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

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Abby Olena The smallest terrestrial mammal, the Etruscan shrew (Suncus etruscus), is about as big as a person’s thumb and no heavier than a couple of paper clips. To have enough energy to survive, it must eat eight or more times its body weight daily and therefore doesn’t hibernate. Instead, according to a study published November 30 in PNAS, in winter, these shrews lose 28 percent of the volume from their somatosensory cortex, which likely helps them conserve energy. “This phenomenon of an animal that is not a hibernator still implementing these energy saving strategies is just stunning,” says Christine Schwartz, a neuroscientist who studies hibernation at the University of Wisconsin La Crosse and was not involved in the work. Scientists have shown before that red-toothed shrews, which belong to a group separate from the Etruscan shrew, are born and grow to their full body size in a single summer. Then in autumn, they start to shrink all over—in their spine length, skull, brain, bones, organs such as the liver, and body weight—reaching their smallest size in the winter. Somewhere around February, they start to grow again and reach a second size peak as they sexually mature in the spring. Then they reproduce just once, and, shortly after, die. This cycle is known as Dehnel’s phenomenon. When Saikat Ray was a graduate student in Michael Brecht's lab at the Bernstein Center for Computational Neuroscience in Berlin, he was curious to see if Dehnel’s phenomenon also exists in white-toothed shrews, the subfamily that includes the Etruscan shrew. They already had a colony of Etruscan shrews in the lab, says Ray, who is now a postdoc in Nachum Ulanovsky’s lab at the Weizmann Institute in Israel, because the animals’ tiny brains are a helpful model system for studying more of the brain at once than are the brains of larger mammals, such as mice or rats. © 1986–2020 The Scientist.

Keyword: Neurogenesis
Link ID: 27602 - Posted: 12.05.2020

by Laura Dattaro Autistic boys with large brains in early childhood still have large brains in adolescence, according to a new study. Autistic girls, too, have brains that grow differently from those of their non-autistic peers. The findings challenge the long-standing idea that brain enlargement in autism is temporary. Previous studies indicated that young children on the spectrum have larger brains than their non-autistic peers but older people with autism do not. To explain the difference, researchers speculated that a pruning process follows early brain overgrowth. But the changes are a mirage, the researchers behind the new study say: Because having a large brain is associated with a low intelligence quotient (IQ) and severe autism traits, and because older children with such characteristics are often excluded from imaging studies, the prior results reflect only a lack of older participants with large brains. “This whole idea of this early overgrowth followed by normalization is just an artifact of sampling bias,” says lead investigator Christine Wu Nordahl, associate professor of psychiatry and behavioral sciences at the University of California, Davis MIND Institute. “It was sort of like, ‘Wow, why didn’t we ever think about this before?’ But it’s pretty clear that that’s what’s happening.” Autistic and non-autistic children also show different development patterns in their white matter — fibers that connect regions of the brain — in early childhood, a second study from Nordahl’s group shows. Some of the differences correlate with changes in the children’s autism traits over time. © 2020 Simons Foundation

Keyword: Autism; Brain imaging
Link ID: 27598 - Posted: 11.30.2020

by Peter Hess / Mutations in a top autism gene called SYNGAP1 slow the rate at which zebrafish digest food and pass waste. The findings may explain why some people with SYNGAP1 mutations have gastrointestinal (GI) problems. Researchers presented the unpublished work on Tuesday and Wednesday at the 2020 International SYNGAP1 Scientific Conference, which took place virtually because of the coronavirus pandemic. They also began recruiting people with SYNGAP1 mutations at the meeting for an ongoing study of gut function. “It’s been in the literature, this link between GI symptoms and [autism], for a long time, with not a lot of progress on the mechanisms,” says lead researcher Julia Dallman, associate professor of biology at the University of Miami in Florida, who presented the findings on Wednesday. In the brain, SYNGAP1 functions mainly at synapses, or the junctions between neurons, and helps the cells exchange chemical messages. Mutations in the gene are strongly linked to autism, seizures, intellectual disability and sleep problems. Prompted by families’ anecdotal reports of constipation, reflux and overeating in people with SYNGAP1 mutations, Dallman and her colleagues decided to explore the gene’s role in the gut. The young zebrafish’s transparent skin allowed the researchers to trace the movement of microscopic fluorescent beads — mixed into the fish’s food — through the gut. In this way, they measured how quickly and how strongly the digestive tract moves food and waste. © 2020 Simons Foundation

Keyword: Autism
Link ID: 27590 - Posted: 11.21.2020

Jon Hamilton During deep sleep, the brain appears to wash away waste products that increase the risk for Alzheimer's disease. A host of new research studies suggest that this stage of sleep — when dreams are rare and the brain follows a slow, steady beat – can help reduce levels of beta-amyloid and tau, two hallmarks of the disease. "There is something about this deep sleep that is helping protect you," says Matthew Walker, a professor of neuroscience and psychology at the University of California, Berkeley. The research comes after decades of observations linking poor sleep to long-term problems with memory and thinking, Walker says. "We are now learning that there is a significant relationship between sleep and dementia, particularly Alzheimer's disease." The strongest evidence involves deep sleep, he says. That's when body temperature drops and the brain begins to produce slow, rhythmic electrical waves. So Walker and a team of scientists set out to answer a question: "Can I look into your future and can I accurately estimate how much beta-amyloid you're going to accumulate over the next two years, the next four years, the next six years, simply on the basis of your sleep tonight?" To find out, Walker's team studied 32 people in their 70s who had taken part in a sleep study that looked for the slow electrical waves that signal deep sleep. None of the participants had memory problems. the brain cells of people with Alzheimer's. © 2020 npr

Keyword: Sleep; Alzheimers
Link ID: 27585 - Posted: 11.18.2020

by Angie Voyles Askham Editing DNA in embryonic and newborn mice by using CRISPR technology can override mutations underlying Angelman syndrome and prevent many of the condition’s traits, according to a new study1. The effects last for at least 17 months and may be permanent, the researchers say. “It’s very exciting,” says Steven Kushner, professor of psychiatry at Columbia University, who was not involved in the study. Angelman syndrome usually stems from a mutation in or deletion of the UBE3A gene. People have two copies of the gene — one from each parent — but typically only the one passed down from the mother is active in neurons. Mutations that stymie that copy can lead to a lack of UBE3A protein in the brain, causing the syndrome’s core traits: developmental delays, motor dysfunction, speech impairments, seizures and, often, autism. These traits improve in response to treatments that activate the silent yet intact paternal copy of UBE3A and boost production of the protein in Angelman syndrome model mice2,3. But these treatments wear off over time, requiring repeated injections into the spinal fluid or brain. The new therapy is effective after only two doses, says lead researcher Mark Zylka, professor of cell biology and physiology at the University of North Carolina at Chapel Hill. The strategy uses the enzyme CRISPR-Cas9 to cut and edit DNA encoding an ‘antisense RNA’ molecule that ordinarily serves to block production of UBE3A protein from the paternal copy of the gene. The technique also rouses the silent paternal copy of the gene in cultured human neurons, suggesting that it might work in people. © 2020 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 27575 - Posted: 11.10.2020

By James Gorman Dogs go through stages in their life, just as people do, as is obvious to anyone who has watched their stiff-legged, white-muzzled companion rouse themselves to go for one more walk. Poets from Homer to Pablo Neruda have taken notice. As have folk singers and story tellers. Now science is taking a turn, in the hope that research on how dogs grow and age will help us understand how humans age. And, like the poets before them, scientists are finding parallels between the two species. Their research so far shows that dogs are similar to us in important ways, like how they act during adolescence and old age, and what happens in their DNA as they get older. They may be what scientists call a “model” for human aging, a species that we can study to learn more about how we age and perhaps how to age better. Most recently, researchers in Vienna have found that dogs’ personalities change over time. They seem to mellow in the same way that most humans do. The most intriguing part of this study is that like people, some dogs are just born old, which is to say, relatively steady and mature, the kind of pup that just seems ready for a Mr. Rogers cardigan. “That’s professor Spot, to you, thank you, and could we be a little neater when we pour kibble into my dish?” Mind you, the Vienna study dogs were all Border collies, so I’m a little surprised that any of them were mature. That would suggest a certain calm, a willingness to tilt the head and muse that doesn’t seem to fit the breed, with its desperate desire to be constantly chasing sheep, geese, children or Frisbees. Another recent paper came to the disturbing conclusion that the calculus of seven dog years for every human year isn’t accurate. To calculate dog years, you must now multiply the natural logarithm of a dog’s age in human years by 16 and then add 31. Is that clear? It’s actually not as hard as it sounds, as long as you have a calculator or internet access. For example the natural log of 6 is 1.8, roughly, which, multiplied by 16 is about 29, which, plus 31, is 60. OK, it’s not that easy, even with the internet. © 2020 The New York Times Company

Keyword: Development of the Brain; Evolution
Link ID: 27574 - Posted: 11.10.2020

By Linda Searing The “baby blues” that women can experience after giving birth usually go away within a week or two, but it now appears that more severe depressive symptoms, known as postpartum depression, may affect some new mothers for at least three years. Research from the National Institutes of Health, which tracked 4,866 women for three years after childbirth, found that about 25 percent of the women reported moderate to high levels of depressive symptoms at some point and that the remaining 75 percent experienced low-level depressive symptoms throughout the study. The “baby blues” typically include such symptoms as mood swings, anxiety and trouble sleeping, whereas postpartum depression symptoms — generally more intense and longer lasting — may include excessive crying, overwhelming fatigue, loss of appetite, difficulty bonding with the baby, feelings of inadequacy, hopelessness and more. The NIH research, published in the journal Pediatrics, encourages pediatricians to screen their tiny patients’ mothers for depressive symptoms during the children’s regular checkups, noting that “mothers’ mental health is critical to children’s well-being and development.” The researchers note that maternal depression increases a child’s risk for cognitive, emotional and behavioral problems. Getting treatment, however, should not only ease a mother’s symptoms but also improve her child’s odds for a favorable developmental outcome.

Keyword: Depression; Development of the Brain
Link ID: 27573 - Posted: 11.10.2020

By Giorgia Guglielmi, Spectrum A small clinical trial of a gene therapy for Angelman syndrome—a rare genetic condition related to autism—is on hold after two participants temporarily lost the ability to walk. The safety issue is important to resolve, experts say, given that the therapy otherwise appears to be effective, and the trial could guide treatment strategies for similar brain conditions. Biopharmaceutical company Ultragenyx in Novato, California, in collaboration with Florida-based biotech startup GeneTx, launched the trial in February to assess the safety of a therapy for Angelman syndrome, a neurodevelopmental condition characterized by intellectual disability, balance and motor problems, seizures, sleep problems and, in some cases, autism. Angelman syndrome results from the mutation or absence of a gene called UBE3A. People inherit two copies of UBE3A. Typically, only the maternal copy is active in neurons and the paternal copy is silent. But in people with Angelman syndrome, the maternal copy is mutated or missing, so their brain cells express no active UBE3A protein. The drug developed by Ultragenyx and GeneTx, called GTX-102, is a short snippet of RNA called an antisense oligonucleotide that activates the paternal copy of UBE3A and aims to restore the protein to typical levels. Three other companies—Roche, Biogen, and Ionis—are pursuing similar therapies for the syndrome. On 26 October, Ultragenyx and GeneTx reported that the clinical trial had enrolled five individuals with Angelman syndrome, aged 5 to 15. The plan had been to administer to each participant a dose of GTX-102 once a month over four months. Researchers injected the drug directly into the nutrient-rich solution that envelops the brain and spinal cord through a site in the lower back. © 2020 American Association for the Advancement of Science

Keyword: Autism
Link ID: 27572 - Posted: 11.07.2020

Alison Abbott Two years ago, immunologist and medical-publishing entrepreneur Leslie Norins offered to award US$1 million of his own money to any scientist who could prove that Alzheimer’s disease was caused by a germ. The theory that an infection might cause this form of dementia has been rumbling for decades on the fringes of neuroscience research. The majority of Alzheimer’s researchers, backed by a huge volume of evidence, think instead that the key culprits are sticky molecules in the brain called amyloids, which clump into plaques and cause inflammation, killing neurons. Norins wanted to reward work that would make the infection idea more persuasive. The amyloid hypothesis has become “the one acceptable and supportable belief of the Established Church of Conventional Wisdom”, says Norins. “The few pioneers who did look at microbes and published papers were ridiculed or ignored.” In large part, this was because some early proponents of the infection theory saw it as a replacement for the amyloid hypothesis. But some recent research has provided intriguing hints that the two ideas could fit together — that infection could seed some cases of Alzheimer’s disease by triggering the production of amyloid clumps. The data hint at a radical role for amyloid in neurons. Instead of just being a toxic waste product, amyloid might have an important job of its own: helping to protect the brain from infection. But age or genetics can interrupt the checks and balances in the system, turning amyloid from defender into villain. And that idea suggests new avenues to explore for potential therapies. To test the theory further, scientists are now developing animal models that mimic Alzheimer’s disease more closely. “We are taking the ideas seriously,” says neuroscientist Bart de Strooper, director of the UK Dementia Research Institute at University College London. © 2020 Springer Nature Limited

Keyword: Alzheimers; Neuroimmunology
Link ID: 27571 - Posted: 11.07.2020

By Laura Sanders The fate of a potential new Alzheimer’s drug is still uncertain. Evidence that the drug works isn’t convincing enough for it to be approved, outside experts told the U.S. Food and Drug Administration during a Nov. 6 virtual meeting that at times became contentious. The scientists and clinicians were convened at the request of the FDA to review the evidence for aducanumab, a drug that targets a protein called amyloid-beta that accumulates in the brains of people with Alzheimer’s. The drug is designed to stick to A-beta and stop it from forming larger, more dangerous clumps. That could slow the disease’s progression but not stop or reverse it. When asked whether a key clinical study provided strong evidence that the drug effectively treated Alzheimer’s, eight of 11 experts voted no. One expert voted yes, and two were uncertain. The FDA is not bound to follow the recommendations of the guidance committee, though it has historically done so. If ultimately approved, the drug would be a milestone, says neurologist and neuroscientist Arjun Masurkar of New York University Langone’s Alzheimer’s Disease Research Center. Aducanumab “would be the first therapy that actually targets the underlying disease itself and slows progression.” Developed by the pharmaceutical company Biogen, which is based in Cambridge, Mass., the drug is controversial. That’s because two large clinical trials of aducanumab have yielded different outcomes, one positive and one negative (SN: 12/5/19). The trials were also paused at one point, based on analyses that suggested the drug didn’t work. © Society for Science & the Public 2000–2020.

Keyword: Alzheimers
Link ID: 27570 - Posted: 11.07.2020

By Nicholas Bakalar Some studies have suggested that older people who consistently engage in leisure activities are less likely to develop dementia than those who do not, suggesting that failure to participate in such pastimes could spur cognitive deterioration. A new study suggests another explanation: Failure to participate in leisure activities may be a consequence of dementia, not a cause. Researchers studied 8,280 people, average age 56, who were free of dementia at the start of the analysis. Over the next 18 years, the participants underwent periodic physical and psychological examinations, while researchers tracked their involvement in 13 leisure activities — listening to music, gardening, attending cultural events, playing cards, using a home computer and others. By the end of the project, 360 had developed dementia. The study, in Neurology, controlled for smoking, physical activity, education, coronary heart disease and other health and behavioral characteristics that are tied to dementia risk. They found no association between engagement in leisure activities at age 56 and the incidence of dementia over the following 18 years. The researchers concluded that actively pursuing leisure activities may not provide protection against developing dementia. “Dementia develops over a long period of time, so it’s possible that some changes happen before the diagnosis of dementia,” said the lead author, Andrew Sommerlad, a researcher at University College London. “Elderly people withdrawing from activities that they previously enjoyed may be developing early signs of dementia.” © 2020 The New York Times Company

Keyword: Alzheimers
Link ID: 27563 - Posted: 11.04.2020

By Laura Sanders Nearly 2,000 years ago, a cloud of scorching ash from Mount Vesuvius buried a young man as he lay on a wooden bed. That burning ash quickly cooled, turning some of his brain to glass. This confluence of events in A.D. 79 in the town of Herculaneum, which lay at the western base of the volcano, preserved the usually delicate neural tissue in a durable, glassy form. New scrutiny of this tissue has revealed signs of nerve cells with elaborate tendrils for sending and receiving messages, scientists report October 6 in PLOS ONE. That the young man once possessed these nerve cells, or neurons, is no surprise; human brains are packed with roughly 86 billion neurons (SN: 8/7/19). But samples from ancient brains are sparse. Those that do exist have become a soaplike substance or mummified, says Pier Paolo Petrone, a biologist and forensic anthropologist at the University of Naples Federico II in Italy. But while studying the Herculaneum site, Petrone noticed something dark and shiny inside this man’s skull. He realized that those glassy, black fragments “had to be the remains of the brain.” Petrone and colleagues used scanning electron microscopy to study glassy remains from both the man’s brain and spinal cord. The researchers saw tubular structures as well as cell bodies that were the right sizes and shapes to be neurons. In further analyses, the team found layers of tissue wrapped around tendrils in the brain tissue. This layering appears to be myelin, a fatty substance that speeds signals along nerve fibers. The preserved tissue was “something really astonishing and incredible,” Petrone says, because the conversion of objects to glass, a process called vitrification, is relatively rare in nature. “This is the first ever discovery of ancient human brain remains vitrified by hot ash during a volcanic eruption.” © Society for Science & the Public 2000–2020.

Keyword: Development of the Brain
Link ID: 27558 - Posted: 10.31.2020

R. Douglas Fields As I opened my copy of Science at home one night, an unfamiliar word in the title of a new study caught my eye: dopaminylation. The term refers to the brain chemical dopamine’s ability, in addition to transmitting signals across synapses, to enter a cell’s nucleus and control specific genes. As I read the paper, I realized that it completely upends our understanding of genetics and drug addiction. The intense craving for addictive drugs like alcohol and cocaine may be caused by dopamine controlling genes that alter the brain circuitry underlying addiction. Intriguingly, the results also suggest an answer to why drugs that treat major depression must typically be taken for weeks before they’re effective. I was shocked by the dramatic discovery, but to really understand it, I first had to unlearn some things. “Half of what you learned in college is wrong,” my biology professor, David Lange, once said. “Problem is, we don’t know which half.” How right he was. I was taught to scoff at Jean-Baptiste Lamarck and his theory that traits acquired through life experience could be passed on to the next generation. The silly traditional example is the mama giraffe stretching her neck to reach food high in trees, resulting in baby giraffes with extra-long necks. Then biologists discovered we really can inherit traits our parents acquired in life, without any change to the DNA sequence of our genes. It’s all thanks to a process called epigenetics — a form of gene expression that can be inherited but isn’t actually part of the genetic code. This is where it turns out that brain chemicals like dopamine play a role. All genetic information is encoded in the DNA sequence of our genes, and traits are passed on in the random swapping of genes between egg and sperm that sparks a new life. Genetic information and instructions are coded in a sequence of four different molecules (nucleotides abbreviated A, T, G and C) on the long double-helix strand of DNA. The linear code is quite lengthy (about 6 feet long per human cell), so it’s stored neatly wound around protein bobbins, similar to how magnetic tape is wound around spools in cassette tapes. All Rights Reserved © 2020

Keyword: Drug Abuse; Epigenetics
Link ID: 27555 - Posted: 10.28.2020

Sara Reardon In Alysson Muotri’s laboratory, hundreds of miniature human brains, the size of sesame seeds, float in Petri dishes, sparking with electrical activity. These tiny structures, known as brain organoids, are grown from human stem cells and have become a familiar fixture in many labs that study the properties of the brain. Muotri, a neuroscientist at the University of California, San Diego (UCSD), has found some unusual ways to deploy his. He has connected organoids to walking robots, modified their genomes with Neanderthal genes, launched them into orbit aboard the International Space Station, and used them as models to develop more human-like artificial-intelligence systems. Like many scientists, Muotri has temporarily pivoted to studying COVID-19, using brain organoids to test how drugs perform against the SARS-CoV-2 coronavirus. But one experiment has drawn more scrutiny than the others. In August 2019, Muotri’s group published a paper in Cell Stem Cell reporting the creation of human brain organoids that produced coordinated waves of activity, resembling those seen in premature babies1. The waves continued for months before the team shut the experiment down. This type of brain-wide, coordinated electrical activity is one of the properties of a conscious brain. The team’s finding led ethicists and scientists to raise a host of moral and philosophical questions about whether organoids should be allowed to reach this level of advanced development, whether ‘conscious’ organoids might be entitled to special treatment and rights not afforded to other clumps of cells and the possibility that consciousness could be created from scratch. The idea of bodiless, self-aware brains was already on the minds of many neuroscientists and bioethicists. Just a few months earlier, a team at Yale University in New Haven, Connecticut, announced that it had at least partially restored life to the brains of pigs that had been killed hours earlier. By removing the brains from the pigs’ skulls and infusing them with a chemical cocktail, the researchers revived the neurons’ cellular functions and their ability to transmit electrical signals2.

Keyword: Consciousness; Development of the Brain
Link ID: 27552 - Posted: 10.28.2020

By Nicholas Bakalar Long-term exposure to noise may be linked to an increased risk for Alzheimer’s disease and other forms of dementia. Researchers did periodic interviews with 5,227 people 65 and older participating in a study on aging. They assessed them with standard tests of orientation, memory and language, and tracked average daytime noise levels in their neighborhoods for the five years preceding the cognitive assessments. About 11 percent had Alzheimer’s disease, and 30 percent had mild cognitive impairment, which often progresses to full-blown dementia. Residential noise levels varied widely, from 51 to 78 decibels, or from the level of a relatively quiet suburban neighborhood to that of an urban setting near a busy highway. The study is in Alzheimer’s & Dementia. After controlling for education, race, smoking, alcohol consumption, neighborhood air pollution levels and other factors, they found that each 10 decibel increase in community noise level was associated with a 36 percent higher likelihood of mild cognitive impairment, and a 29 percent increased risk for Alzheimer’s disease. The associations were strongest in poorer neighborhoods, which also had higher noise levels. The reasons for the connection are unknown, but the lead author, Jennifer Weuve, an associate professor of epidemiology at Boston University, suggested that excessive noise can cause sleep deprivation, hearing loss, increased heart rate, constriction of the blood vessels and elevated blood pressure, all of which are associated with an increased risk for dementia. © 2020 The New York Times Company

Keyword: Alzheimers; Hearing
Link ID: 27551 - Posted: 10.28.2020

The plant compound apigenin improved the cognitive and memory deficits usually seen in a mouse model of Down syndrome, according to a study by researchers at the National Institutes of Health and other institutions. Apigenin is found in chamomile flowers, parsley, celery, peppermint and citrus fruits. The researchers fed the compound to pregnant mice carrying fetuses with Down syndrome characteristics and then to the animals after they were born and as they matured. The findings raise the possibility that a treatment to lessen the cognitive deficits seen in Down syndrome could one day be offered to pregnant women whose fetuses have been diagnosed with Down syndrome through prenatal testing. The study appears in the American Journal of Human Genetics. Down syndrome is a set of symptoms resulting from an extra copy or piece of chromosome 21. The intellectual and developmental disabilities accompanying the condition are believed to result from decreased brain growth caused by increased inflammation in the fetal brain. Apigenin is not known to have any toxic effects, and previous studies have indicated that it is an antioxidant that reduces inflammation. Unlike many compounds, it is absorbed through the placenta and the blood brain barrier, the cellular layer that prevents potentially harmful substances from entering the brain. Compared to mice with Down symptoms whose mothers were not fed apigenin, those exposed to the compound showed improvements in tests of developmental milestones and had improvements in spatial and olfactory memory. Tests of gene activity and protein levels showed the apigenin-treated mice had less inflammation and increased blood vessel and nervous system growth. Guedj, F. et al. Apigenin as a candidate prenatal treatment for Trisomy 21: effects in human amniocytes and the Ts1Cje mouse model. American Journal of Human Genetics. 2020.

Keyword: Development of the Brain; Genes & Behavior
Link ID: 27546 - Posted: 10.24.2020

Jon Hamilton Medical research was an early casualty of the COVID-19 pandemic. After cases began emerging worldwide, thousands of clinical trials unrelated to COVID-19 were paused or canceled amid fears that participants would be infected. But now some researchers are finding ways to carry on in spite of the coronavirus. "It's been a struggle of course," says Joshua Grill, who directs the Institute for Memory Impairments and Neurological Disorders at the University of California, Irvine. "But I think there's an imperative for us to find ways to move forward." Grill got a close-up view of the challenge in July when COVID-19 cases were spiking nationwide as he was trying to launch a study. UC Irvine and dozens of other research centers had just begun enrolling participants in the AHEAD study, a global effort that will test whether an investigational drug can slow down the earliest brain changes associated with Alzheimer's disease. Finding individuals willing and able to sign up for this sort of research is difficult even without a pandemic, says Grill, who also co-directs recruitment for the Alzheimer's Clinicals Trial Consortium, funded by the National Institute on Aging. "We're asking people do a lot, including enroll in long studies that require numerous visits," he says, "and in the AHEAD study, taking an investigational drug or placebo that's injected into a vein." Participants will receive either a placebo or a drug called BAN2401, made by Eisai, which is meant to reduce levels of amyloid, a toxic protein associated with Alzheimer's. People in the study will also have positron emission tomography, or PET, scans of their brains to measure changes in amyloid and another toxic protein called tau. © 2020 npr

Keyword: Alzheimers
Link ID: 27545 - Posted: 10.24.2020

By Jeremy Hsu Artificial intelligence could soon help screen for Alzheimer’s disease by analyzing writing. A team from IBM and Pfizer says it has trained AI models to spot early signs of the notoriously stealthy illness by looking at linguistic patterns in word usage. Other researchers have already trained various models to look for signs of cognitive impairments, including Alzheimer’s, by using different types of data, such as brain scans and clinical test results. But the latest work stands out because it used historical information from the multigenerational Framingham Heart Study, which has been tracking the health of more than 14,000 people from three generations since 1948. If the new models’ ability to pick up trends in such data holds up in forward-looking studies of bigger and more diverse populations, researchers say they could predict the development of Alzheimer’s a number of years before symptoms become severe enough for typical diagnostic methods to pick up. And such a screening tool would not require invasive tests or scans. The results of the Pfizer-funded and IBM-run study were published on Thursday in EClinicalMedicine. The new AI models provide “an augmentation to expert practitioners in how you would see some subtle changes earlier in time, before the clinical diagnosis has been achieved,” says Ajay Royyuru, vice president of health care and life sciences research at IBM. “It might actually alert you to some changes that [indicate] you ought to then go do a more complete exam.” To train these models, the researchers used digital transcriptions of handwritten responses from Framingham Heart Study participants who were asked to describe a picture of a woman who is apparently preoccupied with washing dishes while two kids raid a cookie jar behind her back. These descriptions did not preserve the handwriting from the original responses, says Rhoda Au, director of neuropsychology at the Framingham study and a professor at Boston University. © 2020 Scientific American,

Keyword: Alzheimers; Language
Link ID: 27544 - Posted: 10.24.2020

Catherine Offord Overactivation of the brain’s immune cells, called microglia, may play a role in cognitive impairments associated with Down syndrome, according to research published today (October 6) in Neuron. Researchers in Italy identified elevated numbers of the cells in an inflammation-promoting state in the brains of mice with a murine version of the syndrome as well as in postmortem brain tissue from people with the condition. The team additionally showed that drugs that reduce the number of activated microglia in juvenile mice could boost the animals’ performance on cognitive tests. “This is a fabulous study that gives a lot of proof of principle to pursuing some clinical trials in people,” says Elizabeth Head, a neuroscientist at the University of California, Irvine, who was not involved in the work. “The focus on microglial activation, I thought, was very novel and exciting,” she adds, noting that more research will be needed to see how the effects of drugs used in the study might translate from mice to humans. Down syndrome is caused by an extra copy of part or all of human chromosome 21, and is the most commonly occurring chromosomal condition in the US. Children with Down syndrome often experience cognitive delays compared to typically developing children, although there’s substantial variation and the effects are usually mild or moderate. People with the syndrome also have a higher risk of certain medical conditions, including Alzheimer’s disease. © 1986–2020 The Scientist.

Keyword: Development of the Brain; Glia
Link ID: 27537 - Posted: 10.21.2020

By Nicholas Bakalar A mother’s psychological distress during pregnancy may increase the risk for asthma in her child, a new study suggests. Researchers had the parents of 4,231 children fill out well-validated questionnaires on psychological stress in the second trimester of pregnancy, and again three years later. The mothers also completed questionnaires at two and six months after giving birth. The study, in the journal Thorax, found that 362 of the mothers and 167 of the fathers had clinically significant psychological distress during the mothers’ pregnancies. When the children were 10 years old, parents reported whether their child had ever been diagnosed with asthma. As an extra measure, the researchers tested the children using forced expiratory volume, or FEV, a standard clinical test of lung function. After controlling for age, smoking during pregnancy, body mass index, a history of asthma and other factors, they found that maternal depression and anxiety during pregnancy was significantly associated with both diagnoses of asthma and poorer lung function in their children. There was no association between childhood asthma and parents’ psychological distress in the years after pregnancy, and no association with paternal psychological stress at any time. “Of course, this could be only one of many causes of asthma,” said the lead author, Dr. Evelien R. van Meel of Erasmus University in Rotterdam, “but we corrected for many confounders, and we saw the effect only in mothers. This seems to suggest that there’s something going on in the uterus. But this is an observational study, and we can’t say that it’s a causal effect.” © 2020 The New York Times Company

Keyword: Depression; Development of the Brain
Link ID: 27534 - Posted: 10.21.2020