Veronique Greenwood Inside a series of tubes in a bright, warm room at Harvard Medical School, hundreds of fruit flies are staying up late. It has been days since any of them have slept: The constant vibrations that shake their homes preclude rest, cling as they might to the caps of the tubes for respite. Not too far away in their own tubes live other sleepless flies, animated with the calm persistence of those consigned to eternal day. A genetic tweak to certain neurons in their brains keeps them awake for as long as they live. They do not live long. The shaken flies and the engineered flies both die swiftly — in fact, the engineered ones survive only half as long as well-rested controls. After days of sleeplessness, the flies’ numbers tumble, then crash. The tubes empty out. The lights shine on. We all know that we need sleep to be at our best. But profound sleep loss has more serious and immediate effects: Animals completely deprived of sleep die. Yet scientists have found it oddly hard to say exactly why sleep loss is lethal. Sleep is primarily seen as a neurological phenomenon, and yet when deprived creatures die, they have a puzzlingly diverse set of failures in the body outside the nervous system. Insufficient sleep in humans and lab animals, if chronic, sets up health problems that surface over time, such as heart disease, high blood pressure, obesity and diabetes. But those conditions are not what slays creatures that are 100% sleep deprived within days or weeks. What does sleep do that makes it deadly to go without? Could answering that question explain why we need sleep in the first place? Under the pale light of the incubators in Dragana Rogulja’s lab at Harvard Medical School, sleepless flies have been living and dying as she pursues the answers. Simons Foundation © 2020

Keyword: Sleep; Neuroimmunology
Link ID: 27285 - Posted: 06.06.2020

By Meredith Wadman In January, one of the first publications on those sickened by the novel coronavirus in Wuhan, China, reported that three out of every four hospitalized patients were male. Data from around the world have since confirmed that men face a greater risk of severe illness and death from COVID-19 than women and that children are largely spared. Now, scientists investigating how the virus does its deadly work have zeroed in on a possible reason: Androgens—male hormones such as testosterone—appear to boost the virus’ ability to get inside cells. A constellation of emerging data supports this idea, including COVID-19 outcomes in men with prostate cancer and lab studies of how androgens regulate key genes. And preliminary observations from Spain suggest that a disproportionate number of men with male pattern baldness—which is linked to a powerful androgen—end up in hospitals with COVID-19. Researchers are rushing to test already approved drugs that block androgens’ effects, deploying them early in infection in hopes of slowing the virus and buying time for the immune system to beat it back. “Everybody is chasing a link between androgens … and the outcome of COVID-19,” says Howard Soule, executive vice president at the Prostate Cancer Foundation, who on 13 May ran a Zoom call presenting the newest research that drew 600 scientists and physicians. A second call scheduled for today will discuss incipient clinical trials. Epidemiological data from around the world have confirmed the early reports of male vulnerability. In Lombardy in Italy, for example, men comprised 82% of 1591 patients admitted to intensive care units (ICUs) from 20 February to 18 March, according to a JAMA paper. And male mortality exceeded that of women in every adult age group in another JAMA study of 5700 New York City patients hospitalized with COVID-19. © 2020 American Association for the Advancement of Science.

Keyword: Hormones & Behavior; Sexual Behavior
Link ID: 27284 - Posted: 06.04.2020

Hundreds of published studies over the last decade have claimed it's possible to predict an individual’s patterns of thoughts and feelings by scanning their brain in an MRI machine as they perform some mental tasks. But a new analysis by some of the researchers who have done the most work in this area finds that those measurements are highly suspect when it comes to drawing conclusions about any individual person’s brain. Watching the brain through a functional MRI machine (fMRI) is still great for finding the general brain structures involved in a given task across a group of people, said Ahmad Hariri, a professor of psychology and neuroscience at Duke University who led the reanalysis. “Scanning 50 people is going to accurately reveal what parts of the brain, on average, are more active during a mental task, like counting or remembering names,” Hariri said Functional MRI measures blood flow as a proxy for brain activity. It shows where blood is being sent in the brain, presumably because neurons in that area are more active during a mental task. The problem is that the level of activity for any given person probably won’t be the same twice, and a measure that changes every time it is collected cannot be applied to predict anyone’s future mental health or behavior. Hariri and his colleagues reexamined 56 published papers based on fMRI data to gauge their reliability across 90 experiments. Hariri said the researchers recognized that “the correlation between one scan and a second is not even fair, it’s poor.” © Copyright 2020 Duke University.

Keyword: Brain imaging
Link ID: 27283 - Posted: 06.04.2020

by Chloe Williams / A new flexible electrode array can detect the activity of neurons in a rat’s brain at high resolution for more than a year1. The device could be used to study how neuronal activity is altered in autism. Arrays usually have wires connected to each electrode to pick up its signal, but this design is bulky and works only in arrays consisting of 100 electrodes or fewer, limiting the array’s coverage and resolution. Devices with thousands of electrodes have integrated switches to consolidate signals into fewer wires. But these devices usually have a lifespan of only a few days. Their polymer-based coatings are often permeable to water or contain tiny defects that allow body fluids to seep into the device and current to leak out, damaging both the device and brain tissue. The new device combines electronic switches and a specialized protective coating so that scientists can record activity at the surface of the brain at high resolution over extended periods of time. The array, called Neural Matrix, consists of 1,008 surface electrodes laid out in 28 columns and 36 rows. Switches, or transistors, built into the array combine signals from all the electrodes in a column to a single output wire. The signals from each electrode in the column are recorded via the wire in a specific sequence, making it possible to separate them later. © 2020 Simons Foundation

Keyword: Brain imaging
Link ID: 27282 - Posted: 06.04.2020

By Marina Wang The classic eye exam may be about to get an upgrade. Researchers have developed an online vision test—fueled by artificial intelligence (AI)—that produces much more accurate diagnoses than the sheet of capital letters we’ve been staring at since the 19th century. If perfected, the test could also help patients with eye diseases track their vision at home. “It’s an intriguing idea” that reveals just how antiquated the classic eye test is, says Laura Green, an ophthalmologist at the Krieger Eye Institute. Green was not involved with the work, but she studies ways to use technology to improve access to health care. The classic eye exam, known as the Snellen chart, has been around since 1862. The farther down the sheet a person can read, the better their vision. The test is quick and easy to administer, but it has problems, says Chris Piech, a computer scientist at Stanford University. Patients start to guess at letters when they become blurry, he says, which means they can get different scores each time they take the test. Piech is no stranger to the Snellen test. At age 10, doctors diagnosed him with chronic uveitis, an inflammatory eye disease. “I was sitting through all these tests and it was pretty obvious to me that it was terribly inaccurate,” he says. He wanted to find a way to remove human error from the Snellen exam, while improving its accuracy. © 2020 American Association for the Advancement of Science.

Keyword: Vision; Robotics
Link ID: 27281 - Posted: 06.04.2020

In a nationwide study, NIH funded researchers found that the presence of abnormal bundles of brittle blood vessels in the brain or spinal cord, called cavernous angiomas (CA), are linked to the composition of a person’s gut bacteria. Also known as cerebral cavernous malformations, these lesions which contain slow moving or stagnant blood, can often cause hemorrhagic strokes, seizures, or headaches. Current treatment involves surgical removal of lesions when it is safe to do so. Previous studies in mice and a small number of patients suggested a link between CA and gut bacteria. This study is the first to examine the role the gut microbiome may play in a larger population of CA patients. Led by scientists at the University of Chicago, the researchers used advanced genomic analysis techniques to compare stool samples from 122 people who had at least one CA as seen on brain scans, with those from age- and sex-matched, control non-CA participants, including samples collected through the American Gut Project(link is external). Initially, they found that on average the CA patients had more gram-negative bacteria whereas the controls had more gram-positive bacteria, and that the relative abundance of three gut bacterial species distinguished CA patients from controls regardless of a person’s sex, geographic location, or genetic predisposition to the disease. Moreover, gut bacteria from the CA patients appeared to produce more lipopolysaccharide molecules which have been shown to drive CA formation in mice. According to the authors, these results provided the first demonstration in humans of a “permissive microbiome” associated with the formation of neurovascular lesions in the brain.

Keyword: Stroke
Link ID: 27280 - Posted: 06.04.2020

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 Nicholas Bakalar Women who take benzodiazepines, such as Valium or Xanax, before becoming pregnant may be at increased risk for ectopic pregnancy, a new study found. An ectopic, or tubal, pregnancy is one in which a fertilized egg grows outside the uterus, often in a fallopian tube, and it is a life-threatening event. The egg must be removed with medication or surgery. Benzodiazepines, sold by prescription under several brand names, are widely prescribed for anxiety, sleep problems and seizures. The study, in Human Reproduction, used an insurance database of 1,691,366 pregnancies to track prescriptions for benzodiazepines in the 90 days before conception. Almost 18,000 of the of the women had used the drugs, and the scientists calculated that these women were 47 percent more likely to have a tubal pregnancy than those who did not. The study controlled for other risks for tubal pregnancy, including sexually transmitted infections, pelvic infection, use of an intrauterine device, smoking and fertility treatments. “Women planning a pregnancy who are using these drugs should talk to their care provider to see whether a change in treatment is possible, and then slowly change treatment before going off their contraceptive,” said the lead author, Elizabeth Wall-Wieler, a postdoctoral fellow at Stanford University. “Women for whom there is no alternative, or who have an unplanned pregnancy, should let their care provider know, and those pregnancies should be monitored carefully. The key to treating ectopic pregnancy is to treat it early.” © 2020 The New York Times Company

Keyword: Drug Abuse; Sexual Behavior
Link ID: 27278 - Posted: 06.04.2020

By Robert Martone When a concert opens with a refrain from your favorite song, you are swept up in the music, happily tapping to the beat and swaying with the melody. All around you, people revel in the same familiar music. You can see that many of them are singing, the lights flashing to the rhythm, while other fans are clapping in time. Some wave their arms over their head, and others dance in place. The performers and audience seem to be moving as one, as synchronized to one another as the light show is to the beat. A new paper in the journal NeuroImage has shown that this synchrony can be seen in the brain activities of the audience and performer. And the greater the degree of synchrony, the study found, the more the audience enjoys the performance. This result offers insight into the nature of musical exchanges and demonstrates that the musical experience runs deep: we dance and feel the same emotions together, and our neurons fire together as well. In the study, a violinist performed brief excerpts from a dozen different compositions, which were videotaped and later played back to a listener. Researchers tracked changes in local brain activity by measuring levels of oxygenated blood. (More oxygen suggests greater activity, because the body works to keep active neurons supplied with it.) Musical performances caused increases in oxygenated blood flow to areas of the brain related to understanding patterns, interpersonal intentions and expression. Data for the musician, collected during a performance, was compared to those for the listener during playback. In all, there were 12 selections of familiar musical works, including “Edelweiss,” Franz Schubert’s “Ave Maria,” “Auld Lang Syne” and Ludwig van Beethoven’s “Ode to Joy.” The brain activities of 16 listeners were compared to that of a single violinist. © 2020 Scientific American,

Keyword: Hearing
Link ID: 27277 - Posted: 06.03.2020

Patti Neighmond Having trouble getting to sleep these days? You're not alone. For people with a history of insomnia, sleep problems are magnified right now. And many who never struggled before are suddenly experiencing interruptions in their nightly rest or difficulty falling asleep. It's pretty typical that in moments of anxiety, sleep suffers, but the situation we're all living through today means the anxiety never stops, says neurologist and sleep specialist Dr. Douglas Kirsch, past president of the American Academy of Sleep Medicine. For occasional insomnia, the problems go away when the specific trigger is resolved. But now, he says, there's no resolution or relief from "the constant inflow of anxiety-provoking news." And that spells trouble for sleep. Family doctors and sleep specialists say many people who are feeling grief, frustration and anxiety, whether about the pandemic, financial worries or racial inequalities and unrest in the U.S., are finding themselves unable to sleep. And it's not just the worry. It's the interrupted schedules and isolation of the pandemic too. Here's why it's not all in your head and what they say you can do about it. We're suffering "collective social anxiety" — tame it to sleep better Before the pandemic, Arlene Rentas, a busy currency trader in Charlotte, N.C., kept a regular schedule and slept like clockwork. She would awaken at 5:30 in the morning and be out the door by 7 a.m., home by 8 p.m. and, after a quick run, in bed around 10 p.m. © 2020 npr

Keyword: Sleep; Stress
Link ID: 27276 - Posted: 06.03.2020

Ruth Williams Experiments in mice and observations in humans have suggested the bone protein osteocalcin acts as a hormone regulating, among other things, metabolism, fertility, exercise capacity and acute stress. That interpretation is now partially in doubt. Two independent papers published yesterday (May 28) in PLOS Genetics, each of which presents a new osteocalcin knockout mouse strain, report that glucose metabolism and fertility were unaffected in the animals. While some researchers praise the studies, others highlight weaknesses. “I thought they were very good papers. I think the authors should be congratulated for very comprehensive studies of both skeletal and extraskeletal functions of osteocalcin,” says emeritus bone researcher Caren Gundberg of Yale School of Medicine who was not involved in the research. Skeletal biologist Gerard Karsenty of Columbia University disagrees. “There have been 25 laboratories in the world . . . that have shown osteocalcin is a hormone,” says Karsenty. These two papers “do not affect the work of [those] groups,” he adds, “because they are . . . technically flawed.” This tiny protein, one of the most abundant in the body, is produced and secreted by bone-forming osteoblast cells. In the 40 or so years since osteocalcin’s discovery, its precise function, or functions—whether in the bone or endocrine system—have not been fully pinned down. Studies from Karsenty’s lab more than 10 years ago were the first to indicate that osteocalcin could act as a hormone, regulating glucose metabolism. But the suggested hormonal function has been questioned for its relevance to humans. For example, while studies in people have shown that levels of osteocalcin in the blood are correlated with diabetes, whether this is a cause or effect is unclear. © 1986–2020 The Scientist.

Keyword: Hormones & Behavior; Obesity
Link ID: 27275 - Posted: 06.03.2020

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

Ruth Williams With their tiny brains and renowned ability to memorize nectar locations, honeybees are a favorite model organism for studying learning and memory. Such research has indicated that to form long-term memories—ones that last a day or more—the insects need to repeat a training experience at least three times. By contrast, short- and mid-term memories that last seconds to minutes and minutes to hours, respectively, need only a single learning experience. Exceptions to this rule have been observed, however. For example, in some studies, bees formed long-lasting memories after a single learning event. Such results are often regarded as circumstantial anomalies, and the memories formed are not thought to require protein synthesis, a molecular feature of long-term memories encoded by repeated training, says Martin Giurfa of the University of Toulouse. But the anomalous findings, together with research showing that fruit flies and ants can form long-term memories after single experiences, piqued Giurfa’s curiosity. Was it possible that honeybees could reliably do the same, and if so, what molecular mechanisms were required? Giurfa reasoned that the ability to form robust memories might depend on the particular type of bee and the experience. Within a honeybee colony, there are nurses, who clean the hive and feed the young; guards, who patrol and protect the hive; and foragers, who search for nectar. Whereas previous studies have tested bees en masse, Giurfa and his colleagues focused on foragers, tasking them with remembering an experience relevant to their role: an odor associated with a sugary reward. © 1986–2020 The Scientist.

Keyword: Learning & Memory; Evolution
Link ID: 27272 - 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

Diana Kwon What if you could boost your brain’s processing capabilities simply by sticking electrodes onto your head and flipping a switch? Berkeley, California–based neurotechnology company Humm has developed a device that it claims serves that purpose. Their “bioelectric memory patch” is designed to enhance working memory—the type of short-term memory required to temporarily hold and process information—by noninvasively stimulating the brain. In recent years, neurotechnology companies have unveiled direct-to-consumer (DTC) brain stimulation devices that promise a range of benefits, including enhancing athletic performance, increasing concentration, and reducing depression. Humm’s memory patch, which resembles a large, rectangular Band-Aid, is one such product. Users can stick the device to their forehead and toggle a switch to activate it. Electrodes within the patch generate transcranial alternating current stimulation (tACS), a method of noninvasively zapping the brain with oscillating waves of electricity. The company recommends 15 minutes of stimulation to give users up to “90 minutes of boosted learning” immediately after using the device. The product is set for public release in 2021. Over the last year or so, Humm has generated much excitement among investors, consumers, and some members of the scientific community. In addition to raising several million dollars in venture capital funding, the company has drawn interest both from academic research labs and from the United States military. According to Humm cofounder and CEO Iain McIntyre, the US Air Force has ordered approximately 1,000 patches to use in a study at their training academy that is set to start later this year. © 1986–2020 The Scientist

Keyword: Learning & Memory
Link ID: 27269 - 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

By Laura Sanders I’m on deadline, but instead of focusing, my mind buzzes with unrelated tidbits. My first-grader’s tablet needs an update before her online school session tomorrow. Heartbreaking deaths from COVID-19 in New York City make me tear up again. Was that a kid’s scream from upstairs? Do I need to run up there, or will my husband take care of it? These hornets of thoughts drive out the clear thinking my job demands. Try as I might to conjure up a coherent story, the relevant wisps float away. I’m scattered, worried and tired. And even though we’re all socially isolated, I’m not alone. The pandemic — and its social and economic upheavals — has left people around the world feeling like they can’t string two thoughts together. Stress has really done a number on us. That’s no surprise to scientists who study stress. Our brains are not built to do complex thinking, planning and remembering in times of massive upheaval. Feeling impaired is “a natural biological response,” says Amy Arnsten, a neuroscientist at Yale School of Medicine. “This is how our brains are wired.” Decades of research have chronicled the ways stress can disrupt business as usual in our brains. Recent studies have made even more clear how stress saps our ability to plan ahead and have pointed to one way that stress changes how certain brain cells operate. Scientists recognize the pandemic as an opportunity for a massive, real-time experiment on stress. COVID-19 foisted on us a heavy mix of health, economic and social stressors. And the end date is nowhere in sight. Scientists have begun collecting data to answer a range of questions. But one thing is clear: This pandemic has thrown all of us into uncharted territory. © Society for Science & the Public 2000–2020

Keyword: Stress
Link ID: 27266 - Posted: 05.28.2020