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“Bench-to-bedside” describes research that has progressed from basic science in animal models that has led to therapies used in patients. Now, a study in the journal Brain describes what could be considered a direct “aquarium-to-bedside” approach, taking a drug discovered in a genetic zebrafish model of epilepsy and testing it, with promising results, in a small number of children with the disease. The study was supported by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. “This is the first time that scientists have taken a potential therapy discovered in a fish model directly into people in a clinical trial,” said Vicky Whittemore, Ph.D., program director at the NINDS. “These findings suggest that it may be possible to treat neurological disorders caused by genetic mutations through an efficient and precision medicine-style approach.” Scott C. Baraban, Ph.D., the William K. Bowes Jr. Endowed Chair in Neuroscience Research and professor of neurological surgery at the University of California, San Francisco (UCSF), postdoctoral fellow Aliesha Griffin, Ph.D., and colleagues used a zebrafish model of Dravet syndrome to test the drug lorcaserin and found that it suppressed seizure activity in the fish. Dravet syndrome is a severe form of pediatric epilepsy characterized by frequent daily drug-resistant seizures and developmental delays. It is caused by a genetic mutation, which Dr. Baraban’s group was able to introduce into the zebrafish to cause epilepsy. Dr. Baraban and his colleague Kelly Knupp, M.D. at the University of Colorado, Denver, then tested lorcaserin in five children with Dravet syndrome. The children were resistant to other anti-epileptic drugs and participated in this study through a compassionate use, off-label program.
By Tamar Haspel In his new book “The Case Against Sugar,” journalist Gary Taubes makes, as you might easily guess, a spirited case against sugar. His argument is based on the straightforward idea that sugar contributes to obesity and disease well beyond its calorie content, because it affects human metabolism in a way that encourages fat storage. In his new book, the science journalist Gary Taubes takes a hard-nosed look at sugar — and further advances the idea that not all calories are created equal. But there are competing theories of obesity. Who’s right? The debate is often framed as being over the nature of calories themselves, with scientists holding that calories are units of energy — each one no different than the other. Sugar is a carbohydrate, and the body converts carbs to glucose which is then absorbed into the bloodstream. This, in turn, triggers the pancreas to release insulin, the hormone that enables the body to use energy or store it as fat. If a person doesn’t eat many carbohydrates, the pancreas doesn’t release as much insulin, and less fat is stored, forcing the body’s metabolism to increase and burn off that energy. In practical terms, the theory goes, such a person will have an easier time losing weight — or avoiding gaining it. This hypothesis is called, appropriately, the carbohydrate/insulin, or C/I, model, and it is the basis for any number of popular low-carb diets, including Atkins, the Paleo diet, and others. It is also a “minority position” among food scientists, Taubes concedes, and many mainstream nutrition authorities reject it. Copyright 2017 Undark
Link ID: 23208 - Posted: 02.09.2017
By Meredith Wadman A pair of Boston University (BU) brain researchers is pushing back against demands by the National Hockey League (NHL) that they release data, brain pathology slides, and interview records of former NHL players and their families. The scientists accumulated the records during their research on chronic traumatic encephalopathy (CTE), a neurodegenerative disease that has been linked to repetitive head trauma. In affidavits unsealed yesterday in a class action lawsuit brought against the league by former players, BU neuroscientists Robert Stern and Ann McKee argued that giving the league the records would compromise both their ongoing research and the privacy of the players and families involved. The affidavits were first reported on yesterday by Rick Westhead of the Canadian sports network TSN. The NHL first subpoenaed the documents in September 2015. Stern and McKee, a neuropsychologist and a neuropathologist, respectively, at BU’s Chronic Traumatic Encephalopathy Center, have studied the brains of former professional athletes, including hockey players, and are currently using MRI imaging to study scores of living National Football League and college football players in a large study funded by the National Institutes of Health. They say that assurances that players’ privacy will be protected are essential for the success of that $16 million study. In the current litigation, the NHL’s medical expert, Rudy Castellani, asked the BU scientists for copies of gross pathology photographs, all brain slides, and clinical data of former NHL players in order to “verify the accuracy of the reports, evaluate for other pathological processes that may be significant, and conduct a full, independent neuropathological analysis of the cases.” (The scientists interviewed the former NHL players in some cases, and, in others, their surviving family members.) © 2017 American Association for the Advancement of Science.
Keyword: Brain Injury/Concussion
Link ID: 23207 - Posted: 02.09.2017
Swedish researchers say a simple blood test is effective at differentiating symptoms of Parkinson's disease from similar disorders, but it isn't ready for clinical use. In its early stages, neurologists say Parkinson's is difficult to distinguish from rarer disorders, called atypical parkinsonian disorders. They have overlapping symptoms that tend to worsen more quickly and are more likely to lead to death. Researchers are on the hunt for biomarkers to help diagnosis these disorders. One potential biomarker, a nerve protein that can be detected when nerve cells die, is found in higher concentrations in spinal fluid collected by lumbar puncture. Now medical scientists have also found the protein in less invasive blood tests. For the study published in Wednesday's online issue of the journal Neurology, Dr. Oskar Hansson of Sweden's Lund University and his team examined 504 people in three groups. Two of the groups, in England and Sweden, included healthy people and those who had been living with one of the disorders for an average of four to six years. The third group of 109 patients had the diseases for three years or less. "The results of the present study strongly indicate that NfL when measured in blood can be used to distinguish between patients with Parkinson's disease and patients with progressive supranuclear palsy multiple system atrophy and corticobasal degeneration with high diagnostic accuracy," the study's authors said. ©2017 CBC/Radio-Canada.
Link ID: 23206 - Posted: 02.09.2017
In a study of mice and monkeys, National Institutes of Health funded researchers showed that they could prevent and reverse some of the brain injury caused by the toxic form of a protein called tau. The results, published in Science Translational Medicine, suggest that the study of compounds, called tau antisense oligonucleotides, that are genetically engineered to block a cell’s assembly line production of tau, might be pursued as an effective treatment for a variety of disorders. Cells throughout the body normally manufacture tau proteins. In several disorders, toxic forms of tau clump together inside dying brain cells and form neurofibrillary tangles, including Alzheimer’s disease, tau-associated frontotemporal dementia, chronic traumatic encephalopathy and progressive supranuclear palsy. Currently there are no effective treatments for combating toxic tau. "This compound may literally help untangle the brain damage caused by tau,” said Timothy Miller, M.D., Ph.D., the David Clayson Professor of Neurology at Washington University, St. Louis, and the study's senior author. Antisense oligonucleotides are short sequences of DNA or RNA programmed to turn genes on or off. Led by Sarah L. DeVos, a graduate student in Dr. Miller’s lab, the researchers tested sequences designed to turn tau genes off in mice that are genetically engineered to produce abnormally high levels of a mutant form of the human protein. Tau clusters begin to appear in the brains of 6-month-old mice and accumulate with age. The mice develop neurologic problems and die earlier than control mice.
Link ID: 23205 - Posted: 02.09.2017
Scientists who spent years listening to the communication calls of one of our closest ape relatives say their eavesdropping has shed light on the origin of human language. Dr Adriano Reis e Lameira from Durham University recorded and analysed almost 5,000 orangutan "kiss squeaks". He found that the animals combined these purse-lipped, "consonant-like" calls to convey different messages. This could be a glimpse of how our ancestors formed the earliest words. The findings are published in the journal Nature Human Behaviour. "Human language is extraordinarily advanced and complex - we can pretty much transmit any information we want into sound," said Dr Reis e Lameira. "So we tend to think that maybe words evolved from some rudimentary precursor to transmit more complex messages. "We were basically using the orangutan vocal behaviour as a time machine - back to a time when our ancestors were using what would become [those precursors] of consonants and vowels." The team studied kiss squeaks in particular because, like many consonants - the /t/, /p/, /k/ sounds - they depend on the action of the lips, tongue and jaw rather than the voice. "Kiss squeaks do not involve vocal fold action, so they're acoustically and articulatory consonant-like," explained Dr Reis e Lameira. In comparison to research into vowel-like primate calls, the scientists explained, the study of consonants in the evolution of language has been more difficult. But as Prof Serge Wich from Liverpool John Moores University, a lead author in the study, said, they are crucial "building blocks" in the evolution of language. "Most human languages have a lot more consonants than vowels," said Prof Wich. "And if we have more building blocks, we have more combinations." © 2017 BBC.
By Catherine Offord As an undergraduate at Auburn University in the early 2000s, Jeremy Day was thinking of becoming an architect. But an opportunity to work on a research project investigating reward learning in rodents changed the course of his career. “It really hooked me,” he says. “It made me immediately wonder what mechanisms were underlying that behavior in the animal’s brain.” It’s a question Day has pursued ever since. In 2004, he enrolled in a PhD program at the University of North Carolina at Chapel Hill and began studying neural reward signaling under the mentorship of neuroscientist Regina Carelli. “He was a stellar student by all accounts,” Carelli recalls. “He was very clear on the type of work he wanted to do, even that early on in his career.” Focusing on the nucleus accumbens, a brain region involved in associative learning, Day measured dopamine levels in rats undergoing stimulus-reward experiments. Although a rat’s brain released dopamine on receipt of a reward early in training, Day found that, as the rodent became accustomed to specific cues predicting those rewards, this dopamine spike shifted to accompany the cues instead, indicating a changing role for the chemical during learning.1 Day completed his PhD in 2009, but realized that to better understand dopamine signaling and errors in the brain’s reward system that lead to addiction, he would need a broader skill set. “I had a strong background in systems neuroscience, but my training in molecular neuroscience was not as strong,” he explains. So he settled on “a field that I knew almost nothing about?”—epigenetics—and joined David Sweatt’s lab at the University of Alabama at Birmingham (UAB) as a postdoc. For someone used to a field where “data come in as it’s happening,” Day says, “transitioning to a molecular lab where you might do an assay and you don’t get an answer for a week or two was a culture shock.” © 1986-2017 The Scientist
Having a thicker outer layer of the brain is linked to an increased likelihood of having autism. The cerebral cortex is the wrinkled outer layer of the brain that is responsible for many of our most human traits, including thought, language and consciousness. This layer is typically thicker in men than in women, and its structure has been linked to differences in personality. Now brain scans have shown that women who have a more male-like brain structure are three times more likely to have been diagnosed with autism. The study compared the brains of 98 men and women with high functioning autism with those of 98 people who don’t have autism. These findings provide new insights into the brain’s role in sex differences in autism, according to the team that did the study. Autism is thought to be two to five times more common in men than in women, and some think the condition is caused by having an “extreme male brain”. Journal reference: JAMA Psychiatry, DOI: 10.1001/jamapsychiatry.2016.3990 © Copyright Reed Business Information Ltd.
by Linda Rodriguez McRobbie If you ask Jill Price to remember any day of her life, she can come up with an answer in a heartbeat. What was she doing on 29 August 1980? “It was a Friday, I went to Palm Springs with my friends, twins, Nina and Michelle, and their family for Labour Day weekend,” she says. “And before we went to Palm Springs, we went to get them bikini waxes. They were screaming through the whole thing.” Price was 14 years and eight months old. What about the third time she drove a car? “The third time I drove a car was January 10 1981. Saturday. Teen Auto. That’s where we used to get our driving lessons from.” She was 15 years and two weeks old. The first time she heard the Rick Springfield song Jessie’s Girl? “March 7 1981.” She was driving in a car with her mother, who was yelling at her. She was 16 years and two months old. Price was born on 30 December 1965 in New York City. Her first clear memories start from around the age of 18 months. Back then, she lived with her parents in an apartment across the street from Roosevelt Hospital in Midtown Manhattan. She remembers the screaming ambulances and traffic, how she used to love climbing on the living room couch and staring out of the window down 9th Avenue. When she was five years and three months old, her family – her father, a talent agent with William Morris who counted Ray Charles among his clients; her mother, a former variety show dancer, and her baby brother – moved to South Orange, New Jersey. They lived in a three-storey, red brick colonial house with a big backyard and huge trees, the kind of place people left the city for. Jill loved it.
Keyword: Learning & Memory
Link ID: 23201 - Posted: 02.08.2017
Bruce Bower A small, poorly understood segment of the population stays mentally healthy from age 11 to 38, a new study of New Zealanders finds. Everyone else encounters either temporary or long-lasting mental disorders. Only 171 of 988 participants, or 17 percent, experienced no anxiety disorders, depression or other mental ailments from late childhood to middle age, researchers report in the February Journal of Abnormal Psychology. Of the rest, half experienced a transient mental disorder, typically just a single bout of depression, anxiety or substance abuse by middle age. “For many, an episode of mental disorder is like influenza, bronchitis, kidney stones, a broken bone or other highly prevalent conditions,” says study coauthor Jonathan Schaefer, a psychologist at Duke University. “Sufferers experience impaired functioning, many seek medical care, but most recover.” The remaining 408 individuals (41 percent) experienced one or more mental disorders that lasted several years or more. Their diagnoses included more severe conditions such as bipolar and psychotic disorders. Researchers analyzed data for individuals born between April 1972 and March 1973 in Dunedin, New Zealand. Each participant’s general health and behavior were assessed 13 times from birth to age 38. Eight mental health assessments occurred from age 11 to 38. |© Society for Science & the Public 2000 - 2016.
Link ID: 23200 - Posted: 02.08.2017
Squid and their cephalopod brethren have been the inspiration for many a science fiction creature. Their slippery appendages, huge proportions, and inking abilities can be downright shudder-inducing. (See: Arrival.) But you should probably be more concerned by the cephalopod’s huge brain—which not only helps it solve tricky puzzles, but also lets it converse in its own sign language. Right now, you’re probably imagining twisted tentacles spelling out creepy cephalopod communiqués. But it’s not that: Certain kinds of squid send messages by manipulating the color of their skin. “Their body patterning is fantastic, fabulous,” says Chuan-Chin Chiao, a neuroscientist at National Tsing Hua University in Taiwan. They can display bands, or stripes, or turn completely dark or light. And Chiao is trying to crack their code. Chiao got his inspiration from physiologist B. B. Boycott, who in the 1960s showed that the cuttlefish brain was the control center for changing skin color. Boycott copied his technique from neurosurgeon Wilder Penfield, who treated epilepsy patients by burning out the misbehaving bits of their brains. While their grey matter was exposed for surgery, Penfield also applied a gentle current through the electrodes in his patients’ brains. You know, just to see what would happen. A zap in one spot above the ears caused a tingle in the left hand. In another spot, tingles in the leg. And so Penfield discovered that the sensory cortex is a homunculus, with specific brain areas mapping onto different parts of your body. Over time, scientists tried the electrical stimulation technique on all kinds of animals—including Boycott’s cuttlefish.
Keyword: Animal Communication
Link ID: 23199 - Posted: 02.08.2017
By Anil Ananthaswamy Next time a nurse sticks a needle into your arm, don’t look away: it’ll be less painful. A new study shows that we feel less pain when we are looking at our body – and that this effect works with virtual reality too. In 2009, Patrick Haggard and Matthew Longo of University College London showed that looking at your own body has an analgesic effect. The researchers shone infrared laser light on the skin of volunteers. Those who were looking at their body rather than at a neutral object said that they felt less pain. Scalp electrodes revealed that this analgesic effect was linked to weaker activity in parts of the brain’s cortex that process pain – although why this happens is unclear. Since then, two different teams have tested the effect using the rubber hand illusion – in which a rubber hand is placed next to a person’s real hand, which is hidden from view. Stroking both the real and rubber hands with paint brushes convinces them that the rubber hand is their own. Extending this illusion, the teams wanted to know: can looking at a rubber hand that feels like one’s own alleviate pain in your real hand? The studies were contradictory: one study showed an analgesic effect, but the other did not. Maria Sanchez-Vives at the University of Barcelona, Spain, and her colleagues argue that differences in the position of the rubber hand and real hand may have led to the differing results. To test the effect of the rubber hand’s position, her team used virtual reality to induce the illusion. Instead of seeing a real rubber hand, participants were shown one via a VR headset instead. © Copyright Reed Business Information Ltd.
Keyword: Pain & Touch
Link ID: 23198 - Posted: 02.08.2017
By Lenny Bernstein Forty million American adults have lost some hearing because of noise, and half of them suffered the damage outside the workplace, from everyday exposure to leaf blowers, sirens, rock concerts and other loud sounds, the Centers for Disease Control and Prevention reported Tuesday. A quarter of people ages 20 to 69 were suffering some hearing deficits, the CDC reported in its Morbidity and Mortality Weekly Report, even though the vast majority of the people in the study claimed to have good or excellent hearing. The researchers found that 24 percent of adults had “audiometric notches” — a deterioration in the softest sound a person can hear — in one or both ears. The data came from 3,583 people who had undergone hearing tests and reported the results in the 2011-2012 National Health and Nutrition Examination Survey (NHANES). The review's more surprising finding — which the CDC had not previously studied — was that 53 percent of those people said they had no regular exposure to loud noise at work. That means the hearing loss was caused by other environmental factors, including listening to music through headphones with the volume turned up too high. “Noise is damaging hearing before anyone notices or diagnoses it,” said Anne Schuchat, the CDC's acting director. “Because of that, the start of hearing loss is underrecognized.” The study revealed that 19 percent of people between the ages of 20 and 29 had some hearing loss, a finding that Schuchat called alarming. © 1996-2017 The Washington Post
Link ID: 23197 - Posted: 02.08.2017
By JANE E. BRODY Dizziness is not a disease but rather a symptom that can result from a huge variety of underlying disorders or, in some cases, no disorder at all. Readily determining its cause and how best to treat it — or whether to let it resolve on its own — can depend on how well patients are able to describe exactly how they feel during a dizziness episode and the circumstances under which it usually occurs. For example, I recently experienced a rather frightening attack of dizziness, accompanied by nausea, at a food and beverage tasting event where I ate much more than I usually do. Suddenly feeling that I might faint at any moment, I lay down on a concrete balcony for about 10 minutes until the disconcerting sensations passed, after which I felt completely normal. The next morning I checked the internet for my symptom — dizziness after eating — and discovered the condition had a name: Postprandial hypotension, a sudden drop in blood pressure when too much blood is diverted to the digestive tract, leaving the brain relatively deprived. The condition most often affects older adults who may have an associated disorder like diabetes, hypertension or Parkinson’s disease that impedes the body’s ability to maintain a normal blood pressure. Fortunately, I am thus far spared any disorder linked to this symptom, but I’m now careful to avoid overeating lest it happen again. “An essential problem is that almost every disease can cause dizziness,” say two medical experts who wrote a comprehensive new book, “Dizziness: Why You Feel Dizzy and What Will Help You Feel Better.” Although the vast majority of patients seen at dizziness clinics do not have a serious health problem, the authors, Dr. Gregory T. Whitman and Dr. Robert W. Baloh, emphasize that doctors must always “be on the alert for a serious disease presenting as ‘dizziness,’” like “stroke, transient ischemic attacks, multiple sclerosis and brain tumors.” © 2017 The New York Times Company
Link ID: 23196 - Posted: 02.07.2017
By James Gallagher Health and science reporter, BBC News website Deaf mice have been able to hear a tiny whisper after being given a "landmark" gene therapy by US scientists. They say restoring near-normal hearing in the animals paves the way for similar treatments for people "in the near future". Studies, published in Nature Biotechnology, corrected errors that led to the sound-sensing hairs in the ear becoming defective. The researchers used a synthetic virus to nip in and correct the defect. "It's unprecedented, this is the first time we've seen this level of hearing restoration," said researcher Dr Jeffrey Holt, from Boston Children's Hospital. Hair defect About half of all forms of deafness are due to an error in the instructions for life - DNA. In the experiments at Boston Children's Hospital and Harvard Medical School, the mice had a genetic disorder called Usher syndrome. It means there are inaccurate instructions for building microscopic hairs inside the ear. In healthy ears, sets of outer hair cells magnify sound waves and inner hair cells then convert sounds to electrical signals that go to the brain. The hairs normally form these neat V-shaped rows. But in Usher syndrome they become disorganised - severely affecting hearing. The researchers developed a synthetic virus that was able to "infect" the ear with the correct instructions for building hair cells. © 2017 BBC.
By Julia Shaw We all have times of day when we are not at our best. For me, before 10am, and between 2-4pm, it’s as though my brain just doesn’t work the way it should. I labor to come up with names, struggle to keep my train of thought, and my eloquence drops to the level expected of an eight-year-old. In an effort to blame my brain for this, rather than my motivation, I reached out to a researcher in the area of sleep and circadian neuroscience. Andrea Smit, a PhD student working with Professors John McDonald and Ralph Mistlberger at Simon Fraser University in Canada, was happy to help me find excuses for why my memory is so terribly unreliable at certain times of day. Humans have daily biological rhythms, called circadian rhythms, which affect almost everything that we do. They inform our bodies when it is time to eat and sleep, and they dictate our ability to remember things. According to Smit, “Chronotype, the degree to which someone is a “morning lark” or a “night owl,” is a manifestation of circadian rhythms. In a recent study, Smit used EEG, a type of brain scan, to study the interaction between chronotypes and memory. “Testing extreme chronotypes at multiple times of day allowed us to compare attentional abilities and visual short term memory between morning larks and night owls. Night owls were worse at suppressing distracting visual information and had a worse visual short term memory in the morning as compared with the afternoon,” she says. “Our research shows that circadian rhythms interact with memories even at very early stages of processing within the brain.” © 2017 Scientific American
Aylin Woodward Fearful, flighty chickens raised for eating can hurt themselves while trying to avoid human handlers. But there may be a simple way to hatch calmer chicks: Shine light on the eggs for at least 12 hours a day. Researchers at the University of California, Davis bathed eggs daily in light for different time periods during their three-week incubation. When the chickens reached 3 to 6 weeks old, the scientists tested the birds’ fear responses. In one test, 120 chickens were randomly selected from the 1,006-bird sample and placed one by one in a box with a human “predator” sitting visibly nearby. The chickens incubated in light the longest — 12 hours — made an average of 179 distress calls in three minutes, compared with 211 from birds incubated in complete darkness, animal scientists Gregory Archer and Joy Mench report in January in Applied Animal Behaviour Science. Chickens exposed to lots of light as eggs “would sit in the closest part of the box to me and just chill out,” Archer says. The others spent their time trying to get away. How light has its effect is unclear. On commercial chicken farms, eggs typically sit in warm, dark incubation rooms. The researchers are now testing light's effects in large, commercial incubators. Using light exposure to raise less-fearful chickens could reduce broken bones during handling at processing plants, Archer says. It might also decrease harmful anxious behaviors, such as feather pecking of nearby chickens. G. S. Archer and J. A. Mench. Exposing avian embryos to light affects post-hatch anti-predator fear responses. Applied Animal Behaviour Science. Vol. 186, January 2017, p. 80. doi: 10.1016/j.applanim.2016.10.014. © Society for Science & the Public 2000 - 2016
By Meredith Wadman The Humane Society of the United States (HSUS) today put the U.S. Department of Agriculture (USDA) on notice that it intends to use legal tools to force the agency to restore tens of thousands of documents on animal welfare that it removed from its website on Friday. In this letter to the U.S. Department of Justice, the animal welfare organization reminded the government that under the terms of a 2009 legal settlement with HSUS, USDA had agreed to make public some of the records it has now scrubbed from its public database. HSUS, its lawyers write, “is exercising its rights under [the 2009 settlement] and intends to take further action unless USDA agrees to reconsider this bizarre reversal of the agency’s longstanding policy” of making inspection records and others publicly available. The animal organization’s letter notes that under the terms of the 2009 settlement, the two parties, HSUS and USDA, now have 30 days to settle their differences. After that, HSUS can ask the court to reopen the lawsuit. A spokesperson for USDA did not in the course of 3 hours return an email and a call requesting comment. The HSUS letter also argues that USDA’s actions violate laws governing the electronic release of data under the Freedom of Information Act (FOIA). One of the laws requires agencies to “make available for public inspection … [By] electronic means” all FOIA requests that it releases to anyone and that it determines are likely to be asked for again, by others. When they were public, many of USDA’s inspection reports, especially those of troubled facilities, were accessed repeatedly by a number of different users. © 2017 American Association for the Advancement of Science
Keyword: Animal Rights
Link ID: 23192 - Posted: 02.07.2017
Rae Ellen Bichell By the time Kay Schwister got her diagnosis last summer, she couldn't talk anymore. But she could still scowl, and scowl she did. After weeks of decline and no clue what was causing it, doctors had told Schwister — a 53-year-old vocational rehab counselor and mother of two from Chicago — that she had an incurable disease called Creutzfeldt-Jakob disease, or CJD. The disease was shrinking Kay's brain, and riddling it with holes. She would likely only live a few more weeks, the doctors said. It was a diagnosis that no one could ever want. But the fact that Schwister was able to get a firm diagnosis while still alive is a relatively new development that represents a step forward in understanding a group of devastating neurological disorders. And, some biochemists say, it could lead to better ways of diagnosing brain diseases that are much more common, including Parkinson's and Alzheimer's. For Kay Schwister it all started in the spring of 2016, when she started getting headaches and feeling dizzy all the time. Aging, she told herself, just didn't feel very good. Over the next few weeks, she got steadily worse. "She got to the point where she was so nauseous and so dizzy that she stopped driving and actually stopped working," says her husband, Tim Schwister. By the time Kay entered the emergency room last June her speech had changed. She was enunciating things in a strange way, and finishing each sentence on a really high note. Doctors drew blood and spinal fluid and tested it for things like multiple sclerosis and mercury poisoning. Those tests came back negative. Soon, Kay couldn't talk or walk. © 2017 npr
Link ID: 23191 - Posted: 02.06.2017
By SHARON LERNER IN the fall, I began to research an article that I gave the working title “The Last Days of Chlorpyrifos.” A widely used pesticide, chlorpyrifos affects humans as well as the bugs it kills. Back in the halcyon days before the election, the optimism of the title seemed warranted. After years of study, the Environmental Protection Agency had announced in October 2015 that it could no longer vouch for the safety of chlorpyrifos on food. The agency had acknowledged for decades that chlorpyrifos can cause acute poisoning and in the early 2000s it had prohibited its use in most home products and reduced the amounts that could be used on some crops. But the 2015 announcement stemmed from the agency’s recognition of mounting evidence that prenatal exposure to chlorpyrifos could have lasting effects on children’s brains. Though the process of re-evaluating the safety of the pesticide had stretched on for years, at long last, chlorpyrifos seemed to be going down. Another report was expected to provide all the ammunition necessary to stop its use on fruits and vegetables, and I was eager to document its demise. For a reporter who covers the environment, this was going to be the rare happy story. The election of President Trump has thrown that outcome — indeed, the fate of many of the E.P.A.’s public health protections — into question. On Monday, Mr. Trump signed an executive order requiring federal agencies to scrap two regulations for every one they institute on small businesses. In its first week, his administration suspended 30 environmental regulations issued under President Barack Obama. And Myron Ebell, who oversaw the agency’s transition team, suggested recently that the E.P.A.’s staff may soon be reduced by as much as two-thirds. How will the agency’s mission “to protect human health and the environment” fare under this assault? What happens with chlorpyrifos may be our best indication. “I think it’ll be a very early test of their commitment to environmental protection,” Jim Jones, who oversaw the evaluation of chlorpyrifos as the E.P.A.’s assistant administrator for chemical safety and pollution prevention, told me, not long after he stepped down on Inauguration Day. © 2017 The New York Times Company