By Judith Graham, Ask Edith Smith, a proud 103-year-old, about her friends, and she’ll give you an earful. There’s Johnetta, 101, whom she’s known for 70 years and who has Alzheimer’s disease. “I call her every day and just say ‘Hi, how are you doing?’ She never knows, but she says hi back, and I tease her,” Smith said. There’s Katie, 93, whom Smith met during a long teaching career with the Chicago Public Schools. “Every day we have a good conversation. She’s still driving and lives in her own house, and she tells me what’s going on.” Then there’s Rhea, 90, whom Smith visits regularly at a retirement facility. And Mary, 95, who doesn’t leave her house anymore, “so I fix her a basket about once a month of jelly and little things I make and send it over by cab.” And fellow residents at Smith’s Chicago senior community, whom she recognizes with a card and a treat on their birthdays. “I’m a very friendly person,” Smith said, when asked to describe herself. That may be one reason why this lively centenarian has an extraordinary memory for someone her age, suggests a recent study by researchers at Northwestern University highlighting a notable link between brain health and positive relationships. For nine years, these experts have been examining “SuperAgers”—men and women over age 80 whose memories are as good—or better—than people 20 to 30 years younger. Every couple of years, the group fills out surveys about their lives and gets a battery of neuropsychological tests, brain scans and a neurological examination, among other evaluations. © 2017 Scientific American,

Keyword: Stress
Link ID: 24455 - Posted: 12.26.2017

By Katarina Zimmer | CRISPR-Cas9 gene editing can extend survival in a mouse model of amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative disease, according to a study published yesterday (December 20) in Science Advances. “The treatment did not make the ALS mice normal and it is not yet a cure,” study coauthor David Schaffer, a professor of chemical and biomolecular engineering at the University of California, Berkeley, says in a press release. “But based upon what I think is a really strong proof of concept, CRISPR-Cas9 could be a therapeutic molecule for ALS.” ALS, or Lou Gehrig’s disease, affects some 20,000 Americans and is characterized by the premature death of motor neurons in the brain stem and spinal cord. The disease causes progressive muscle deterioration and eventually results in paralysis and death. There are no available treatments to delay the muscle wasting and currently approved drugs can extend survival by a few months at most. Schaffer and his colleagues suspected that ALS could be treated through genome editing because some forms of the disease (around 20 percent of inherited forms and 2 percent of all cases) are caused by dominant mutations in a gene that encodes superoxide dismutase 1 (SOD1), an enzyme that helps protect cells against toxic free radicals. © 1986-2017 The Scientist

Keyword: ALS-Lou Gehrig's Disease ; Genes & Behavior
Link ID: 24454 - Posted: 12.22.2017

Michaeleen Doucleff It's not every day that surgeons develop a new brain surgery that could save tens of thousands of babies, even a hundred thousand, each year. And it's definitely not every day that the surgery is developed in one of the world's poorest countries. But that's exactly what neurosurgeons from Boston and Mbale, Uganda, report Wednesday in the New England Journal of Medicine. The treatment is for a scary condition in which a baby's head swells up, almost like balloon. It's called hydrocephalus, or "water on the brain." But a more accurate description is "spinal fluid inside the brain." Inside our brains, there are four chambers that continually fill up and release spinal fluid. So their volume stays constant. In babies with hydrocephalus, the chambers don't drain properly. They swell up, putting pressure on the brain. If left untreated about half the children will die, and the others will be badly disabled. Traditionally doctors treat hydrocelphalus in the U.S. with what's called a shunt: They place a long tube in the baby's brain, which allows the liquid to drain into the child's stomach. © 2017 npr

Keyword: Development of the Brain
Link ID: 24453 - Posted: 12.22.2017

By Rebecca Keogh Imagine you are at Ikea to pick up a sofa for your new flat. You see one you like, a wine-coloured two-seater with big soft cushions. You imagine what it would look like with your current furniture, and decide that’s the sofa you want. As you continue meandering through the store you find a nice industrial-style lamp and coffee table, so you try to imagine what they might look like with the sofa. But imagining all three items together is more difficult than just imagining the sofa alone. How many pieces of furniture do you think you could rearrange in your mind? Is there a limit to how much we can imagine at once, or is our imagination truly unlimited? viewpoints Limitations to our imagery can constrain what we are able to achieve, both in daily life and in therapeutic interventions. This is the question that my supervisor and I tried to answer in our lab at the University of New South Wales recently. Instead of furniture, we used simple shapes known as Gabor patches, which are essentially circles with lines through them. We also used a visual illusion known as binocular rivalry. Binocular rivalry occurs when two different images are shown, one to each eye, and instead of seeing a mix of the two images you see only one of them, either the image that was presented to the left eye or the image presented to the right eye. Previous work by Joel Pearson (my supervisor) has shown that simply imagining a Gabor patch, or seeing a very weak Gabor patch, will make you more likely to see that image in a subsequent binocular rivalry display. Copyright 2017 Undark

Keyword: Vision; Attention
Link ID: 24452 - Posted: 12.22.2017

A promising approach to post-operative incision-site pain control uses a naturally occurring plant molecule called resiniferatoxin (RTX). RTX is found in Euphorbia resinifera, a cactus-like plant native to Morocco, which is 500 times more potent than the chemical that produces heat in hot peppers, and may help limit the use of opioid medication while in the hospital and during home recovery. In a paper published online in Anesthesiology, the peer-reviewed medical journal of the American Society of Anesthesiologists, researchers found that RTX could be used to block postoperative incisional pain in an animal model. Many medical providers turn to opioids, such as morphine or fentanyl, for moderate to severe post-operative pain relief, but these often come with side effects that can interfere with recovery, including respiratory depression, inhibition of gut motility and constipation, nausea and vomiting. Prolonged use of opioids can produce tolerance and introduces the risk of misuse. RTX is not an opioid and does not act in the brain but rather on the nerve endings in the skin. Scientists found that it can be used to block pain from the surgical incision selectively for approximately 10 days. In the study, researchers pre-treated the skin incision site with RTX to render the nerve endings in the skin and subcutaneous tissue along the incision path selectively insensitive to pain. Unlike local anesthetics, which block all nerve activity including motor axons, RTX allows many sensations, like touch and vibration, as well as muscle function, to be preserved. Long after the surgery, and towards the end of healing of an incision wound, the nerve endings eventually grow back. Thus, pain from the skin incision is reduced during the recovery period.

Keyword: Pain & Touch
Link ID: 24451 - Posted: 12.22.2017

By Catherine Offord Jerrold Olefsky has spent much of the last decade trying to decipher the connection between obesity and the risk for type 2 diabetes. It’s now known that “in obesity, the adipose tissue becomes highly inflamed and fills up with macrophages and other immune cells,” Olefsky, an endocrinologist at the University of California, San Diego, explains. “This inflammation is very important for causing insulin resistance,” in which cells fail to respond to hormonal signals to take up glucose. But a crucial piece of the puzzle has been missing. “Insulin resistance is a systemic thing,” Olefsky says. For inflamed fat tissue to trigger it, “somehow, all the tissues must talk to each other. We just didn’t know how.” Research has not supported a major role for early suspects such as cytokines. But reading a paper a few years ago on the role of tiny vesicles called exosomes in intercellular communication in cancer, Olefsky was struck by the fact that, “Well, gee, all these cells make exosomes.” Known to carry microRNAs (miRNAs)—small nucleic acids that influence gene expression—exosomes seemed like plausible candidates for an inter-tissue communication system in obesity. Olefsky’s group isolated macrophages from adipose tissue in obese and lean mice and harvested exosomes produced by the cells in vitro. Then, the researchers added these vesicles to cultured muscle, liver, and fat cells—major insulin targets in the body. While lean-type exosomes made recipient cells “super insulin-sensitive,” Olefsky says, obese-type exosomes induced insulin resistance. In vivo work showed a similar effect: lean mice injected with obese-type exosomes became insulin resistant without gaining weight, while obese mice treated with lean-type exosomes stayed obese, but developed normalized insulin sensitivity. © 1986-2017 The Scientist

Keyword: Obesity
Link ID: 24450 - Posted: 12.22.2017

Hannah Devlin Science correspondent Deafness has been prevented in mice using gene editing for the first time, in an advance that could transform future treatment of genetic hearing loss. The study found that a single injection of a gene editing cocktail prevented progressive deafness in baby animals that were destined to lose their hearing. “We hope that the work will one day inform the development of a cure for certain forms of genetic deafness in people,” said Prof David Liu, who led the work at Harvard University and MIT. Nearly half of all cases of deafness have a genetic root, but current treatment options are limited. However, the advent of new high-precision gene editing tools such as Crispr has raised the prospect of a new class of therapies that target the underlying problem. The study, published in the journal Nature, focused on a mutation in a gene called Tmc1, a single wrong letter in the genetic code, that causes the loss of the inner ear’s hair cells over time. The delicate hairs, which sit in a spiral-shaped organ called the cochlea, vibrate in response to sound waves. Nerve cells pick up the physical motion and transmit it to the brain, where it is perceived as sound. If a child inherits one copy of the mutated Tmc1 gene they will suffer progressive hearing loss, normally starting in the first decade of life and resulting in profound deafness within 10 to 15 years. However, since most people affected by the mutation will also have a healthy version of the gene, inherited from their other parent, the scientists wanted to explore whether deleting the faulty version worked as a treatment. © 2017 Guardian News and Media Limited

Keyword: Hearing; Genes & Behavior
Link ID: 24449 - Posted: 12.21.2017

Laura Sanders Globs of an inflammation protein beckon an Alzheimer’s protein and cause it to accumulate in the brain, a study in mice finds. The results, described in the Dec. 21/28 Nature, add new details to the relationship between brain inflammation and Alzheimer’s disease. Researchers suspect that this inflammatory cycle is an early step in the disease, which raises the prospect of being able to prevent the buildup of amyloid-beta, the sticky protein found in brains of people with Alzheimer’s disease. “It is a provocative paper,” says immunologist Marco Colonna of Washington University School of Medicine in St. Louis. Finding an inflammatory protein that can prompt A-beta to clump around it is “a big deal,” he says. Researchers led by Michael Heneka of the University of Bonn in Germany started by studying specks made of a protein called ASC that’s produced as part of the inflammatory response. (A-beta itself is known to kick-start this inflammatory process.) Despite being called specks, these are large globs of protein that are created by and then ejected from brain immune cells called microglia when inflammation sets in. A-beta then accumulates around these ejected ASC specks in the space between cells, Haneke and colleagues now propose. Specks of a type of inflammation protein called ASC (red) form the core of amyloid-beta plaques (green) in the brain of a 4-month-old mouse (top) and in the brain of a person who had Alzheimer’s disease (bottom). |© Society for Science & the Public 2000 - 2017.

Keyword: Alzheimers
Link ID: 24448 - Posted: 12.21.2017

By Kasra Zarei Depression and antidepressant use are at all-time highs in the year 2017, but for about a third of those affected, depression still doesn’t get better with medication—and for these patients, transcranial magnetic stimulation (TMS), which uses powerful magnets to stimulate brain cells noninvasively, can be a viable option. To be clear, TMS isn’t new; it was first approved by the FDA in 2008. What’s new is that the evidence for its safety and effectiveness has only gotten stronger. TMS is now generally covered by insurance companies for treatment-resistant depression, and new studies have shown that combining it with traditional treatments like psychotherapy can lead to significantly higher response rates. Some scientists also now believe TMS can be a dominant therapy compared to antidepressants, based on its lower cost, higher net monetary benefit and better quality of life outcomes produced. Although there are still many questions about TMS left unanswered, it is a treatment with a strong presence in fighting depression and much promise as personalized TMS grows closer to becoming a reality. According to the World Health Organization, an estimated 350 million people worldwide suffer from depression, making it the leading cause of disability worldwide. As many as 30 percent of people with depression are resistant to medication, and show suicide thoughts and attempts, and an overall poor quality of life. With traditional treatment options ineffective, these patients need a solution. © 2017 Scientific American

Keyword: Depression
Link ID: 24447 - Posted: 12.21.2017

By NICHOLAS BAKALAR Eating leafy greens may help slow mental decline. Researchers studied 960 men and women ages 58 to 99 who completed food frequency questionnaires and had two or more cognitive assessments over an average of almost five years of follow-up. Among many other foods, the researchers recorded the number of servings of lettuce, spinach, kale and collard greens. At least twice over the course of the study they administered cognitive tests covering memory, spatial ability and perceptual speed. Those who ate the most leafy vegetables — one to two servings a day — scored the equivalent of 11 years younger on tests of mental ability than those who ate little or none. Greens contain lutein, folate, beta carotene and other nutrients known to affect aging. Could the same effect be obtained with supplements containing these nutrients? Probably not. “The evidence for supplements is not positive, either from observational studies or clinical trials,” said the lead author, Martha Clare Morris, a professor of epidemiology at Rush University in Chicago. “The nutrients in food have many different forms and interactions. A specific formulation put in a pill with the same effect? That’s wishful thinking.” The study, in Neurology, controlled for smoking, physical activity and other factors, but it is observational, and does not prove cause and effect. © 2017 The New York Times Company

Keyword: Alzheimers
Link ID: 24446 - Posted: 12.21.2017

Laurel Hamers The hardy souls who manage to push shorts season into December might feel some kinship with the thirteen-lined ground squirrel. The critter hibernates all winter, but even when awake, it’s less sensitive to cold than its nonhibernating relatives, a new study finds. That cold tolerance is linked to changes in a specific cold-sensing protein in the sensory nerve cells of the ground squirrels and another hibernator, the Syrian hamster, researchers report in the Dec. 19 Cell Reports. The altered protein may be an adaptation that helps the animals drift into hibernation. In experiments, mice, which don’t hibernate, strongly preferred to hang out on a hot plate that was 30° Celsius versus one that was cooler. Syrian hamsters (Mesocricetus auratus) and the ground squirrels (Ictidomys tridecemlineatus), however, didn’t seem to notice the chill until plate temperatures dipped below 10° Celsius, notes study coauthor Elena Gracheva, a neurophysiologist at Yale University. Further work revealed that a cold-sensing protein called TRPM8 wasn’t as easily activated by cold in the squirrels and hamsters as in rats. Found in the sensory nerve cells of vertebrates, TRPM8 typically sends a sensation of cold to the brain when activated by low temperatures. It’s what makes your fingertips feel chilly when you’re holding a glass of ice water. It’s also responsible for the cooling sensation in your mouth after you chew gum made with menthol. |© Society for Science & the Public 2000 - 2017

Keyword: Miscellaneous
Link ID: 24445 - Posted: 12.20.2017

By Melissa McCradden Do girls take longer than boys to recover after a concussion? A recent study of middle- and high school athletes they found that the female athletes took twice as long to be symptom-free as the male athletes. Shockingly, the female athletes took nearly a full month to report being symptom-free, while the male athletes took less than two weeks. It was reported widely across the media as evidence the young women may have a special problem with concussions. This conclusion, unfortunately, is not well supported. Meta-analyses (which look at the full body of literature on a topic) have found conflicting evidence regarding male-female differences in concussion recovery. Consensus statements on sport-related concussion have not deemed there to be sufficient reason to distinguish between the genders for return-to-play protocols or guidelines on handling the injury. And the study itself has important flaws. There are hundreds of thousands of female athletes who have scholarships, professional careers, and Olympic hopes at stake, and let’s not forget the basic principle that our girls deserve equal opportunity as the boys to participate in sports. These conclusions have real consequences, and we need to get our information right. One of the strongest predictive factors for prolonged post-concussion symptoms is expectation of recovery—those who believe they will recover quickly are more likely to do so. So if we label women in this way, it can have a direct, negative effect on their recovery from concussion. © 2017 Scientific American

Keyword: Brain Injury/Concussion; Sexual Behavior
Link ID: 24444 - Posted: 12.20.2017

by Ben Guarino Each year between February and June, the fish gather to spawn in Mexico's Colorado River Delta. The fish, a type of croaker called the Gulf corvina, meet in water as cloudy as chocolate milk. It's a reunion for the entire species, all members of which reproduce within a dozen-mile stretch of the delta. When the time is right, a few days before the new or full moons, the male fish begin to sing. To humans, the sound is machine guns going off just below the waterline. To female fish, the rapid burr-burr-burr is a Bing Crosby croon. Make that Bing cranked up to 11. Marine biologists who recorded the sound describe the animals as the “loudest fish ever documented,” said Timothy J. Rowell, at the Scripps Institution of Oceanography in California. Rowell and Brad E. Erisman, a University of Texas at Austin fisheries scientist, spent four days in 2014 snooping on the fish with sonar and underwater microphones. The land surrounding the delta is desolate, Rowell said. Fresh water that once fed wild greenery has been diverted to faucets and hoses. But the delta is alive with the sound of fish. “When you arrive at the channels of the delta, you can hear it in the air even while the engine is running on the boat,” Rowell said. © 1996-2017 The Washington Post

Keyword: Hearing; Animal Communication
Link ID: 24443 - Posted: 12.20.2017

Scientists have found a new way to explain the hearing loss caused by cisplatin, a powerful drug used to treat many forms of cancer. Using a highly sensitive technique to measure and map cisplatin in mouse and human inner ear tissues, researchers found that forms of cisplatin build up in the inner ear. They also found a region in the inner ear that could be targeted for efforts to prevent hearing loss from cisplatin. The study is published in Nature Communications (link is external), and was supported by the National Institute on Deafness and other Communications Disorders (NIDCD), part of the National Institutes of Health. Cisplatin and similar platinum-based drugs are prescribed for an estimated 10 to 20 percent of all cancer patients. The NIH’s National Cancer Institute supported research that led to the 1965 discovery of cisplatin and continued development leading to its success as an essential weapon in the battle against cancer. The drugs cause permanent hearing loss in 40 to 80 percent of adult patients and at least half of children who receive the drug. The new findings help explain why cisplatin is so toxic to the inner ear, and why hearing loss gets worse after each treatment, can occur long after treatment, and is more severe in children than adults. “Hearing loss can have a major impact on a person’s life,” said James F. Battey, Jr., M.D., Ph.D., director of NIDCD. “Many adults with hearing loss struggle with social isolation and depression, among other conditions. Children who lose their hearing often have problems with social development and keeping up at school. Helping to preserve hearing in cancer patients who benefit from these drugs would be a major contribution to the quality of their lives.”

Keyword: Hearing
Link ID: 24442 - Posted: 12.20.2017

By Simon Makin The brain's reward system learns the actions that produce positive outcomes, such as obtaining food or sex. It then reinforces the desire to initiate those behaviors by inducing pleasure in anticipation of the relevant action. But in some circumstances this system can become oversensitized to pleasurable but harmful behaviors, producing pathological impulses like drug addiction, binge eating and compulsive gambling. But what if we could spot impulsive urges in the brain and intervene to prevent the act? This is the promise of a new study published December 18 in Proceedings of the National Academy of Sciences, led by neurosurgeon Casey Halpern, of Stanford University. His team identified a “signature” of impulsive urges in part of the brain's reward-learning circuitry, the nucleus accumbens. Delivering electrical pulses to this region on detecting this activity reduced binge-eating behavior in mice. They also observed the same signature in a human brain, suggesting the technique has potential for treating a range of conditions involving compulsive behaviors. “We've identified a brain biomarker of loss of control,” Halpern says. “If we can use that to prevent any of these potentially dangerous actions, we can help a lot of people.” Researchers used a variation on deep-brain stimulation (DBS) in their experiments, a well-established treatment to diminish the shaking present in Parkinson's disease that is also showing promise in other conditions including depression and obsessive-compulsive disorder. Exactly how DBS has beneficial effects is still being debated, but there can be side effects. When treating movement disorders, patients may experience tingling and muscle contraction, says neurosurgeon Tipu Aziz of the University of Oxford. The long-term consequences in other regions are unknown but could include seizures, or effects on cognition, he says. © 2017 Scientific American,

Keyword: Drug Abuse; Obesity
Link ID: 24441 - Posted: 12.20.2017

Esther Landhuis Picture this: While reaching for the cookie jar — or cigarette or bottle of booze or other temptation — a sudden slap denies your outstretched hand. When the urge returns, out comes another slap. Now imagine those "slaps" occurring inside the brain, protecting you in moments of weakness. In a report published Monday in the Proceedings of the National Academy of Sciences, Stanford neuroscientists say they've achieved this sort of mind-reading in binge-eating mice. They found a telltale pattern of brain activity that comes up seconds before the animals start to pig out — and delivering a quick zap to that part of the brain kept the mice from overindulging. Whether this strategy could block harmful impulses in people remains unclear. For now the path seems promising. The current study used a brain stimulation device already approved for hard-to-treat epilepsy. And based on the new findings, a clinical trial testing this off-the-shelf system for some forms of obesity could start as early as next summer, says Casey Halpern, the study's leader and an assistant professor of neurosurgery at Stanford. He thinks the approach could also work for eating disorders and a range of other addictive or potentially life-threatening urges. As a physician-researcher, Halpern specializes in deep brain stimulation (DBS), a surgical treatment in which battery-powered implants send electrical pulses to brain areas where signals go awry. © 2017 npr

Keyword: Obesity; Drug Abuse
Link ID: 24440 - Posted: 12.19.2017

/ By Carrie Arnold Jim and Ida Hall buried their daughter Jerra in a family plot at the bottom of a grassy rise. Several times a year, Jim Hall drives just over a mile from his home on North Main Street in the town of St. Louis, Michigan to Jerra’s headstone in the back corner of Oak Grove Cemetery in his 1997 Chevy pickup. In the 12 years since complications from a rare heart defect claimed the life of their brown-haired toddler, her family continues to cover her grave with stuffed animals (frogs were her favorite). Hall gently sweeps off the leaves and debris covering the childhood paraphernalia and wipes his callused hands on a pair of worn jeans, his tall frame stooped by grief. He stops and stares at the inscription: “Two years, two months, too little.” “We didn’t know what else to write,” he said. “When your daughter is born with a heart condition and doesn’t survive, you just wonder.” Jim Hall’s exposure to PBB as a child makes him valuable in the hunt for the answer to a burning scientific question: Can a father’s exposure to environmental toxins impact the health of his progeny? Jerra’s headstone sits where an umbrella of majestic oaks gives way to the dreadlocks of vines and grasses of a small wetland in the geographic center of Michigan’s Lower Peninsula, a little more than a mile from the chemical plant that once produced a toxic flame retardant called PBB, short for polybrominated biphenyl. Hall can’t help but think it may have killed his little girl. Copyright 2017 Undark

Keyword: Development of the Brain; Epigenetics
Link ID: 24439 - Posted: 12.19.2017

By Elizabeth Quigley BBC Scotland news Scientists are close to establishing what causes a smell associated with sufferers of Parkinson's disease. They hope it could lead to the first diagnostic test for the disease. The breakthrough came after Joy Milne astonished doctors with her ability to detect the disease through smell under scientific conditions. A team from Manchester has found distinctive molecules that seem to be concentrated on the skin of Parkinson's patients. One in 500 people in the UK has Parkinson's - that is 127,000 across Britain. Musky smell It can leave them struggling to walk, speak and sleep. Currently there is no definitive test for the disease, with clinicians diagnosing patients by observing symptoms. This is how the disease has been diagnosed since 1817, when James Parkinson first established it as a recognised medical condition. However, that could change because of Joy Milne from Perth, whose husband Les was told he had Parkinson's at the age of 45. About a decade before her consultant anaesthetist husband was diagnosed, Joy noticed she could detect an unusual musky smell. Joy said: "We had a very tumultuous period, when he was about 34 or 35, where I kept saying to him, 'you've not showered. You've not brushed your teeth properly'. "It was a new smell - I didn't know what it was. I kept on saying to him, and he became quite upset about it. So I just had to be quiet." The retired nurse only linked the odour to the disease after meeting people with the same distinctive smell at a Parkinson's UK support group. © 2017 BBC.

Keyword: Parkinsons; Chemical Senses (Smell & Taste)
Link ID: 24438 - Posted: 12.19.2017

By Mary Bates Whip spiders, also known as tailless whip scorpions, are actually neither spiders nor scorpions. These strange creatures belong to a separate arachnid order called Amblypygi, meaning “blunt rump,” a reference to their lack of tails. Little was known about whip spiders before the turn of this century, but a recent flurry of behavioral and neurophysiological studies has opened a window into their unique sensory world. Researchers have discovered that some of the more than 150 species engage in curious behaviors, including homing, territorial defense, cannibalism, and tender social interactions—all mediated by a pair of unusual sensory organs. Like all arachnids, whip spiders have eight legs. However, they walk on only six. The front two legs are elongated, antennae-like sensory structures called antenniform legs. These legs, three to four times longer than the walking legs, are covered with different types of sensory hairs. They constantly sweep the environment in a whiplike motion, earning whip spiders their common name. Whip spiders use their antenniform legs the way a blind person uses a cane—except that in addition to feeling their environment, whip spiders can smell, taste, and hear with their antenniform legs. All aspects of a whip spider’s life center on the use of these legs, including hunting—whip spiders are dangerous predators, if you’re a small invertebrate that shares the arachnids’ tropical and subtropical ecosystems. When Eileen Hebets, a biologist at the University of Nebraska–Lincoln, recorded the prey capture behavior of the whip spider Phrynus marginemaculatus, she observed a well-choreographed pattern. © 1986-2017 The Scientist

Keyword: Chemical Senses (Smell & Taste); Pain & Touch
Link ID: 24437 - Posted: 12.19.2017

By Sarah DeWeerdt Older men and women are more likely than young ones to have a child with autism, according to multiple studies published in the past decade. Especially regarding fathers, this effect is one of the most consistent findings in the epidemiology of autism. The link between a mother’s age and autism is more complex: Women seem to be at an increased risk both when they are much older and much younger than average, according to some studies. Nailing down why either parent’s age influences autism risk has proved difficult, however. How do we know that older men are at elevated risk of fathering a child with autism? Epidemiologists have gathered data on large numbers of families and calculated how often men of different ages have a child with autism. The first rigorous study of this type, published in 2006, drew on medical records of 132,000 Israeli adolescents. It showed that men in their 30s were 1.6 times as likely to have a child with autism as men younger than 30. Men in their 40s had a sixfold increase in risk. Since then, scientists have conducted similar analyses of data on children born in California, Denmark and Sweden, as well as of an international data set on 5.7 million children. Nearly all of this research has shown an increased prevalence of autism among the children of older fathers. At what age does the risk increase for men? No one knows. The age ranges and ages of the men differ across studies, making results hard to compare. Overall, the findings indicate that the risk increases steadily over time rather than suddenly rising after a certain age. © 1996-2017 The Washington Post

Keyword: Autism; Epigenetics
Link ID: 24436 - Posted: 12.18.2017