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

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By Veronique Greenwood Planarians have unusual talents, to say the least. If you slice one of the tiny flatworms in half, the halves will grow back, giving you two identical worms. Cut a flatworm’s head in two, and it will grow two heads. Cut an eye off a flatworm — it will grow back. Stick an eye on a flatworm that lacks eyes — it’ll take root. Pieces as small as one-279th of a flatworm will turn into new, whole flatworms, given the time. This process of regeneration has fascinated scientists for more than 200 years, prompting myriad zany, if somewhat macabre, experiments to understand how it is possible for a complex organism to rebuild itself from scratch, over and over and over again. In a paper published Friday in Science, researchers revealed a tantalizing glimpse into how the worms’ nervous systems manage this feat. Specialized cells, the scientists report, point the way for neurons stretching from newly grown eyes to the brain of the worm, helping them connect correctly. The research suggests that cellular guides hidden throughout the planarian body may make it possible for the worm’s newly grown neurons to retrace their steps. Gathering these and other insights from the study of flatworms may someday help scientists interested in helping humans regenerate injured neurons. María Lucila Scimone, a researcher at M.I.T.’s Whitehead Institute for Biomedical Research, first noticed these cells while studying Schmidtea mediterranea, a planarian common to bodies of freshwater in Southern Europe and North Africa. During another experiment, she noted that they were expressing a gene involved in regeneration. The team looked more closely and realized that some of the regeneration-related cells were positioned at key branching points in the network of nerves between the worms’ eyes and their brains. When the researchers transplanted an eye from one animal to another, the neurons growing from the new eye always grew toward these cells. When the nerve cells reached their target, they kept growing along the route that would take them to the brain. Removing those cells meant the neurons got lost and did not reach the brain. © 2020 The New York Times Company

Keyword: Development of the Brain; Regeneration
Link ID: 27340 - Posted: 07.01.2020

By Melinda Wenner Moyer For three months, Chelsea Alionar has struggled with fevers, headaches, dizziness and a brain fog so intense it feels like early dementia. She came down with the worst headache of her life on March 9, then lost her sense of taste and smell. She eventually tested positive for the coronavirus. But her symptoms have been stranger, and lasted longer, than most. “I tell the same stories repeatedly; I forget words I know,” she told me. Her fingers and toes have been numb, her vision blurry and her fatigue severe. The 37-year-old is a one of the more than 4,000 members of a Facebook support group for Covid survivors who have been ill for more than 80 days. The more we learn about the coronavirus, the more we realize it’s not just a respiratory infection. The virus can ravage many of the body’s major organ systems, including the brain and central nervous system. Among patients hospitalized for Covid-19 in Wuhan, China, more than a third experienced nervous system symptoms, including seizures and impaired consciousness. Earlier this month, French researchers reported that 84 percent of Covid patients who had been admitted to the I.C.U. experienced neurological problems, and that 33 percent continued to act confused and disoriented when they were discharged. According to Dr. Mady Hornig, a psychiatrist and epidemiologist at the Columbia University Mailman School of Public Health, the possibility that neurological issues “will persist and create disability, or difficulties, for individuals downstream is really looking more and more likely.” Infections have long been implicated in neurological diseases. Syphilis and H.I.V. can induce dementia. Zika is known to invade developing brains and limit their growth, while untreated Lyme disease can cause nerve pain, facial palsy and spinal cord inflammation. One man with SARS developed delirium that progressed into coma, and was found to have the virus in his brain tissue after his death. © 2020 The New York Times Company

Keyword: Alzheimers; Learning & Memory
Link ID: 27335 - Posted: 06.29.2020

Jon Hamilton A research effort based at the Allen Institute in Seattle, Wash., will tap leading scientists from several institutions to dive even deeper into brain genetics and physiology. The aim: Find clues to the earliest beginnings of Alzheimer's. Allen Institute Three research institutions in Seattle have joined forces to study how Alzheimer's disease takes root in the brain. The consortium will create a new research center at the Allen Institute for Brain Science to study tissue from brains donated by people who died with Alzheimer's. UW Medicine and the Kaiser Permanente Washington Health Research Group are also part of the effort, which will be funded by a five-year $40.5 million grant from the National Institute on Aging, a part of the National Institutes of Health. The project, with its emphasis on basic research, represents part of a global do-over for the Alzheimer's field, which has weathered a series of failed attempts to develop a drug that could slow or stop the disease. "The premise of this project here is that we need to take a step back," says Ed Lein, a senior scientist at the Allen Institute and the center's lead investigator. That's a marked change from a decade ago, when there was great excitement about experimental drugs that could scrub away the sticky brain plaques thought to cause Alzheimer's. Studies have shown that the drugs do their job, removing a toxic protein called amyloid-beta from the brain. But they don't help patients avoid memory loss or cognitive problems. © 2020 npr

Keyword: Alzheimers
Link ID: 27331 - Posted: 06.27.2020

Nicola Davis People living with inflammatory bowel disease (IBD) have more than twice the risk of developing dementia, researchers have revealed in the latest study to link gut health to neurological diseases. A growing body of research suggests changes in the gastrointestinal tract may affect the brain through two-way communication known as the gut-brain axis. Scientists have previously found signs that the abnormally folded proteins involved in Parkinson’s disease may arise in the gut and travel to the brain via the vagus nerve, while changes to the microbial community in the gut – the gut microbiome – have been linked with conditions ranging from mental health problems to motor neurone disease and Parkinson’s disease. In addition, previous work has shown people with IBD have a higher risk of Parkinson’s disease. Researchers now say they have found that people with IBD – inflammatory conditions including ulcerative colitis and Crohn’s disease, which have symptoms including stomach pain and bloody stools – have a greater chance of developing dementia than those without, and tend to be diagnosed with dementia several years earlier. “The findings suggest that there may be a connection between IBD and neurocognitive decline,” said Dr Bing Zhang, first author of the research from the University of California San Francisco. While the study does not prove IBD causes dementia, Zhang and his colleagues outlined a number of ways the two may be linked, noting chronic inflammation has been suggested to trigger processes involved in Alzheimer’s disease, and blood clots and stroke – features involved in vascular dementia. © 2020 Guardian News & Media Limited or its affiliated companies.

Keyword: Alzheimers; Neuroimmunology
Link ID: 27326 - Posted: 06.26.2020

by Peter Hess / Inherited mutations in a gene called ACTL6B lead to autism, epilepsy and intellectual disability, according to a new study1. The mutations are recessive, which means that they lead to autism only if a person inherits them in both copies of the gene — one from each parent, who are silent carriers. Most other mutations implicated in autism are spontaneous, or ‘de novo,’ mutations, which are not inherited. The study suggests that recessive mutations in ACTL6B could be a relatively common cause of autism, says co-lead researcher Joseph Gleeson, professor of neurosciences and pediatrics at the University of California, San Diego. ACTL6B helps to control the expression of other genes in brain cells by encoding part of a protein complex called BAF. This complex tightens and loosens chromatin, the bundle of DNA and protein crammed inside a cell’s nucleus, during transcription. Scientists have linked autism to mutations in many other chromatin regulation genes — including several that encode other parts of the BAF complex. ACTL6B mutations have previously been associated with neurodevelopmental conditions, but the new study makes a strong case that they are tied to autism, says Gaia Novarino, professor of neuroscience at the Institute of Science and Technology in Klosterneuburg, Austria, who was not involved in the study. The work also provides a comprehensive look at how mutations in ACTL6B affect the brains of people, mice and flies, and suggests that the gene plays a common role across species. © 2020 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 27325 - Posted: 06.26.2020

By Nicholas Bakalar Five behaviors are associated with a lower risk for Alzheimer’s disease, a new study in Neurology suggests, and the more of them you follow, the lower your risk. Researchers used detailed diet and lifestyle information from two databases, one of 1,845 people whose average age was 73, the other of 920 people whose average age was 81. All were free of Alzheimer’s disease at the start of the study. They followed them for an average of about six years, during which 608 developed Alzheimer’s disease. The researchers scored the participants on their adherence to five behaviors: not smoking, consistent moderate or intense physical activity, light to moderate alcohol consumption, a high-quality Mediterranean-style diet, and engagement in late-life cognitively challenging activity. Compared to those with none or one of the healthy lifestyle factors, those with two or three had a 37 percent reduced risk for Alzheimer dementia, and those with four or five had a 60 percent reduced risk. The lead author, Dr. Klodian Dhana, an assistant professor of medicine at Rush Medical College, said that the paper focuses on modifiable risk factors. All five of these factors are related to each other, he added, and work best in combination. “My top recommendations are to engage in cognitively stimulating activities such as reading books and newspapers and playing brain-stimulating games, like chess and checkers,” he said. “Also, exercising regularly and following a diet for a healthy brain that includes green leafy vegetables every day, berries, nuts, poultry, fish, and limited fried food.” © 2020 The New York Times Company

Keyword: Alzheimers
Link ID: 27317 - Posted: 06.24.2020

by Laura Dattaro Children with autism are more likely than typical children to have had problems falling asleep as infants, according to a new study1. These infants also have more growth in the hippocampus, the brain’s memory hub, from age 6 to 24 months. The study is the first to link sleep problems to altered brain development in infants later diagnosed with autism. Sleep difficulties are common in autistic children: Nearly 80 percent of autistic preschoolers have trouble sleeping2. But little is known about the interplay between sleep and brain development in early life, says lead investigator Annette Estes, director of the UW Autism Center at the University of Washington in Seattle. The researchers examined the sleep patterns and brain scans of infants who have autistic older siblings, a group known as ‘baby sibs.’ Baby sibs are 20 times as likely to be diagnosed with autism as are children in the general population, and they often show signs of autism early in life. The study shows an association between sleep problems and brain structure in babies who have autism. But it is too early to say whether sleep troubles contribute to brain changes and autism traits or vice versa, or whether some common factor underlies all three, Estes says. It is also not clear what, if any, connection exists between these findings and the well-documented sleep problems in older autistic children. © 2020 Simons Foundation

Keyword: Autism; Sleep
Link ID: 27314 - Posted: 06.22.2020

By Elizabeth Pennisi When Muhammad Ali duked it out with Joe Frazier in the boxing ring, it’s unlikely anyone thought about what was happening to the genes inside their heads. But a new study in fighting fish has demonstrated that as the fish spar, genes in their brains begin to turn on and off in a coordinated way. It’s still unclear what those genes are doing or how they influence the skirmish, but similar changes may be happening in humans. The work is “a really cool example of the way that social interactions can get under the skin,” says Alison Bell, a behavioral ecologist at the University of Illinois, Urbana-Champaign, who was not involved with the study. The molecular basis of how animals, humans included, coordinate behaviors is a mystery. Whether it be mating or fighting, “animals need to be really good at this, but we don’t particularly know how they do it,” says Hans Hofmann, an evolutionary social neuroscientist at the University of Texas, Austin. When molecular biologist Norihiro Okada at Kitasato University in Japan first saw Siamese fighting fish (Betta splendens) on TV, he realized the animals could help solve this mystery. Native to Thailand, these goldfish-size swimmers have been bred to have very large, vibrantly colored fins and tails. Aquarium owners tend to keep their pets, or “bettas” as they are often called, separate. The fish are territorial and can get into fights that last more than 1 hour, with strikes, bites, and chases (as seen in the video below). They will even lock jaws in a fish version of an arm wrestle. Okada and colleagues videotaped more than a dozen hours of fights between 17 pairs of fish and then analyzed what happened—and when—in each fight. The longer the fight, the more the fish synchronize their behavior, timing their circling, striking, and biting more than anyone had ever realized, the researchers report today in PLOS Genetics. © 2020 American Association for the Advancement of Science.

Keyword: Aggression; Epigenetics
Link ID: 27310 - Posted: 06.19.2020

Combining more healthy lifestyle behaviors was associated with substantially lower risk for Alzheimer’s disease in a study that included data from nearly 3,000 research participants. Those who adhered to four or all of the five specified healthy behaviors were found to have a 60% lower risk of Alzheimer’s. The behaviors were physical activity, not smoking, light-to-moderate alcohol consumption, a high-quality diet, and cognitive activities. Funded by the National Institute on Aging (NIA), part of the National Institutes of Health, this research was published in the June 17, 2020, online issue of Neurology, the medical journal of the American Academy of Neurology. The research team reviewed data from two NIA-funded longitudinal study populations: The Chicago Health and Aging Project (CHAP)(link is external) and the Memory and Aging Project (MAP)(link is external). They selected participants from those studies who had data available on their diet, lifestyle factors, genetics, and clinical assessments for Alzheimer’s disease. The resulting data pool included 1,845 participants from CHAP and 920 from MAP. The researchers scored each participant based on five healthy lifestyle factors, all of which have important health benefits: At least 150 minutes per week of moderate- to vigorous-intensity physical activity – Physical activity is an important part of healthy aging. Not smoking – Established research has confirmed that even in people 60 or older who have been smoking for decades, quitting will improve health. Light-to-moderate alcohol consumption – Limiting use of alcohol may help cognitive health. A high-quality, Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND) diet, which combines the Mediterranean diet and Dietary Approaches to Stop Hypertension (DASH) diet – The MIND diet focuses on plant-based foods linked to dementia prevention. Engagement in late-life cognitive activities – Being intellectually engaged by keeping the mind active may benefit the brain.

Keyword: Alzheimers
Link ID: 27309 - Posted: 06.19.2020

By Lisa Friedman and Coral Davenport WASHINGTON — The Trump administration on Thursday finalized a decision not to impose any limits on perchlorate, a toxic chemical compound found in rocket fuel that contaminates water and has been linked to fetal and infant brain damage. The move by the Environmental Protection Agency was widely expected, after The New York Times reported last month that Andrew Wheeler, the E.P.A. administrator, had decided to effectively defy a court order that required the agency to establish a safe drinking-water standard for the chemical by the end of June. In addition to not regulating, the E.P.A. overturned the underlying scientific finding that declared perchlorate a serious health risk for five million to 16 million people in the United States. The E.P.A. said California and Massachusetts and other states had already taken regulatory steps to reduce the contamination. “Today’s decision is built on science and local success stories and fulfills President Trump’s promise to pare back burdensome ‘one-size-fits-all’ overregulation for the American people,” Mr. Wheeler said in a statement. “State and local water systems are effectively and efficiently managing levels of perchlorate. Our state partners deserve credit for their leadership on protecting public health in their communities, not unnecessary federal intervention.” Environmentalists said both moves showed a disregard for science, the law and public health, and they criticized the agency for claiming credit for state regulations done in the face of federal inaction. “Today’s decision is illegal, unscientific and unconscionable,” said Erik D. Olson, the senior strategic director for health at the Natural Resources Defense Council, an advocacy group. “The Environmental Protection Agency is threatening the health of pregnant moms and young children with toxic chemicals in their drinking water at levels that literally can cause loss of I.Q. points. Is this what the Environmental Protection Agency has come to?” © 2020 The New York Times Company

Keyword: Neurotoxins; Development of the Brain
Link ID: 27308 - Posted: 06.19.2020

by Tessa van Leeuwen, Rob van Lier Have you ever considered what your favorite piece of music tastes like? Or the color of Tuesday? If the answer is yes, you might be a synesthete. For people with synesthesia, ordinary sensory events, such as listening to music or reading text, elicit experiences involving other senses, such as perceiving a taste or seeing a color. Synesthesia is not to be confused with common metaphors — such as saying someone ‘sees red’ to describe anger. Instead, synesthetic associations are perceptual, highly specific and idiosyncratic, and typically stable beginning in childhood. And many types exist: A taste can have a shape, a word can have a color, the months of the year may be experienced as an array around the body. In the general population, the phenomenon is relatively rare: Only 2 to 4 percent of people have it. But as much as 20 percent of people with autism experience synesthesia1,2. Why would two relatively rare conditions occur together so often? Over the past few years, researchers have found that people with synesthesia or autism share many characteristics. Synesthetes often have sensory sensitivities and attention differences, as well as other autism traits3,4. The two conditions also share brain connectivity patterns and possibly genes, suggesting they have common biological underpinnings. © 2020 Simons Foundation

Keyword: Autism
Link ID: 27304 - Posted: 06.17.2020

by Peter Hess Early behavioral signs predict seizures in autistic children, according to a new study1. Previous work has shown that 5 to 46 percent of people with autism experience seizures. And autistic adults with epilepsy have, on average, less cognitive ability and weaker daily living skills than their autistic peers who do not have seizures2. The new study shows that people with autism who begin having seizures during childhood show small but significant behavioral differences before they ever experience a seizure, compared with those who do not develop epilepsy. They score lower than their peers on measures of quality of life and adaptive behaviors, which include communication, daily living skills, socialization and motor skills. They score higher on a measure of hyperactivity. The results suggest that seizures and certain behavioral issues in autism could have common origins, says co-lead investigator Jamie Capal, associate professor of pediatrics and neurology at the University of North Carolina at Chapel Hill. “I think it really does show us that in individuals with autism who eventually have epilepsy, there is some shared mechanism early on that we just haven’t been able to identify,” Capal says. Early signs: To investigate the relationship between childhood behaviors in autism and the development of seizures, the researchers analyzed data on 472 autistic children aged 2 to 15 from the Autism Treatment Network, a medical registry that includes 12 clinics in the United States and Canada. None of the children had experienced seizures before enrolling in the network, but 22 developed seizures two to six years after enrollment. © 2020 Simons Foundation

Keyword: Autism; Epilepsy
Link ID: 27294 - Posted: 06.09.2020

Amber Dance They told Marcelle Girard her baby was dead. Back in 1992, Girard, a dentist in Gatineau, Canada, was 26 weeks pregnant and on her honeymoon in the Dominican Republic. When she started bleeding, physicians at the local clinic assumed the baby had died. But Girard and her husband felt a kick. Only then did the doctors check for a fetal heartbeat and realize the baby was alive. The couple was medically evacuated by air to Montreal, Canada, then taken to the Sainte-Justine University Hospital Center. Five hours later, Camille Girard-Bock was born, weighing just 920 grams (2 pounds). Babies born so early are fragile and underdeveloped. Their lungs are particularly delicate: the organs lack the slippery substance, called surfactant, that prevents the airways from collapsing upon exhalation. Fortunately for Girard and her family, Sainte-Justine had recently started giving surfactant, a new treatment at the time, to premature babies. After three months of intensive care, Girard took her baby home. Today, Camille Girard-Bock is 27 years old and studying for a PhD in biomedical sciences at the University of Montreal. Working with researchers at Sainte-Justine, she’s addressing the long-term consequences of being born extremely premature — defined, variously, as less than 25–28 weeks in gestational age. Families often assume they will have grasped the major issues arising from a premature birth once the child reaches school age, by which time any neurodevelopmental problems will have appeared, Girard-Bock says. But that’s not necessarily the case. Her PhD advisers have found that young adults of this population exhibit risk factors for cardiovascular disease — and it may be that more chronic health conditions will show up with time.

Keyword: Development of the Brain
Link ID: 27279 - Posted: 06.04.2020

By Laura Sanders The heart has its own “brain.” Now, scientists have drawn a detailed map of this little brain, called the intracardiac nervous system, in rat hearts. The heart’s big boss is the brain, but nerve cells in the heart have a say, too. These neurons are thought to play a crucial role in heart health, helping to fine-tune heart rhythms and perhaps protecting people against certain kinds of heart disease. But so far, this local control system hasn’t been mapped in great detail. To make their map, systems biologist James Schwaber at Thomas Jefferson University in Philadelphia and colleagues imaged male and female rat hearts with a method called knife-edge scanning microscopy, creating detailed pictures of heart anatomy. Those images could then be built into a 3-D model of the heart. The scientists also plucked out individual neurons and measured the amount of gene activity within each cell. These measurements helped sort the heart’s neurons into discrete groups. Most of these neuron clusters dot the top of the heart, where blood vessels come in and out. Some of these clusters spread down the back of the heart, and were particularly abundant on the left side. With this new view of the individual clusters, scientists can begin to study whether these groups have distinct jobs. The comprehensive, 3-D map of the heart’s little brain could ultimately lead to targeted therapies that could treat or prevent heart diseases, the authors write online May 26 in iScience. © Society for Science & the Public 2000–2020.

Keyword: Development of the Brain
Link ID: 27274 - Posted: 06.03.2020

by Emily Anthes The overproduction of proteins in brain cells called microglia causes social impairments, cognitive deficits and repetitive behavior in male mice, a new study has found.1 These behavioral differences are not present in female mice, or in mice that produce excess protein in other brain cells, including neurons or star-shaped support cells known as astrocytes. Microglia help eliminate excess synapses — connections between brain cells — that form early in life; this pruning process is crucial to healthy brain development. But male mice that have been engineered to overproduce proteins in these cells have enlarged microglia. That, in turn, lowers the cells’ mobility and may prevent them from migrating to synapses that need eliminating. In support of that idea, the mice have too many synapses, the researchers found — a result that mirrors evidence that certain brain regions may be overconnected in people with autism. “Increased protein synthesis in microglia is sufficient to cause autism phenotypes in mice,” says lead investigator Baoji Xu, professor of neuroscience at the Scripps Research Institute in Jupiter, Florida. “Problems in microglia could be an important pathological mechanism for autism.” Malfunctioning microglia: The researchers studied mice that produce excess levels of EIF4E, a protein that facilitates the synthesis of other proteins. Mutations in several genes linked to autism — including TSC1, TSC2, PTEN and FMR1 — are associated with elevated levels of an active form of EIF4E and, as a result, many other proteins in the brain. Mice that overproduce EIF4E also display autism-like behavior, researchers have previously found. © 2020 Simons Foundation

Keyword: Autism; Glia
Link ID: 27273 - Posted: 06.01.2020

By Tina Hesman Saey A genetic variant that raises one’s risk of developing Alzheimer’s disease may also make people more susceptible to COVID-19. People with two copies of a version of the APOE gene called APOE4 are 14 times as likely to develop Alzheimer’s disease as people with two copies of the APOE3 version of the gene (SN: 9/22/17). Those people were also more than twice as likely to test positive for the coronavirus than people with two copies of the APOE3 version, researchers report May 26 in the Journals of Gerontology: Series A. The results come from a study of more than 600 people in England diagnosed with COVID-19 from March 16 to April 26. Two previous studies showed that people with dementia were more likely to have severe cases or to die of COVID-19. This new study found that even people with no signs of dementia or other diseases associated with having APOE4 were still more susceptible to COVID-19 than people with the APOE3 version. Among nearly 400,000 participants in the large genetic database called the UK Biobank, only 3 percent have two copies of APOE4, while 69 percent have two copies of APOE3. The remainder have one of each version. But the APOE4 version was more common than expected among people diagnosed with COVID-19, the study found. Of 622 people who tested positive for the coronavirus, 37 had two copies of APOE4. On a population scale, that means about 410 of every 100,000 people with two copies of that version of the gene would test positive, the researchers calculate. That compares with 179 of every 100,000 people with two copies of APOE3 testing positive. © Society for Science & the Public 2000–2020.

Keyword: Alzheimers; Genes & Behavior
Link ID: 27271 - Posted: 06.01.2020

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

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

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

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

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

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

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

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