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

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By Andrea Petersen Anne Firmender, 74, was working with her psychologist to come up with a list of her positive attributes. “I cook for others,” said Ms. Firmender. “It’s giving,” encouraged the psychologist, Dimitris Kiosses. “Good kids,” continued Ms. Firmender, who has four grown children and four grandchildren. “And great mother,” added Dr. Kiosses. Ms. Firmender smiled. Dr. Kiosses typed up the list and handed a printout to Ms. Firmender to take home. “When you’re feeling down and hard on yourself, you can remind yourself of your strengths,” he told her. Ms. Firmender, who has a history of mental health problems, was in therapy for depression. But she also has mild cognitive impairment and can have trouble remembering what day it is. So Dr. Kiosses was treating her with a novel approach called Problem Adaptation Therapy, or PATH. The therapy, developed at Weill Cornell Medicine in New York City and White Plains, N.Y., focuses on solving tangible problems that fuel feelings of sadness and hopelessness. It incorporates tools, like checklists, calendars, signs and videos, to make it accessible for people with memory issues. A caregiver is often involved. The approach is one of several new psychotherapies to treat anxiety and depression in people with cognitive impairments, including early to moderate dementia. Another, the Peaceful Mind program, developed by researchers at Baylor College of Medicine and elsewhere for patients with anxiety and dementia, simplifies traditional cognitive behavioral therapy and focuses on scheduling pleasurable activities and skills, like deep breathing. Therapy sessions are short and take place in patients’ homes. A program designed by researchers at University College London gives cards to patients to take home to remind them of key strategies. One that says “Stop and Think” prompts them to pause when they have panicky and unhelpful thoughts to help keep those thoughts from spiraling and creating more anxiety. © 2019 The New York Times Company

Keyword: Alzheimers; Depression
Link ID: 26884 - Posted: 12.09.2019

By Laura Sanders Call it a comeback — maybe. After being shelved earlier this year for lackluster preliminary results, a drug designed to slow Alzheimer’s progression is showing new signs of life. A more in-depth look at the data from two clinical trials suggests that patients on the biggest doses of the drug, called aducanumab, may indeed benefit, the company reported December 5. People who took the highest amounts of the drug declined about 30 percent less, as measured by a commonly used Alzheimer’s scale, than people who took a placebo, Samantha Haeberlein of the biotechnology company Biogen reported at the Clinical Trials on Alzheimer’s Disease meeting in San Diego. With these encouraging results in hand, Biogen, based in Cambridge, Mass., plans to seek drug approval from the U.S. Food and Drug Administration in early 2020. The results are “exhilarating, not just to the scientific community but our patients as well,” Sharon Cohen, a behavioral neurologist at the Toronto Memory Program, said during a panel discussion at the meeting. Cohen participated in the clinical trials and has received funding from Biogen. The presentation marks “an important moment for the Alzheimer’s field,” says Rebecca Edelmayer, director of scientific engagement for the Alzheimer’s Association in Chicago. Alzheimer’s disease slowly kills cells in the brain, gradually erasing people’s abilities to remember, navigate and think clearly. Current Alzheimer’s medicines can hold off symptoms temporarily, but don’t fight the underlying brain destruction. A treatment that could actually slow or even stop the damage would have a “huge impact for patients and their caregivers,” she says. © Society for Science & the Public 2000–2019

Keyword: Alzheimers
Link ID: 26879 - Posted: 12.06.2019

By Kelly Servick When Samantha Budd Haeberlein, Biogen’s head of clinical development, took the stage in San Diego, California, before a room full of Alzheimer’s disease researchers and physicians this morning, she knew she had some explaining to do. In October, the pharmaceutical company, based in Cambridge, Massachusetts, unexpectedly revived an experimental Alzheimer’s drug that it had declared a failure 7 months earlier. Ever since, scientists and industry analysts have been hungry for more detail about two large clinical trials meant to prove that Biogen’s drug, an antibody called aducanumab, slows down cognitive decline in the early stages of disease. At the Clinical Trials on Alzheimer’s Disease congress today, Budd Haeberlein tried to clarify what has emboldened the company to apply to the U.S. Food and Drug Administration (FDA) for market approval for aducanumab early next year. After analyzing more patient data than were available at the time of a discouraging preliminary analysis, she explained, the company found evidence that the higher of two tested doses led to 22% less cognitive decline after 78 weeks than a placebo in one trial. However, the other trial failed to show any benefit, leaving some researchers with a grim outlook on the drug. “I surely don’t think that it should be given market approval on the basis of these data,” says Robert Howard, a psychiatrist at University College London who has run clinical trials of potential Alzheimer’s treatments. More positive results from a subset of patients that weren’t preselected at the trial’s launch are not convincing, he says. “[Biogen has] broken all the rules, really, about how you analyze data and report it.” © 2019 American Association for the Advancement of Science.

Keyword: Alzheimers
Link ID: 26878 - Posted: 12.06.2019

Richard Harris Scientists know that if they transfuse blood from a young mouse to an old one, then they can stave off or even reverse some signs of aging. But they don't know what in the blood is responsible for this remarkable effect. Researchers now report that they've identified hundreds of proteins in human blood that wax and wane in surprising ways as we age. The findings could provide important clues about which substances in the blood can slow aging. The scientists studied nearly 3,000 proteins in blood plasma that was drawn from more than 4,000 people with a span of ages from 18 to 95. The project focused on proteins that change in both men and women. "When we went into this, we assumed you aged gradually, so we would see these changes taking place relatively steadily as individuals get older," said Tony Wyss-Coray, a professor of neurology at Stanford University. Instead, Wyss-Coray and his colleagues report in Nature Medicine on Thursday that these proteins change in three distinct waves, the first of which happens "very surprisingly" during our 30s, peaking around age 34. "Then we found a second wave around 60, and then we found a third one, the most prominent one, really around 80 years of age," Wyss-Coray said. (An earlier version of their paper is freely available on the bioRxiv preprint server.) This observation raises a host of questions about the biology of aging. What age-related transition is occurring in our 30s? And what do the changes in the blood actually mean? "Most of the proteins in the blood are actually from other tissue sources," he said. "So we can start to ask where ... these proteins come from and if they change with age," he said. For example, in proteins traced back to the liver, "that would tell us that the liver is aging." © 2019 npr

Keyword: Alzheimers
Link ID: 26876 - Posted: 12.06.2019

Ian Sample Science editor Scientists have created artificial neurons that could potentially be implanted into patients to overcome paralysis, restore failing brain circuits, and even connect their minds to machines. The bionic neurons can receive electrical signals from healthy nerve cells, and process them in a natural way, before sending fresh signals on to other neurons, or to muscles and organs elsewhere in the body. One of the first applications may be a treatment for a form of heart failure that develops when a particular neural circuit at the base of the brain deteriorates through age or disease and fails to send the right signals to make the heart pump properly. Rather than implanting directly into the brain, the artificial neurons are built into ultra-low power microchips a few millimetres wide. The chips form the basis for devices that would plug straight into the nervous system, for example by intercepting signals that pass between the brain and leg muscles. “Any area where you have some degenerative disease, such as Alzheimer’s, or where the neurons stop firing properly because of age, disease, or injury, then in theory you could replace the faulty biocircuit with a synthetic circuit,” said Alain Nogaret, a physicist who led the project at the University of Bath. The breakthrough came when researchers found they could model live neurons in a computer program and then recreate their firing patterns in silicon chips with more than 94% accuracy. The program allows the scientists to mimic the full variety of neurons found in the nervous system. © 2019 Guardian News & Media Limited

Keyword: Robotics; Learning & Memory
Link ID: 26872 - Posted: 12.04.2019

Shawna Williams In September of this year, pharmaceutical companies Biogen and Eisai announced that they were halting Phase 3 clinical trials of a drug, elenbecestat, aimed at thwarting amyloid-β buildup in Alzheimer’s disease. Although the drug had seemed so promising that the companies elected to test it in two Phase 3 trials simultaneously, preliminary analyses determined that elenbecestat’s risks outweighed its benefits, and the drug shouldn’t be moved to market. The cancellation “amounts to a further step in the unwinding of Biogen’s expensive, painful, and ultimately fruitless investment in Alzheimer’s disease (AD) drug development,” analyst Geoffrey Porges told Reuters at the time. Biogen’s misfortune is just the latest in a slew of late-stage Alzheimer’s drug failures. Six months earlier, the company had halted another set of parallel Phase 3 trials due to lack of efficacy of a different drug candidate, aducanumab (though after further data analysis, Biogen announced that it will seek approval for aducanumab after all). And between 2013 and 2018, Pfizer, Eli Lilly, Merck, and Johnson & Johnson all terminated Phase 3 or Phase 2/3 trials due to poor early results. Yet some Alzheimer’s researchers say they think they’ve spotted a silver lining in this cloud of bad news—a hint in the data from these studies about how future work might meet with more success. In some of these trials, Alzheimer’s patients who were at earlier stages of the disease did better than those with more advanced cognitive decline, says Colin Masters, a neuroscientist at Florey Institute of Neuroscience and Mental Health in Australia who was not involved in the trials. This indicates that the key to finding an effective treatment might be to catch subjects before their condition advances too far, he adds. © 1986–2019 The Scientist

Keyword: Alzheimers
Link ID: 26868 - Posted: 12.04.2019

By Claudia Wallis For more than 25 years one idea has dominated scientific thinking about Alzheimer's disease: the amyloid cascade hypothesis. It holds that the disorder, which afflicts about one in 10 Americans age 65 or older, is caused by a buildup in the brain of abnormal amyloid-beta protein, which eventually destroys neurons and synapses, producing the tragic symptoms of dementia. There's plenty of evidence for this. First, the presence of sticky clumps or “plaques” containing amyloid is a classic hallmark of the disease (along with tangles of a protein called tau). It was what Alois Alzheimer saw in the autopsied brain of patient zero in 1906. Second, families with inherited defects in amyloid precursor protein (APP) or in genes encoding proteins that process APP are plagued by early-onset Alzheimer's. Third, mice genetically engineered to churn out excess amyloid tend to develop memory problems and do better when the amyloid pileup is stopped. This evidence and more has led grant makers and drug companies to pour billions of dollars into amyloid-targeting therapies. More than a dozen have been tested, and one by one they have flopped. One of the biggest heartbreaks came last March, when a promising antibody to amyloid, called aducanumab, performed no better than placebo in patients with very early Alzheimer's. Meanwhile researchers pursuing nonamyloid approaches were often left out in the cold, struggling to get grants and to have their work published. Science journalist Sharon Begley spent more than a year reporting on the lost opportunities in an article for the Web site Stat entitled “The Maddening Saga of How an Alzheimer's ‘Cabal’ Thwarted Progress toward a Cure for Decades.” Begley notes that the amyloid crowd was “neither organized nor nefarious,” but its outsized influence stifled other avenues of investigation. © 2019 Scientific American

Keyword: Alzheimers
Link ID: 26867 - Posted: 12.04.2019

By Donald McCarthy I lived only half a childhood. Friendships were difficult, because I often did not know what to say. I had little patience for small talk and a dislike of new situations. Thrust into unfamiliar surroundings, my whole body would warm, my hands would shake, and I would feel a tightening in my chest and a deep, almost primal urge to scream. Even as an adult, I felt like I viewed reality through a foggy window. I thought it was simply me — that my personality was just odd — and I would need to learn to cope with the fact that I did not fit in well with most people. Then, at age 28, I was diagnosed with autism spectrum disorder (ASD). My diagnosis was a relief. Suddenly, I knew why I felt the way I did, and why I had a hard time living the way others did. But I can only imagine how much better my life would have been if I had been diagnosed as a child and had the chance to understand myself at a younger age. Might I have made emotional connections with my peers, instead of just with Bruce Springsteen songs and characters in Stephen King novels? It turns out I’m not alone. Many people go more than half of their lives before learning that they are autistic; the exact number remains a mystery, as research on adults with autism has been scarce. Although public awareness of ASD and its symptoms has improved in recent decades, many children still slip through the cracks, especially girls and children of color. We as a society have the power and resources to change that; all we need is the will. Consider the science: There is little question among psychologists specializing in autism that an early diagnosis can change a person’s life for the better. Therapy aimed at reworking the way a young person with ASD thinks and comprehends has shown success. Children who undergo therapy see results that allow them to curb undesirable behavior, improve social interactions, and better their own quality of life.

Keyword: Autism
Link ID: 26856 - Posted: 11.29.2019

By Meredith Wadman Tony Magana, chief of neurosurgery at Mekelle University School of Medicine in Ethiopia’s Tigray province, confronts his country’s high prevalence of neural tube defects nearly every day. His team operates on more than 400 babies annually to repair these severe, often lethal birth malformations, in which babies can be born without brains or with their spinal cords protruding from their backs. “Probably every other day we see a child that is so bad we can’t help them,” Magana says. The holes where the spinal cord protrudes “are so big that you can’t close them.” This month, a team of nutrition experts converged in Addis Ababa to lay groundwork for an unproven but possibly highly effective intervention: fortifying Ethiopia’s salt supply with folic acid, a synthetic form of the B vitamin folate. In the first 4 weeks of pregnancy, folate is essential to proper closure of the neural tube, which gives rise to the brain and spinal cord, and since the mid-1990s, more than 80 countries have mandated flour fortification with folic acid. Ethiopia, where fewer than one-third of people eat flour, is not among them. Last year, a pair of studies that surveyed births at 11 public hospitals there shook the global health community. The studies—one co-authored by Magana—found that among every 10,000 births, between 126 and 131 babies suffered from neural tube defects (NTDs). That’s seven times their global prevalence and 26 times the prevalence in high-income, flour-fortifying countries such as the United States. According to Ethiopian government data, 84% of Ethiopian women of reproductive age have folate levels in their red blood cells that put them at risk of giving birth to a child with an NTD. © 2019 American Association for the Advancement of Science

Keyword: Development of the Brain
Link ID: 26851 - Posted: 11.26.2019

A disturbing aspect of Canada's opioid crisis is that more babies are being born to mothers who use fentanyl and other opioid drugs. The Canadian Institute for Health Information says more than 1,800 infants per year are born with symptoms of opioid withdrawal. A study presented Monday at the 105th Scientific Assembly and Annual Meeting of the Radiological Society of North America suggests that prenatal exposure to opioids may have a significant impact on the brain development of unborn children. A team of obstetricians, neonatologists, psychologists and radiologists led by Dr. Rupa Radhakrishnan, a radiologist at Indiana University School of Medicine, did functional MRI brain scans on 16 full-term infants. Eight of the infants had mothers who used opioids during pregnancy and eight had mothers who did not use opioids. The brain imaging technique used by the researchers is called resting state functional MRI (fMRI). The technique enabled researchers to measure brain activity by detecting changes in blood flow. The technique permits researchers to measure how well different regions of the brain talk to one another. The researchers found abnormal connections to and from a part of the brain called the amygdala. It's a region that is responsible for the perception and regulation of emotions such as anger, fear, sadness and aggression. This is one of the first studies to suggest that the brain function of infants may be affected by prenatal exposure to opioids. Abnormal function in the amygdala could make it difficult for children exposed to opioids to regulate their emotions. That could have serious implications on their social development and on their behaviour. The researchers say the study is small. They say they aren't certain as to the clinical implications of this study. A long-term outcome study is underway to understand better the functional brain changes caused by prenatal opioid exposure and their associated long-term developmental outcomes. How newborns face opioid withdrawal This research may become even more important should current trends continue, and we see an increase in the number of infants exposed to opioids prenatally. ©2019 CBC/Radio-Canada

Keyword: Development of the Brain; Drug Abuse
Link ID: 26850 - Posted: 11.26.2019

By Nicholas Bakalar Long-term exposure to air pollution is associated with lower scores on tests of mental acuity, researchers have found. And one reason may be that air pollution causes changes in brain structure that resemble those of Alzheimer’s disease. The scientists studied 998 women ages 73 to 87 and free of dementia, periodically giving them tests of learning and memory. They used magnetic resonance imaging to detect brain atrophy, or wasting, and then scored the deterioration on its degree of similarity to the brain atrophy characteristic of Alzheimer’s disease. They matched Environmental Protection Agency data on air pollution to the women’s residential addresses. Over 11 years of follow-up, they found that the greater the women’s exposure to PM 2.5, the tiny particulate matter that easily penetrates the lungs and bloodstream, the lower their scores on the cognitive tests. After excluding cases of dementia and stroke, they also found a possible reason for the declining scores: The M.R.I. results showed that increased exposure to PM 2.5 was associated with increased brain atrophy, even before clinical symptoms of dementia had appeared. The study is in the journal Brain. “PM 2.5 alters brain structure, which then accelerates memory decline,” said the lead author, Diana Younan, a postdoctoral researcher at the University of California. “I just want people to be aware that air pollution can affect their health, and possibly their brains.” © 2019 The New York Times Company

Keyword: Neurotoxins; Development of the Brain
Link ID: 26849 - Posted: 11.26.2019

By Tina Hesman Saey Picking embryos based on genetics might not give prospective parents the “designer baby” they’re after. DNA predictions of height or IQ might help would-be parents select an embryo that would grow into a child who is, at most, only about three centimeters taller or about three IQ points smarter than an average embryo from the couple, researchers report November 21 in Cell. But offspring predicted by their DNA to be the tallest among siblings were actually the tallest in only seven of 28 real families, the study found. And in five of those families, the child predicted to be tallest was actually shorter than the average for the family. Even if it were ethical to select embryos based on genetic propensity for height or intelligence, “the impact of doing so is likely to be modest — so modest that it’s not likely to be practically worth it,” says Amit Khera, a physician and geneticist at the Center for Genomics Medicine at Massachusetts General Hospital in Boston who was not involved in the new study. For years, couples have been able to use genetic diagnosis to screen out embryos carrying a disease-causing DNA variant. The procedure, called preimplantation genetic diagnosis, or PGD, involves creating embryos through in vitro fertilization. Clinic staff remove a single cell from the embryo and test its DNA for genetic variants that cause cystic fibrosis, Tay-Sachs or other life-threatening diseases caused by defects in single genes. © Society for Science & the Public 2000–2019

Keyword: Genes & Behavior; Intelligence
Link ID: 26847 - Posted: 11.23.2019

By Nicholas Bakalar People who never learned to read and write may be at increased risk for dementia. Researchers studied 983 adults 65 and older with four or fewer years of schooling. Ninety percent were immigrants from the Dominican Republic, where there were limited opportunities for schooling. Many had learned to read outside of school, but 237 could not read or write. Over an average of three and a half years, the participants periodically took tests of memory, language and reasoning. Illiterate men and women were 2.65 times as likely as the literate to have dementia at the start of the study, and twice as likely to have developed it by the end. Illiterate people, however, did not show a faster rate of decline in skills than those who could read and write. The analysis, in Neurology, controlled for sex, hypertension, diabetes, heart disease and other dementia risk factors. “Early life exposures and early life social opportunities have an impact on later life,” said the senior author, Jennifer J. Manly, a professor of neuropsychology at Columbia. “That’s the underlying theme here. There’s a life course of exposures and engagements and opportunities that lead to a healthy brain later in life.” “We would like to expand this research to other populations,” she added. “Our hypothesis is that this is relevant and consistent across populations of illiterate adults.” © 2019 The New York Times Company

Keyword: Language; Alzheimers
Link ID: 26838 - Posted: 11.21.2019

By Knvul Sheikh Shortly after the birth of her first son, Monika Jones learned that he had a rare neurological condition that made one side of his brain abnormally large. Her son, Henry, endured hundreds of seizures a day. Despite receiving high doses of medication, his little body seemed like a rag doll as one episode blended into another. He required several surgeries, starting when he was 3 1/2 months old, eventually leading to a complete anatomical hemispherectomy, or the removal of half of his brain, when he turned 3. The procedure was first developed in the 1920s to treat malignant brain tumors. But its success in children who have brain malformations, intractable seizures or diseases where damage is confined to half the brain, has astonished even seasoned scientists. After the procedure, many of the children are able to walk, talk, read and do everyday tasks. Roughly 20 percent of patients who have the procedure go on to find gainful employment as adults. Now, research published Tuesday in the journal Cell Reports suggests that some individuals recover so well from the surgery because of a reorganization in the remaining half of the brain. Scientists identified the variety of networks that pick up the slack for the removed tissue, with some of the brain’s specialists learning to operate like generalists. “The brain is remarkably plastic,” said Dorit Kliemann, a cognitive neuroscientist at the California Institute of Technology, and the first author of the study. “It can compensate for dramatic loss of brain structure, and in some cases the remaining networks can support almost typical cognition.” The study was partially funded by a nonprofit organization that Mrs. Jones and her husband set up to advocate for others who need surgery to stop seizures. The study’s findings could provide encouragement for those seeking hemispherectomies beyond early childhood. © 2019 The New York Times Company

Keyword: Development of the Brain; Laterality
Link ID: 26837 - Posted: 11.20.2019

By Michele C. Hollow As soon as James Griffin gets off the school bus he tells his mom, “Go dance, go dance.” James is 14 and has autism, and his speech is limited. He’s a participant in a program for children on the autism spectrum at the University of Delaware that is studying how dance affects behavior and verbal, social and motor skills. One afternoon while dancing, he spun around, looked at his mother, smiled and shouted, “I love you.” His mom, Rachelan Griffin, said she had waited his whole life to hear him say those words. “I think that the program is a big part of that, because he was dancing when he said it,” she said. According to Anjana Bhat, an associate professor in the department of physical therapy at the University of Delaware, “Parents report that their children with autism enjoy musical activities and show more positive interactions with others through greater eye contact, smiling and speaking after engaging in a dance and music program.” James is one of about a dozen children on the autism spectrum who meet individually with Dr. Bhat’s graduate and undergraduate students for the dance study, which also uses yoga and musical activities. Some children also participated in robotic therapy, in which a humanoid robot helps them learn to follow dance moves. “Across many different studies we find that social skills like smiling and verbalization are substantially higher when children with autism engage in socially embedded movements versus sedentary games like checkers or building a Lego set,” Dr. Bhat said. © 2019 The New York Times Company

Keyword: Autism
Link ID: 26835 - Posted: 11.20.2019

Robin McKie Major psychological disorders such as schizophrenia will continue to affect humans because men and women are continually generating genetic mutations that disrupt brain development. This will be the key conclusion of Professor Sir Michael Owen, director of Cardiff University’s centre for neuropsychiatric genetics and genomics, when he gives the annual Darwin Lecture at the Royal Society of Medicine this week. Understanding such conditions at an evolutionary level will be crucial to developing treatments, Owen believes. Thirty years ago, the new technology of DNA analysis raised hopes that schizophrenia – a condition that can track through families – would soon reveal links to one or two specific genes, said Owen. Treatments might then be relatively easy to develop, it was thought. Instead scientists found that hundreds of genes, each having a tiny effect, dictate whether or not a person will be susceptible to the condition. Characterised by profound behavioural changes, hallucinations, and delusions, these transformations in behaviour can have profound consequences, he added. For example, men with schizophrenia have – on average – only a quarter as many children as males in the general population while women with the condition have about half as many as unaffected females. That low reproduction rate should have had one clear result, Owen told the Observer last week. “Schizophrenia cases should have declined and disappeared long ago as those affected were out bred by those unaffected. This has not happened. A steady level of 1% people continue to be affected.” © 2019 Guardian News & Media Limited

Keyword: Schizophrenia; Genes & Behavior
Link ID: 26831 - Posted: 11.19.2019

Lorenz Wagner Henry Markram, the neuroscientist behind the billion-dollar Blue Brain Project to build a supercomputer model of the brain, has set the goal of decoding all disturbances of the mind within a generation. This quest is personal for him. The driving force behind his grand ambition has been his son Kai, who suffers from autism. Raising Kai made Henry Markram question all that he thought he knew about neuroscience, and then inspired his groundbreaking research that would upend the conventional wisdom about autism, leading to his now-famous theory of the Intense World Syndrome. When Kai was first diagnosed, his father consulted studies and experts. He knew as much about the human brain as almost anyone but still felt as helpless as any parent confronted with this condition in his child. What’s more, the scientific consensus that autism was a deficit of empathy didn’t mesh with Markram’s experience of his son. He became convinced that the disorder, which has seen a 657 percent increase in diagnoses over the past decade, was fundamentally misunderstood. Bringing his world-class research to bear on the problem, he devised a radical new theory of the disorder: People like Kai don’t feel too little; they feel too much. Their senses are too delicate for this world. The following is an extract condensed from "The Boy Who Felt Too Much: How a Renowned Neuroscientist Changed Our View of Autism Forever," by Lorenz Wagner, just out from Arcade Publishing, which tells this remarkable story. The car was coasting. Kai heard the wheels crunch as it drew to a halt outside his house. The car door opened, and a young man hopped out. He popped the hood and disappeared beneath it. “You’ve got to be kidding me!” he fumed. © 2019 Salon.com, LLC

Keyword: Autism
Link ID: 26828 - Posted: 11.18.2019

Ruth Williams Throughout the animal kingdom, there are numerous examples of neurons that respond to multiple stimuli and faithfully transmit information about those various inputs. In the mouse, for example, there are certain neurons that respond to both temperature and potentially damaging touch. In the fruit fly, there are neurons that sense light, temperature, pain, and proprioceptive stimuli—those arising as a result of body position and movement. And in C. elegans, two sensory neurons, known as PVD neurons, that run the length of the body on either side are thought to regulate proprioception as well as responses to harsh touch and cold temperature. Scientists have now figured out how a single PVD neuron can relay two different stimuli: while harsh touch results in typical firing of the neuron—an impulse that travels the length of the cell—proprioception causes a localized response in one part of the cell with no apparent involvement of the rest. The findings are reported today (November 14) in Developmental Cell. “[The] paper illustrates that different parts of the neuron do different things,” says neuroscientist Scott Emmons of Albert Einstein College of Medicine who did not participate in the research, “and that just makes the whole system much more complex to interpret,” he says. To examine how a single neuron interprets distinct inputs and drives corresponding behaviors, neuroscientist Kang Shen of Stanford University and colleagues focused on PVD neuron–regulated escape behavior when a worm is poked with a wire and the worm’s normal wiggling motion as it responds to proprioceptive stimuli. © 1986–2019 The Scientist

Keyword: Pain & Touch; Development of the Brain
Link ID: 26823 - Posted: 11.16.2019

Emily Makowski China’s approval of the drug oligomannate earlier this month for treating mild to moderate Alzheimer’s disease has been met with surprise and skepticism from some members of the scientific community, who claim that the preclinical data raise questions about the underlying mechanism of the drug. One microbiome researcher has pointed out inconsistencies between the researchers’ data and their proposed mechanism for how oligomannate could treat Alzheimer’s. “The field is seeing this [research] with a large dose of skepticism,” Malú Tansey, a neuroimmunologist at the University of Florida College of Medicine, tells The Scientist. On November 2, Shanghai Green Valley Pharmaceuticals announced that oligomannate, an oligosaccharide mixture derived from brown algae, had been approved by the National Medical Product Administration (NMPA), China’s equivalent of the US Food and Drug Administration. The announcement followed the completion of a Phase 3 clinical trial in China that found the drug appeared to slow cognitive decline in Alzheimer’s patients. In addition, researchers led by Meiyu Geng at the Shanghai Institute of Materia Medica published a paper in Cell Research in September on oligomannate’s ability to remodel the gut microbiome in mice and reduce neuroinflammation. There is an emerging link between the gut microbiome and Alzheimer’s disease in humans. In the study, the researchers gave oligomannate to mice that are genetically engineered to show physical and behavioral symptoms similar to Alzheimer’s disease. The team collected mouse feces to study the microorganisms present in gut microbiota, drew blood to analyze the presence of immune cells, and also examined the levels of cytokines, which are inflammatory compounds, in the brain. © 1986–2019 The Scientist

Keyword: Alzheimers
Link ID: 26821 - Posted: 11.16.2019

By Gary Stix Socrates famously railed against the evils of writing. The sage warned that it would “introduce forgetfulness into the soul of those who learn it: they will not practice using their memory because they will put their trust in writing.” He got a few things wrong. For one, people nurture Socrates’ memory because of all of the books written about him. But he also was off the mark in his musings about a forgetfulness of the soul. If anything, it appears that just the opposite holds: a study of hundreds of illiterate people living at the northern end of an island considered to be a world media capital roundly contradicts the father of Western philosophy. Evaluations of the elderly in the environs of Manhattan’s Washington Heights (the neighborhood immortalized by a Lin-Manuel Miranda musical) reveal that the very act of reading or writing—largely apart from any formal education—may help protect against the forgetfulness of dementia. “The people who were illiterate in the study developed dementia at an earlier age than people who were literate in the study,” says Jennifer J. Manly, senior author of the paper, which appeared on November 13in Neurology. Earlier studies trying to parse this topic had not been able to disentangle the role of reading and writing from schooling to determine whether literacy, by itself, could be a pivotal factor safeguarding people against dementia later in life. The researchers conducting the new study, who are mostly at Columbia University’s Vagelos College of Physicians and Surgeons, recruited 983 people with four years or less of schooling who were part of the renowned Washington Heights–Inwood Columbia Community Aging Project. Of that group, 238 were illiterate, which was determined by asking the participants point-blank, “Did you ever learn to read or write?”—followed by reading tests administered to a subsample. Even without much time in school, study subjects sometimes learned from other family members. © 2019 Scientific American

Keyword: Alzheimers; Language
Link ID: 26819 - Posted: 11.14.2019