Anna Ploszajski A man who lost his hand 17 years ago has been given the sense of touch through a brain-controlled robotic prosthetic. Keven Walgamott, whose arm was amputated below the elbow after an accident, can now feel 119 different touch sensations through the prosthetic as if it were his own limb. He is able to distinguish between large, small, soft and hard objects when blindfolded, and handle delicate objects such as grapes and eggs. Everyday tasks such as putting on his wedding ring, peeling a banana or holding a mobile phone are now possible. “The most amazing thing for me is what the team was able to do,” said Walgamott. “[They] take a bunch of mechanical pieces and provide, through a computer, not only the ability to move all fingers and grasp things but be able to feel again.” The prosthetic hand and wrist has been in development for 15 years. Electrodes were implanted in the remaining part of his arm, allowing communication between the prosthetic hand and his brain. The hand can move in six directions and is equipped with 19 sensors that detect touch and positioning. The arrays interpret the signals Walgamott’s brain sends to his arm nerves, and a computer outside the body translates these into digital information, which then instructs the prosthetic to move as the wearer intends. They also provide Walgamott’s nerves with computer-generated touch signals from the prosthesis, which are then interpreted by his brain. © 2019 Guardian News & Media Limited

Keyword: Pain & Touch; Robotics
Link ID: 26449 - Posted: 07.25.2019

By Megan Schmidt | Soaring with the birds. Teeth falling out. A crazy psychopath is chasing you. For many of us, our dreams transport us to a surreal world where logic and reason have no reign. Some of us may even look forward to sleep – and the adventures we’ll go on in our dreams. But does everyone take a nightly trip to dreamland? While most of us remember somewhere around one or two dreams a week, some people report a subconscious experience that’s more like a blank tape. Among us are people who say they never, ever dream. A small subset of the population – around one in every 250 people – report never remembering a single dream in their lives, as a 2015 study found. What is it about people who don’t remember their dreams that sets them apart from the people that do? Is it possible for the brain to stop producing dreams? And could something be wrong in the brains of people who report never dreaming? Raphael Vallat, a neuroscientist specializing in sleep and dream research at the University of California, Berkeley Sleep and Neuroimaging Lab, offered insights to a number of these questions. Vallat says dreaming “is one of the last frontiers in our understanding of the human mind.” And learning about dream recall – the why and how of remembering one’s dreams – may help scientists solve some of the mysteries of the dreaming mind. Work by Vallat and others in the field has uncovered a number of interesting tidbits that seem to separate the dreamers from the so-called nondreamers, or the people seldom or never remember their dreams.

Keyword: Sleep
Link ID: 26448 - Posted: 07.25.2019

By Gretchen Reynolds Weight training may have benefits for brain health, at least in rats. When rats lift weights, they gain strength and also change the cellular environment inside their brains, improving their ability to think, according to a notable new study of resistance training, rodents and the workings of their minds. The study finds that weight training, accomplished in rodents with ladders and tiny, taped-on weights, can reduce or even reverse aspects of age-related memory loss. The finding may have important brain-health implications for those of us who are not literal gym rats. Most of us discover in middle age, to our chagrin, that brains change with age and thinking skills dip. Familiar names, words and the current location of our house keys begin to elude us. But a wealth of helpful past research indicates that regular aerobic exercise, such as walking or jogging, can prop up memory and cognition. In these studies, which have involved people and animals, aerobic exercise generally increases the number of new neurons created in the brain’s memory center and also reduces inflammation. Unchecked, inflammation in the brain may contribute to the development of dementia and other neurodegenerative conditions. Far less has been known, though, about whether and how resistance training affects the brain. A few studies with older people have linked weight training to improved cognition, but the studies have been small and the linkages tenuous. While researchers know that lifting weights builds muscle, it is not yet clear how, at a molecular level, it would affect the cells and functions of the brain. © 2019 The New York Times Company

Keyword: Learning & Memory; Neurogenesis
Link ID: 26447 - Posted: 07.24.2019

Ian Sample Science editor Brain scans of US embassy staff who became ill in mysterious circumstances while serving in Cuba have found potential abnormalities that may be related to their symptoms. The scans taken from 40 US government workers who suffered strange concussion-like symptoms during their deployment to Havana revealed that particular brain features looked different to those in healthy volunteers. Images of the diplomats’ brains found that on average they had lower volumes of white matter, the tissue made from nerve bundles that send messages around the brain. They also showed micro-structural differences and other changes that could affect auditory and visuospatial processing, doctors said. But the medical team that performed the scans said the findings were not conclusive. They do not match what is normally seen in brain injuries and the severity of symptoms did not vary with the extent of the brain differences spotted. “It’s a unique presentation that we have not seen before,” said Ragini Verma, a professor of biomedical imaging on the team at the University of Pennsylvania. “What caused it? I’m completely unequipped to answer that.” Independent experts agreed the findings were inconclusive and said it was still unclear whether the diplomats were victims of any attack or had suffered related brain injuries. The apparent abnormalities might have pre-dated the attacks, they said, and could have more mundane explanations such as anxiety or depression. One said the study did not meet the usual standards for publication. © 2019 Guardian News & Media Limited

Keyword: Brain imaging; Brain Injury/Concussion
Link ID: 26446 - Posted: 07.24.2019

Dave Davies We tend to think of being asleep or awake as an either-or prospect: If you're not asleep, then you must be awake. But sleep disorder specialist and neurologist Guy Leschziner says it's not that simple. "If one looks at the brain during sleep, we now know that actually sleep is not a static state," Leschziner says. "There are a number of different brain states that occur while we sleep." As head of the sleep disorders center at Guy's Hospital in London, Leschziner has treated patients with a host of nocturnal problems, including insomnia, night terrors, narcolepsy, sleep walking, sleep eating and sexsomnia, a condition in which a person pursues sexual acts while asleep. He writes about his experiences in his book The Nocturnal Brain. Leschziner notes that the different parts of the brain aren't always in the same stage of sleep at the same time. When this happens, an individual might order a pizza or go out for a drive — while technically still being fast asleep. "Sometimes these conditions sound very funny," Leschziner says. "But on other occasions they can be really life changing, resulting in major injury or, as one of the cases that I described in the book, in a criminal conviction." On what we know about recall after a sleepwalking episode We used to think that people don't really remember anything that occurs in this stage. That seems to relate to the fact that the brain in parts is in very deep sleep whilst in other parts is awake. What we have learned over the last few years is that actually quite a lot of people have some sort of limited recall. They don't necessarily remember the details of all the events or indeed the entirety of the event, but sometimes they do experience little snippets. © 2019 npr

Keyword: Sleep
Link ID: 26445 - Posted: 07.24.2019

Briar Stewart · A Canadian-born researcher is helping to launch the first substantial study of transgender athletes in a bid to better understand how transitioning and hormone therapy affects athletic performance. The issue of how to include transgender women in competition is centred around rules, rights and biological differences. And the debate about what constitutes an unfair advantage is heated, which is why medical physicist Joanna Harper hopes science can steer the conversation. "Until we have several of these larger-scale studies done worldwide, it's hard to be truly definitive on anything," she said. Harper, who is also an adviser to the International Olympic Committee (IOC), will be moving to the U.K. this fall to help lead the research into transgender athletes. The work will be carried out at Loughborough University, through its School of Sport, Exercise and Health Sciences. Personal motivation It was Harper's own experience that motivated her to try and track transgender athletes both before and after a gender transition. Harper, who is originally from Parry Sound, Ont, but is now based in Portland, Ore., has been a competitive runner for decades. When she was younger and racing as a male, her marathon time was a very quick two hours and 23 minutes. But once she started her transition in 2004 and began taking testosterone blockers and estrogen, her pace slowed. "Within nine months of hormone therapy, I was running 12 per cent slower," she said. "That's the difference between serious male distance runners and serious female distance runners." Harper, now in her 60s, still competes, racing alongside women. She wins some events and loses others, which is why she asserts that if trans women can become hormonally like other women, competition can be "equitable and meaningful." ©2019 CBC/Radio-Canada.

Keyword: Hormones & Behavior; Sexual Behavior
Link ID: 26444 - Posted: 07.24.2019

By Heather King On Sept. 29, 2016, I was at a private book signing in Williamson County, Tenn., for Alberto Gonzales, the former United States attorney general. As the chairwoman for the Montgomery County Young Republicans, I spent a lot of time sharing drinks with Tennessee’s political class. At the end of the evening, I decided to drive home, even though I knew I had drunk too much. I had taken these back roads so many times, I told myself; I could make it home. Twenty minutes into my hourlong trek, I passed out. When I regained consciousness, I was upside down in a ditch. A stranger stopped to pull me out of my car. The police arrived and arrested me immediately. The next morning, reality set in. I had done so much damage in my life that my son, Taj, who was 16 at the time, refused to talk to me. That was the last night I drank. As much as I would love to say that I stopped drinking for Taj, I didn’t. For the first time in many years, I wanted to live more than I wanted to drink. I found myself in this weird dilemma: I could no longer see myself drinking, but I had no idea how to live my life without alcohol. My son was the first person that I told I was going to stop. He didn’t believe me, and rightly so. He had seen plenty of unsuccessful attempts to quit. But he held me, as a parent would hold a child after her first heartbreak, and he told me we would get through it together. At 16 years old, my child was more of an adult than I was at 34. I became a mother at 18 years old. I had never wanted children. Partying my way through high school and getting drunk with my older brother was my only priority. It stayed that way even after I had my son. I never thought I was capable of loving and nurturing a small human; after all, I was raised by a working single mom who rarely showed affection. Not because she didn’t love me; she just wasn’t around. © 2019 The New York Times Company

Keyword: Drug Abuse
Link ID: 26443 - Posted: 07.24.2019

By Knvul Sheikh On Sálvora Island, off the coast of Spain, thousands of yellow-legged gulls dot the grassy cliffs from April to late July. It is a riot of white wings and plaintive calls. Occasionally, the chorus changes as the seabirds engage in courtship and chick-feeding. And when the adults notice a predator, such as a dusky-coated mink, the chorus shifts again, to a characteristic alarm call — ha-ha-ha. These acoustic cues reach not just young and adult gulls but unhatched embryos, too. In 2018, researchers found that when gull eggs hatch, the ones that were exposed to alarm calls were able to crouch and hide from predators a couple of seconds faster than others. A few other bird species, including quails, fairywrens and zebra finches, are known to relay similar cues about the environment to their unhatched young, to prepare hatchlings to fend for themselves. But embryos aren’t receiving wisdom only from their parents. A new study, published Monday in the journal Nature Ecology & Evolution, suggests that they’re also receiving cues from nearby unhatched siblings. “Paying attention to cues from the outside is important for survival,” said Jose C. Noguera, an evolutionary ecologist at the University of Vigo in Spain, who led the study. Embryos that do so develop traits that provide an advantage in avoiding predators, identifying other species of birds or building their own nests in warmer temperatures later in life, he said. © 2019 The New York Times Company

Keyword: Animal Communication; Development of the Brain
Link ID: 26442 - Posted: 07.23.2019

By Lauren Aguirre, STAT Scientists who study Alzheimer’s disease have mostly ignored the role of seizures, but that is beginning to change, and new research suggests they may provide insight into the progression of the disease and pave the way for treatments. It’s no surprise to neurologists that some people experience convulsive seizures in the later stages of the disease. In fact, the second patient ever to receive an Alzheimer’s diagnosis more than a century ago suffered from them. But because brain damage can cause seizures, they were long thought to be just one more casualty of a deteriorating brain. Now evidence is accumulating that such abnormal electrical activity is far more common and occurs much earlier—and perhaps even precedes obvious signs of memory loss. This raises the possibility that seizures may be intimately tied up with the progression of the disease. New research that lends credence to this hypothesis was shared at the Alzheimer’s Association International Conference in Los Angeles this week. One study looked at 55 patients between the ages of 50 and 69 who were admitted to an Israeli medical center with their first known seizure. A quarter of them went on to develop dementia—with a mean time to the diagnosis of eight and a half years. Another study of nearly 300,000 U.S. veterans over the age of 55 found that seizures were associated with twice the risk for developing dementia between one and nine years later. © 2019 Scientific American,

Keyword: Alzheimers; Epilepsy
Link ID: 26441 - Posted: 07.23.2019

Ed Yong On July 22, 2009, the neuroscientist Henry Markram walked onstage at the TEDGlobal conference in Oxford, England, and told the audience that he was going to simulate the human brain, in all its staggering complexity, in a computer. His goals were lofty: “It’s perhaps to understand perception, to understand reality, and perhaps to even also understand physical reality.” His timeline was ambitious: “We can do it within 10 years, and if we do succeed, we will send to TED, in 10 years, a hologram to talk to you.” If the galaxy-brain meme had existed then, it would have been a great time to invoke it. It’s been exactly 10 years. He did not succeed. One could argue that the nature of pioneers is to reach far and talk big, and that it’s churlish to single out any one failed prediction when science is so full of them. (Science writers joke that breakthrough medicines and technologies always seem five to 10 years away, on a rolling window.) But Markram’s claims are worth revisiting for two reasons. First, the stakes were huge: In 2013, the European Commission awarded his initiative—the Human Brain Project (HBP)—a staggering 1 billion euro grant (worth about $1.42 billion at the time). Second, the HBP’s efforts, and the intense backlash to them, exposed important divides in how neuroscientists think about the brain and how it should be studied. Markram’s goal wasn’t to create a simplified version of the brain, but a gloriously complex facsimile, down to the constituent neurons, the electrical activity coursing along them, and even the genes turning on and off within them. From the outset, the criticism to this approach was very widespread, and to many other neuroscientists, its bottom-up strategy seemed implausible to the point of absurdity.

Keyword: Brain imaging
Link ID: 26440 - Posted: 07.23.2019

Tina Hesman Saey A friendly gut bacterium can help lessen ALS symptoms, a study of mice suggests. Mice that develop a degenerative nerve disease similar to amyotrophic lateral sclerosis (ALS), or Lou Gehrig’s disease, fared better when bacteria making vitamin B3 were living in their intestines, researchers report July 22 in Nature. Those results suggest that gut microbes may make molecules that can slow progression of the deadly disease. The researchers uncovered clues that the mouse results may also be important for people with ALS. But the results are too preliminary to inform any changes in treating the disease, which at any given time affects about two out of every 100,000 people, or about 16,000 people in the United States, says Eran Elinav, a microbiome researcher at the Weizmann Institute of Science in Rehovot, Israel. “With respect to ALS, the jury is still out,” says Elinav, also of the German Cancer Research Center in Heidelberg. “We have to prove that what we found in mice is reproducibly found in humans.” Elinav and his colleagues examined the gut microbiomes — bacteria, archaea and other microbes that live in the colon, or large intestine — of mice that produce large amounts of a mutated form of the SOD1 protein. In the mice, as in human ALS patients, faulty SOD1 proteins clump together and lead to the death of nerve cells. |© Society for Science & the Public 2000 - 2019

Keyword: ALS-Lou Gehrig's Disease
Link ID: 26439 - Posted: 07.23.2019

Mariam Alexander It might come as quite a surprise to learn that, as a psychiatrist, if I ever had the misfortune to develop severe depression, my treatment of choice would be electroconvulsive therapy (ECT). Why? Well, to put it simply, ECT is the most rapid treatment for severe depression that we currently have to offer – with a recent study in the BMJ highlighting its effectiveness. For the uninitiated, ECT is a medical procedure in which an anaesthetised patient has a small electrical current applied to their scalp in order to induce a seizure for the purposes of treating severe mental illnesses and occasionally neurological disorders too. Each treatment takes just a few minutes and is usually administered two or three times a week. ECT course length varies depending on the needs of the patient, but on average eight to 12 treatments are given. It’s almost impossible to discuss ECT without the word “barbaric” being used. For anyone who is familiar with the psychiatric era of One Flew Over the Cuckoo’s Nest, this is understandable. But things have moved on a great deal since then. Indeed, if you’re looking for a “b” word to describe the process of contemporary ECT, top of my list would be “boring” – the use of a general anaesthetic and muscle relaxant means there’s probably more drama involved in having a filling than ECT. That’s not to say ECT isn’t a significant intervention, but treatments should always be considered in relation to the condition that needs to be managed. Most people would be totally opposed to the idea of a surgeon amputating their leg. However, if there was an infection rapidly rising from their foot and an amputation was the best option to save their life, I suspect most people would then see it as a necessity. Context is key. © 2019 Guardian News & Media Limited

Keyword: Depression
Link ID: 26438 - Posted: 07.23.2019

Kelly Crowe · CBC News Scientists are slowly chipping away at one of the most mysterious aspects of weight loss: why does the lost weight often seem to come back? It's now clear that it's not simply a matter of willpower. "We know people are good at losing weight with diet and exercise," said Gregory Steinberg, Canada Research Chair in Metabolism and Obesity at McMaster University. "It's not that people just give up." The problem is rooted in the body's physiology. After people lose weight, their bodies' energy use also changes by burning fewer calories. "Quickly you hit a plateau at five to 10 per cent weight loss and you can't lose more weight than that because your metabolism slows down too much," said Steinberg. "This explains why relapse weight gain is so high." But why the body's calorie-burning capacity drops has so far not been explained. "No one knows why," said Steinberg. There are theories that something is putting the brakes on the body's ability to turn up its fat-burning machinery. And last week, a new paper published in Cell Reports, describes one possible system. At New York University, Ann Marie Schmidt is studying a receptor on fat cells that appears to interfere with weight loss. When she created a mouse model without any of those receptors the mice didn't get fat even though they ate more food. "When you delete [the receptor] it completely resets their metabolic program so that they are resistant to the diet-induced obesity," said Schmidt. "It's totally unexpected and it has so many implications for human health." Although scientists have identified the receptor — called RAGE — in humans, so far most of the research has been done in mice. ©2019 CBC/Radio-Canada.

Keyword: Obesity
Link ID: 26437 - Posted: 07.23.2019

Selena Simmons-Duffin Good news came out from the Centers for Disease Control and Prevention Wednesday: Preliminary data shows reported drug overdoses declined 4.2% in 2018, after rising precipitously for decades. "It looks like this is the first turnaround since the opioid crisis began," says Bertha Madras who served on President Trump's opioid commission, and is a professor of psychobiology at Harvard Medical School. She says it won't be entirely clear until the CDC finalizes the numbers but, "I think the tide could be turning." But not everyone was celebrating. Some states actually saw double-digit increases. "It's deflating," Rachel Winograd says. She's an associate research professor at the University of Missouri-St. Louis. "It's incredibly discouraging to see the increase in Missouri in 2018 that happened at the same time as we really ramped up so many efforts to save lives and improve lives in our state." The provisional data shows Missouri deaths increased by 17% — one of 18 states that saw a year-over-year increase. Over the last several years, Missouri has received $65 million in federal grants to address the opioid crisis, Winograd says, and she has helped the state decide where and how to spend that money. They've focused on expanding access to medication-assisted treatment, and "saturating our communities with naloxone — the opiate overdose antidote," she says. © 2019 npr

Keyword: Drug Abuse
Link ID: 26436 - Posted: 07.20.2019

By Jan Hoffman, Katie Thomas and Danny Hakim The Walgreens employee was bewildered by the quantity of opioids the company was shipping to just one store. Its pharmacy in Port Richey, Fla. (population 2,831) was ordering 3,271 bottles of oxycodone a month. “I don’t know how they can even house this many bottles to be honest,” Barbara Martin, whose job was to review suspicious drug orders, wrote to a colleague in a January 2011 email. The next month, the company shipped another outsized order to the same store. The email was among thousands of documents from corporations across the pharmaceutical and retail industries — internal memos, depositions, sales and shipping reports, experts’ analyses, and other confidential information — filed Friday in federal court in Cleveland by lawyers for cities, towns and counties devastated by addiction. They lay out a detailed case of how diverse corporate interests — far beyond the familiar players like Purdue Pharma — fed a deadly opioid epidemic that persisted for nearly two decades. From the team at NYT Parenting: Get the latest news and guidance for parents. We'll celebrate the little parenting moments that mean a lot — and share stories that matter to families. Little-known manufacturers of generic pills, superstores like Walmart and chain retailers like Rite Aid also flooded the country with billions of pills, according to the filings. The devastation was so extreme that one Ohio county resorted to a mobile morgue to handle all the corpses of people who died from overdoses. As the epidemic crested, the suppliers with the greatest sales were not the branded manufacturers but those who made generic prescription drugs. Between 2003 and 2011, lawyers for the plaintiffs said in one filing, Mallinckrodt, the Ireland-based manufacturer of generic and branded drugs, sold 53 million orders of opioids. Yet the company stopped and then reported to federal authorities at most 33 orders as suspicious, a ratio the lawyers described as defying credibility. © 2019 The New York Times Company

Keyword: Drug Abuse
Link ID: 26435 - Posted: 07.20.2019

Scientists say they may have discovered why more women than men have Alzheimer's disease and dementia. It has always been thought that women living longer than men was the reason. But new research presented at an international conference suggests this may not be the whole story. Differences in brain connectivity and sex-specific genes linked to risk could explain the numbers, the researchers say. Most people living with Alzheimer's - the most common cause of dementia - are women. In the UK, about 500,000 women have dementia, compared with 350,000 men. Most people who develop the disease are over the age of 65 but it is not a normal part of ageing. Alzheimer's disease can affect younger people too. Researchers from Vanderbilt University Medical Centre studied brain scans of hundreds of men and women, looking at the pattern of a protein called tau. One of the characteristic features of Alzheimer's is the build-up of proteins called tau and amyloid in the brain. When they form toxic, tangled clumps, this causes brain cells to die, leading to memory problems. The researchers found differences between the sexes in how tau was spread across regions of the brain. Women appeared to have better connectivity between the regions where tau protein builds up - and this had implications for the brain, the study said. With this higher connectivity, women's brains may be at risk of faster spread of tau - and of cognitive decline. Dr Jana Voigt, head of research at Alzheimer's Research UK, said the study revealed "sex-specific differences in brain connectivity that could contribute to differing Alzheimer's risk in men and women". © 2019 BBC.

Keyword: Alzheimers; Sexual Behavior
Link ID: 26434 - Posted: 07.20.2019

By Carl Zimmer In a laboratory at the Stanford University School of Medicine, the mice are seeing things. And it’s not because they’ve been given drugs. With new laser technology, scientists have triggered specific hallucinations in mice by switching on a few neurons with beams of light. The researchers reported the results on Thursday in the journal Science. The technique promises to provide clues to how the billions of neurons in the brain make sense of the environment. Eventually the research also may lead to new treatments for psychological disorders, including uncontrollable hallucinations. “This is spectacular — this is the dream,” said Lindsey Glickfeld, a neuroscientist at Duke University, who was not involved in the new study. In the early 2000s, Dr. Karl Deisseroth, a psychiatrist and neuroscientist at Stanford, and other scientists engineered neurons in the brains of living mouse mice to switch on when exposed to a flash of light. The technique is known as optogenetics. In the first wave of these experiments, researchers used light to learn how various types of neurons worked. But Dr. Deisseroth wanted to be able to pick out any individual cell in the brain and turn it on and off with light. So he and his colleagues designed a new device: Instead of just bathing a mouse’s brain in light, it allowed the researchers to deliver tiny beams of red light that could strike dozens of individual brain neurons at once. To try out this new system, Dr. Deisseroth and his colleagues focused on the brain’s perception of the visual world. When light enters the eyes — of a mouse or a human — it triggers nerve endings in the retina that send electrical impulses to the rear of the brain. There, in a region called the visual cortex, neurons quickly detect edges and other patterns, which the brain then assembles into a picture of reality. © 2019 The New York Times Company

Keyword: Vision
Link ID: 26433 - Posted: 07.19.2019

By Andrew Curry ZURICH, SWITZERLAND—The children living in SOS Children's Villages orphanages in Pakistan have had a rough start in life. Many have lost their fathers, which in conservative Pakistani society can effectively mean losing their mothers, too: Destitute widows often struggle to find enough work to support their families and may have to give up their children. The orphanages, in Multan, Lahore, and Islamabad, provide shelter and health care and send kids to local schools, trying to provide "the best possible support," says University of Zurich (UZH) physician and neuroscientist Ali Jawaid. "But despite that, these children experience symptoms similar to PTSD [post-traumatic stress disorder]," including anxiety and depression. Beyond these psychological burdens, Jawaid wonders about a potential hidden consequence of the children's experience. He has set up a study with the orphanages to probe the disturbing possibility that the emotional trauma of separation from their parents also triggers subtle biological alterations—changes so lasting that the children might even pass them to their own offspring. That idea would have been laughed at 20 years ago. But today the hypothesis that an individual's experience might alter the cells and behavior of their children and grandchildren has become widely accepted. In animals, exposure to stress, cold, or high-fat diets has been shown to trigger metabolic changes in later generations. And small studies in humans exposed to traumatic conditions—among them the children of Holocaust survivors—suggest subtle biological and health changes in their children. © 2019 American Association for the Advancement of Science.

Keyword: Epigenetics; Stress
Link ID: 26432 - Posted: 07.19.2019

Sara Reardon Nearly every scientist who has used mice or rats to study depression is familiar with the forced-swim test. The animal is dropped into a tank of water while researchers watch to see how long it tries to stay afloat. In theory, a depressed rodent will give up more quickly than a happy one — an assumption that has guided decades of research on antidepressants and genetic modifications intended to induce depression in lab mice. But mental-health researchers have become increasingly sceptical in recent years about whether the forced-swim test is a good model for depression in people. It is not clear whether mice stop swimming because they are despondent or because they have learnt that a lab technician will scoop them out of the tank when they stop moving. Factors such as water temperature also seem to affect the results. “We don’t know what depression looks like in a mouse,” says Eric Nestler, a neuroscientist at the Icahn School of Medicine at Mount Sinai in New York City. Now, the animal-rights group People for the Ethical Treatment of Animals (PETA) is jumping into the fray. The group wants the US National Institute of Mental Health (NIMH) in Bethesda, Maryland, to stop supporting the use of the forced-swim test and similar behavioural assessments by its employees and grant recipients. The tests “create intense fear, anxiety, terror, and depression in small animals” without providing useful data, PETA said in a letter to the agency on 12 July. © 2019 Springer Nature Publishing AG

Keyword: Depression; Animal Rights
Link ID: 26431 - Posted: 07.19.2019

Jon Hamilton Researchers are prescribing exercise as if it were a drug in a study that aims to see if it can prevent Alzheimer's disease. "We are testing if exercise is medicine for people with a mild memory problem," says Laura Baker, principal investigator of the nationwide EXERT study and associate director of the Alzheimer's Disease Research Center at Wake Forest School of Medicine. The study, funded by the National Institute on Aging, could help determine whether exercise can protect people from the memory and thinking problems associated with Alzheimer's. "The evidence in science has been building for the last 20 years to suggest that exercise at the right intensity could protect brain health as we age," Baker says. But much of that evidence has come from studies that were small, ran for only a few months or relied on people's own estimates of how much they exercised. The EXERT study is different. It's taking 300 people at high risk for Alzheimer's and randomly assigning them to one of two groups for 18 months. Half the participants do aerobic exercise, like running on a treadmill. The other half do stretching and flexibility exercises for comparison. By subscribing, you agree to NPR's terms of use and privacy policy. This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply. © 2019 npr

Keyword: Alzheimers
Link ID: 26430 - Posted: 07.19.2019