans to great apes, our evolutionary kin (SN: 6/4/09). Human adults tend to laugh while exhaling (SN: 6/10/15), but chimpanzees and bonobos mainly laugh in two ways. One is like panting, with sound produced on both in and out breaths, and the other has outbursts occurring on exhales, like human adults. Less is known about how human babies laugh. So Mariska Kret, a cognitive psychologist at Leiden University in the Netherlands, and colleagues scoured the internet for videos with laughing 3- to 18-month-olds, and asked 15 speech sound specialists and thousands of novices to judge the babies’ laughs. After evaluating dozens of short audio clips, experts and nonexperts alike found that younger infants laughed during inhalation and exhalation, while older infants laughed more on the exhale. That finding suggests that infants’ laughter becomes less apelike with age, the researchers report in the September Biology Letters. Humans start to laugh around 3 months of age, but early on, “it hasn’t reached its full potential,” Kret says. Both babies’ maturing vocal tracts and their social interactions may influence the development of the sounds, the researchers say.

Keyword: Language; Evolution
Link ID: 27983 - Posted: 09.11.2021

by Niko McCarty Brain scans from 16 mouse models of autism reveal at least four distinct patterns of brain activity, a new study suggests. The findings lend fresh support to the popular idea that autism is associated with a range of brain ‘signatures.’ Telltale neural signatures of autism have long proved elusive, with functional magnetic resonance imaging (fMRI) and other brain scanning technologies shouldering the blame for scattered and inconsistent results. “One big question is whether there’s a single signature of dysfunction in the brain of people with autism. And many people consider that to be, like, something that there must be,” says study investigator Alessandro Gozzi, senior researcher at the Istituto Italiano di Tecnologia in Rovereto, Italy. “If we’ve not found it yet, the blame must be on the method: fMRI.” The method gauges small changes in blood flow and oxygenation as an indirect measure of brain activity. For the new study, published in Molecular Psychiatry in August, Gozzi and his colleagues used fMRI to study brain connectivity patterns — or which brain regions ‘talk’ to each other, and to what degree. Brain regions are considered to be in communication if they have synchronous oscillations in blood flow. To tackle the question of reproducibility in fMRI, the researchers conducted their analysis in mice, anesthetizing the animals and fixing their heads in place to prevent any motion that could perturb brain signals. “We moved to a model organism where we can control, in exquisite detail, many of the factors that are considered to be at the basis of this variability, this unreliability in imaging,” Gozzi says. © 2021 Simons Foundation

Keyword: Autism; Brain imaging
Link ID: 27982 - Posted: 09.11.2021

by Angie Voyles Askham Male mice exposed to atypically low levels of a placental hormone in the womb have altered brain development and asocial behaviors, according to a new study. The findings may help explain why preterm birth — which coincides with a deficiency in hormones made by the placenta — is linked to an increased likelihood of having autism. The hormone, called allopregnanolone, crosses the blood-brain barrier, binds to receptors for the chemical messenger gamma-aminobutyric acid (GABA) and helps regulate aspects of neurodevelopment, including the growth of new neurons. Its levels typically peak in the fetus during the second half of gestation. In the new study, researchers engineered a mouse model to have low fetal levels of allopregnanolone, mimicking the hormone’s loss due to preterm birth or placental dysfunction. The male mice in particular have structural changes in the cerebellum, a brain region known for balance and motor control, and exhibit more pronounced autism-like traits than control mice or female model mice. The new model “has a good translational potential for understanding the underlying mechanisms of sex differences in neurodevelopmental conditions such as autism,” says Amanda Kentner, professor of psychology at the Massachusetts College of Pharmacy and Health Sciences in Boston, who was not involved in the work. Injecting a pregnant mouse with allopregnanolone partway through gestation decreased the likelihood that its offspring would have autism-like traits, the researchers found. © 2021 Simons Foundation

Keyword: Autism; Development of the Brain
Link ID: 27977 - Posted: 09.04.2021

By Laura Sanders Clumps of brain cells grown from the stem cells of two people with a neurological syndrome show signs of the disorder. The results, published August 23 in Nature Neuroscience, suggest that personalized brain organoids could be powerful tools to understand complex disorders. Researchers are eager to create brain organoids, human stem cells coaxed into becoming 3-D blobs of brain cells, because of their ability to mimic human brains in the lab (SN: 2/20/18). In the current study, researchers grew two kinds of brain organoids. One kind, grown from healthy people’s stem cells, produced complex electrical activity that echoed the brain waves a full-sized brain makes. These waves, created by the coordinated firing of many nerve cells, are part of how the brain keeps information moving (SN: 3/13/18). The researchers also grew organoids using cells from a 25-year-old woman and a 5-year-old girl with Rett syndrome, a developmental disorder marked by seizures, autism and developmental lags. Rett syndrome is thought to be caused by changes in a gene called MECP2, mutations that the lab-grown organoids carried as well. These organoids looked like those grown from healthy people, but behaved differently in some ways. Their nerve cells fired off signals that were too synchronized and less varied. Some of the brain waves these organoids produced are reminiscent of a brain having a seizure, in which a bolus of electrical activity scrambles normal brain business. © Society for Science & the Public 2000–2021.

Keyword: Development of the Brain
Link ID: 27976 - Posted: 09.04.2021

Jordana Cepelewicz Faced with a threat, the brain has to act fast, its neurons making new connections to learn what might spell the difference between life and death. But in its response, the brain also raises the stakes: As an unsettling recent discovery shows, to express learning and memory genes more quickly, brain cells snap their DNA into pieces at many key points, and then rebuild their fractured genome later. The finding doesn’t just provide insights into the nature of the brain’s plasticity. It also demonstrates that DNA breakage may be a routine and important part of normal cellular processes — which has implications for how scientists think about aging and disease, and how they approach genomic events they’ve typically written off as merely bad luck. The discovery is all the more surprising because DNA double-strand breaks, in which both rails of the helical ladder get cut at the same position along the genome, are a particularly dangerous kind of genetic damage associated with cancer, neurodegeneration and aging. It’s more difficult for cells to repair double-strand breaks than other kinds of DNA damage because there isn’t an intact “template” left to guide the reattachment of the strands. Yet it’s also long been recognized that DNA breakage sometimes plays a constructive role, too. When cells are dividing, double-strand breaks allow for the normal process of genetic recombination between chromosomes. In the developing immune system, they enable pieces of DNA to recombine and generate a diverse repertoire of antibodies. Double-strand breaks have also been implicated in neuronal development and in helping turn certain genes on. Still, those functions have seemed like exceptions to the rule that double-strand breaks are accidental and unwelcome. All Rights Reserved © 2021

Keyword: Learning & Memory; Epigenetics
Link ID: 27975 - Posted: 09.01.2021

by Peter Hess Some mutations in SCN2A, a gene reliably linked to autism, change social behaviors in mice by dampening the electrical activity of their neurons, according to a new study. SCN2A encodes a sodium channel that helps neurons send electrical signals. So-called ‘gain-of-function’ mutations make the channel hyperactive and can lead to epilepsy, whereas ‘loss-of-function’ mutations diminish its activity and are typically associated with autism. The mice in the new study carry the latter type and, as a result, have fewer functioning sodium channels than usual. The animals also react to unfamiliar mice in an atypical way, mirroring social behaviors seen in autistic people with similar SCN2A mutations. “We’re in the position of really connecting a single mutation, or at least a defect in the channel, to the behavior,” says lead investigator Geoffrey Pitt, professor of medicine at Weill Cornell Medicine in New York. “The message that our paper shows is that loss-of-function mutations and decreased sodium current can lead to behaviors.” This study confirms previous work showing that autism-linked mutations in SCN2A dampen channel activity in neurons, and further connects the loss-of-function mutations to clear changes in behavior, says Kevin Bender, associate professor of neurology at the University of California San Francisco, who was not involved in the work. “The behavioral results were actually some of the most robust that I’ve seen in this field to date.” © 2021 Simons Foundation

Keyword: Autism
Link ID: 27968 - Posted: 08.28.2021

By Daniel R. George, Peter J. Whitehouse Aducanumab, marketed as “Aduhelm,” is an antiamyloid monoclonal antibody and the latest in a procession of such drugs to be tested against Alzheimer’s disease. Over the last several decades, billions have been spent targeting the amyloid that clumps together to form the neuritic plaques first documented by German psychiatrist Alois Alzheimer in 1906. This class of drugs has reduced amyloid aggregation; however, since 2000, there has been a virtual 100 percent fail rate in clinical trials, with some therapies actually worsening patient outcomes. In 2019, Aducanumab failed in a futility analysis of two pooled phase III randomized controlled trials, but was later claimed to have yielded a small benefit for a subset of patients in a high-dosage group. The biologic was granted accelerated approval by the FDA based not on its clinical benefit but rather on its ability to lower amyloid on PET scans. Biogen immediately priced the treatment at $56,000 annually, making it potentially one of the most expensive drugs in the country’s history. This predicament is all the more surreal because—in the absence of more decisive evidence—there is no adequate proof that the drug actually clinically benefits people who take it. Aducanumab, which is delivered intravenously, was observed to cause brain swelling or bleeding in 40 percent of high-dose participants as well as higher rates of headache, falls and diarrhea. The FDA’s decision flew in the face of a near-consensus recommendation from its advisory committee not to approve. Three members of that committee have since resigned; several federal investigations have been launched to examine the close relationship between Biogen and the FDA; and the Department of Veterans Affairs and numerous private insurers and high-profile hospital systems have already signaled they want nothing to do with the drug. Meanwhile, Biogen has launched a Web site and comprehensive marketing campaign called “It’s Time,” quizzing potential consumers on their memory loss and ultimately guiding them to experts, imaging and/or infusion sites. © 2021 Scientific American,

Keyword: Alzheimers
Link ID: 27967 - Posted: 08.28.2021

Emma Yasinski Some genetic risk factors for alcohol use disorder overlap with those for neurodegenerative diseases like Alzheimer’s, scientists reported in Nature Communications on August 20. The study, which relied on a combination of genetic, transcriptomic, and epigenetic data, also offers insight into the molecular commonalities among these disorders, and their connections to immune disfunction. “By meshing findings from genome wide association studies . . . with gene expression in brain and other tissues, this new study has prioritized genes likely to harbor regulatory variants influencing risk of Alcohol Use Disorder,” writes David Goldman, a neurogenetics researcher at the National Institute on Alcohol Abuse and Alcoholism (NIAAA), in an email to The Scientist. “Several of these genes are also associated with neurodegenerative disorders—an intriguing connection because of alcohol’s ability to prematurely age the brain.” Over the past several years, researchers have published a handful of massive genome-wide association studies (GWAS) studies identifying loci—regions of the genome that can contain 10 or more individual genes—that likely influence a person’s risk of developing an alcohol use disorder (AUD). In a study published two years ago, Manav Kapoor, a neuroscientist and geneticist at the Icahn School of Medicine at Mount Sinai and first author on the new paper, and his team found evidence that the immune system might be overactive in people with AUD, but the finding left him with more questions. The first was whether excessive drinking directly causes immune dysfunction, or if instead some people’s genetic makeup puts them at risk for both simultaneously. © 1986–2021 The Scientist.

Keyword: Alzheimers; Genes & Behavior
Link ID: 27966 - Posted: 08.28.2021

By Paula Span Learning your odds of eventually developing dementia — a pressing concern for many, especially those with a family history of it — requires medical testing and counseling. But what if everyday behavior, like overlooking a couple of credit card payments or habitually braking while driving, could foretell your risk? A spate of experiments is underway to explore that possibility, reflecting the growing awareness that the pathologies underlying dementia can begin years or even decades before symptoms emerge. “Early detection is key for intervention, at the stage when that would be most effective,” said Sayeh Bayat, the lead author of a driving study funded by the National Institutes of Health and conducted at Washington University in St. Louis. Such efforts could help identify potential volunteers for clinical trials, researchers say, and help protect older people against financial abuse and other dangers. In recent years, many once-promising dementia drugs, particularly for Alzheimer’s disease, have failed in trials. One possible reason, researchers say, is that the drugs are administered too late to be helpful. Identifying risks earlier, when the brain has sustained less damage, could create a pool of potential participants with “preclinical” Alzheimer’s disease, who could then test preventive measures or treatments. It could also bring improvements in daily life. “We could support people’s ability to drive longer, and have safer streets for everyone,” Ms. Bayat offered as an example. © 2021 The New York Times Company

Keyword: Alzheimers; Learning & Memory
Link ID: 27959 - Posted: 08.25.2021

by Peter Hess Children born to mothers who take antipsychotic medications during pregnancy do not have elevated odds of autism or attention deficit hyperactivity disorder (ADHD), nor are they more likely to be born preterm or underweight, according to a study released this past Monday in JAMA Internal Medicine. Some women with schizophrenia, Tourette syndrome or bipolar disorder take antipsychotic drugs, such as aripiprazole, haloperidol or risperidone. Clinicians have long debated whether women should discontinue these medications during pregnancy out of concern for the drugs’ effects on the developing fetus. But children born to mothers who take antipsychotics during pregnancy and to those who do not take them have similar outcomes, the new work shows. “Our findings do not support a recommendation for women to discontinue their regular antipsychotic treatment during pregnancy,” says senior investigator Kenneth Man, research fellow at the University College London School of Pharmacy in the United Kingdom. Prescribing antipsychotics during pregnancy can help prevent potentially dangerous psychotic episodes and ensure that an expectant mother can take care of herself, says Mady Hornig, associate professor of epidemiology at Columbia University, who was not involved in the study. “We certainly don’t want to be cavalier about the use of any medication during pregnancy, but one also wants to balance out the implications of not treating.” © 2021 Simons Foundation

Keyword: Schizophrenia; Development of the Brain
Link ID: 27954 - Posted: 08.21.2021

Ruth Williams In the days before a newborn mouse opens its peepers, nerve impulses that have been sweeping randomly across the retina since birth start flowing consistently in one direction, according to a paper published in Science today (July 22). This specific pattern has a critical purpose, the authors say, helping to establish the brain circuitry to be used later in motion detection. “I love this paper. It blew my mind,” says David Berson, who studies the visual system at Brown University and was not involved in the research. “What it implies is that evolution has built a visual system that can simulate the patterns of activity that it will see later when it’s fully mature and the eyes are open, and that [the simulated pattern] in turn shapes the development of the nervous system in a way that makes it better adapted to seeing those patterns. . . . That’s staggering.” The thread of this concept may be looped, but to unravel it, Berson says, it helps to think of the mammalian visual system, or really any neuronal circuitry, as being formed by a combination of evolution and life experiences—in short, nature and nurture. We might expect that life’s visual experiences, the nurture part, would begin when the eyes open. But, much like a human baby in the womb practices breathing and sucking without ever having experienced air or breastfeeding, the eyes of newborn mice appear to practice seeing before they can actually see. Motion detection is important enough to mouse survival that evolution has selected for gene variants that set up this prevision training, says Berson. © 1986–2021 The Scientist.

Keyword: Vision; Development of the Brain
Link ID: 27950 - Posted: 08.18.2021

Nicola Davis Science correspondent It’s been used to detect eye diseases, make medical diagnoses, and spot early signs of oesophageal cancer. Now it has been claimed artificial intelligence may be able to diagnose dementia from just one brain scan, with researchers starting a trial to test the approach. The team behind the AI tool say the hope is that it will lead to earlier diagnoses, which could improve outcomes for patients, while it may also help to shed light on their prognoses. Dr Timothy Rittman, a senior clinical research associate and consultant neurologist at the University of Cambridge, who is leading the study, told the BBC the AI system is a “fantastic development”. “These set of diseases are really devastating for people,” he said. “So when I am delivering this information to a patient, anything I can do to be more confident about the diagnosis, to give them more information about the likely progression of the disease to help them plan their lives is a great thing to be able to do.” It is expected that in the first year of the trial the AI system, which uses algorithms to detect patterns in brain scans, will be tested in a “real-world” clinical setting on about 500 patients at Addenbrooke’s hospital in Cambridge and other memory clinics across the country. “If we intervene early, the treatments can kick in early and slow down the progression of the disease and at the same time avoid more damage,” Prof Zoe Kourtzi, of Cambridge University and a fellow of national centre for AI and data science the Alan Turing Institute, told the BBC. “And it’s likely that symptoms occur much later in life or may never occur.” © 2021 Guardian News & Media Limited

Keyword: Alzheimers; Development of the Brain
Link ID: 27941 - Posted: 08.11.2021

Jon Hamilton Scientists are working to develop new treatments for Alzheimer's disease by looking beyond amyloid plaques, which have been the focus of most Alzheimer's drug development in the past 20 years. Science Photo Library — ZEPHYR./Getty Images Immune cells, toxic protein tangles and brain waves are among the targets of future Alzheimer's treatments, scientists say. These approaches are noteworthy because they do not directly attack the sticky amyloid plaques in the brain that are a hallmark of Alzheimer's. The plaques have been the focus of most Alzheimer's drug development in the past 20 years. And the drug Aduhelm was given conditional approval by the Food and Drug Administration in June based primarily on the medication's ability to remove amyloid from the brain. But many researchers believe amyloid drugs alone can't stop Alzheimer's. "The field has been moving beyond amyloid for many years now," says Malú Gámez Tansey, co-director of the Center for Translational Research in Neurodegenerative Disease at the University of Florida. Tansey and a number of other researchers offered a wide range of alternative strategies at the Alzheimer's Association International Conference in Denver last month. Here are three of the most promising: © 2021 npr

Keyword: Alzheimers; Development of the Brain
Link ID: 27940 - Posted: 08.11.2021