Nicola Davis Scientists have discovered 17 separate genetic variations that increase the risk of a person developing depression. The findings, which came from analysing DNA data collected from more than 300,000 people, are the first genetics links to the disease found in people of European ancestry. The scientists say the research will contribute to a better understanding of the disease and could eventually lead to new treatments. They also hope it will reduce the stigma that can accompany depression. According to Nice, up to 10% of people seen by practitioners in primary care have clinical depression, with symptoms including a continuously low mood, low self-esteem, difficulties making decisions and lack of energy. Both environmental and genetic factors are thought to be behind depression, with the interaction between the two also thought to be important. But with a large number of genetic variants each thought to make a tiny contribution to the risk of developing the condition, unravelling their identity has proved challenging. While previous studies have turned up a couple of regions in the genome of Chinese women that might increase the risk of depression, the variants didn’t appear to play a role in depression for people of European ancestry. © 2016 Guardian News and Media Limited

Keyword: Depression; Genes & Behavior
Link ID: 22504 - Posted: 08.02.2016

By Andy Coghlan Mysterious shrunken cells have been spotted in the human brain for the first time, and appear to be associated with Alzheimer’s disease. “We don’t know yet if they’re a cause or consequence,” says Marie-Ève Tremblay of Laval University in Québec, Canada, who presented her discovery at the Translational Neuroimmunology conference in Big Sky, Montana, last week. The cells appear to be withered forms of microglia – the cells that keep the brain tidy and free of infection, normally by pruning unwanted brain connections or destroying abnormal and infected brain cells. But the cells discovered by Tremblay appear much darker when viewed using an electron microscope, and they seem to be more destructive. “It took a long time for us to identify them,” says Tremblay, who adds that these shrunken microglia do not show up with the same staining chemicals that normally make microglia visible under the microscope. Compared with normal microglia, the dark cells appear to wrap much more tightly around neurons and the connections between them, called synapses. “It seems they’re hyperactive at synapses,” says Tremblay. Where these microglia are present, synapses often seem shrunken and in the process of being degraded. Tremblay first discovered these dark microglia in mice, finding that they increase in number as mice age, and appear to be linked to a number of things, including stress, the neurodegenerative condition Huntington’s disease and a mouse model of Alzheimer’s disease. “There were 10 times as many dark microglia in Alzheimer’s mice as in control mice,” says Tremblay. © Copyright Reed Business Information Ltd.

Keyword: Alzheimers; Glia
Link ID: 22503 - Posted: 08.02.2016

By Katherine S. Pollard When the first human genome sequence was published in 2001,1 I was a graduate student working as the statistics expert on a team of scientists. Hailing from academia and biotechnology, we aimed to discover differences in gene expression levels between tumors and healthy cells. Like many others, I had high hopes for what we could do with this enormous text file of more than 3 billion As, Cs, Ts, and Gs. Ambitious visions of a precise wiring diagram for human cells and imminent cures for disease were commonplace among my classmates and professors. But I was most excited about a different use of the data, and I found myself counting the months until the genome of a chimpanzee would be sequenced. Chimps are our closest living relatives on the tree of life. While their biology is largely similar to ours, we have many striking differences, ranging from digestive enzymes to spoken language. Humans also suffer from an array of diseases that do not afflict chimpanzees or are less severe in them, including autism, schizophrenia, Alzheimer’s disease, diabetes, atherosclerosis, AIDS, rheumatoid arthritis, and certain cancers. I had long been fascinated with hominin fossils and the way the bones morphed into different forms over evolutionary time. But those skeletons cannot tell us much about the history of our immune system or our cognitive abilities. So I started brainstorming about how to extend the statistical approaches we were using for cancer research to compare human and chimpanzee DNA. My immodest goal was to identify the genetic basis for all the traits that make humans unique. © 1986-2016 The Scientist

Keyword: Evolution; Genes & Behavior
Link ID: 22502 - Posted: 08.02.2016

Carl Zimmer An eye is for seeing, a nose is for smelling. Many aspects of the human body have obvious purposes. But some defy easy explanation. For biologists, few phenomena are as mysterious as the female orgasm. While orgasms have an important role in a woman’s intimate relationships, the evolutionary roots of the experience — a combination of muscle contractions, hormone release, and intense pleasure — have been difficult to uncover. For decades, researchers have put forward theories, but none are widely accepted. Now two evolutionary biologists have joined the fray, offering a new way of thinking about the female orgasm based on a reconstruction of its ancient history. On Monday, in The Journal of Experimental Zoology, the authors conclude that the response originated in mammals more than 150 million years ago as a way to release eggs to be fertilized after sex. Until now, few scientists have investigated the biology of distantly related animals for clues to the mystery. “For orgasms, we kept it reserved for humans and primates,” said Mihaela Pavlicev, an evolutionary biologist at University of Cincinnati College of Medicine and an author of the new paper. “We didn’t look to other species to dig deeper and look for the origin.” The male orgasm has never caused much of a stir among evolutionary biologists. The pleasure is precisely linked to ejaculation, the most important step in passing on a male’s genes to the next generation. That pleasure encourages men to deliver more sperm, which is evolutionarily advantageous. For women, the evolutionary path is harder to figure out. The muscle contractions that occur during an orgasm are not essential for a woman to become pregnant. And while most men can experience an orgasm during sex, it’s less reliable for women. © 2016 The New York Times Company

Keyword: Sexual Behavior; Hormones & Behavior
Link ID: 22501 - Posted: 08.02.2016

By Bahar Gholipour After reflexively reaching out to grab a hot pan falling from the stove, you may be able to withdraw your hand at the very last moment to avoid getting burned. That is because the brain's executive control can step in to break a chain of automatic commands. Several new lines of evidence suggest that the same may be true when it comes to the reflex of recollection—and that the brain can halt the spontaneous retrieval of potentially painful memories. Within the brain, memories sit in a web of interconnected information. As a result, one memory can trigger another, making it bubble up to the surface without any conscious effort. “When you get a reminder, the mind's automatic response is to do you a favor by trying to deliver the thing that's associated with it,” says Michael Anderson, a neuroscientist at the University of Cambridge. “But sometimes we are reminded of things we would rather not think about.” Humans are not helpless against this process, however. Previous imaging studies suggest that the brain's frontal areas can dampen the activity of the hippocampus, a crucial structure for memory, and therefore suppress retrieval. In an effort to learn more, Anderson and his colleagues recently investigated what happens after the hippocampus is suppressed. They asked 381 college students to learn pairs of loosely related words. Later, the students were shown one word and asked to recall the other—or to do the opposite and to actively not think about the other word. Sometimes between these tasks they were shown unusual images, such as a peacock standing in a parking lot. © 2016 Scientific American

Keyword: Learning & Memory
Link ID: 22500 - Posted: 08.01.2016

Aaron E. Carroll I remember thinking, after my pregnant wife’s water broke, minutes after I went to bed, anguishing really, over one thought as we drove to the hospital: “I’m never going to be well rested again.” If there’s one things all new parents wish for, it’s a good night’s sleep. Unfortunately, infants sometimes make that impossible. They wake up repeatedly, needing to be fed, changed and comforted. Eventually, they reach an age when they should sleep through the night. Some don’t, though. What to do with them continues to be a topic of a heated debate in parenting circles. One camp believes that babies should be left to cry it out. These people place babies in their cribs at a certain time, after a certain routine, and don’t interfere until the next morning. No matter how much the babies scream or cry, parents ignore them. After all, if babies learn that tantrums lead to the appearance of a loved one, they will continue that behavior in the future. The official name for this intervention is “Extinction.” The downside, of course, is that it’s unbelievably stressful for parents. Many can’t do it. And not holding fast to the plan can make everything worse. Responding to an infant’s crying after an extended period of time makes the behavior harder to extinguish. To a baby, it’s like a slot machine that hits just as you’re ready to walk away; it makes you want to play more. A modification of this strategy is known as “Graduated Extinction.” Parents allow their infant to cry it out for a longer period each night, until infants eventually put themselves to sleep. On the first night, for instance, parents might commit to not entering the baby’s room for five minutes. The next night, 10 minutes. Then 15, and so on. Or, they could increase the increments on progressive checks each night. When they do go in the room, it’s only to check and make sure the baby is O.K. – no picking up or comforting. This isn’t meant to be a reward for crying, but to allow parents to be assured that nothing is wrong. © 2016 The New York Times Company

Keyword: Sleep; Development of the Brain
Link ID: 22499 - Posted: 08.01.2016

Nicola Davis Female orgasm has perplexed scientists, fuelled an equality movement and propelled Meg Ryan to fame. Now researchers say they might have found its evolutionary roots. The purpose of the euphoric sensation has long puzzled scientists as it is not necessary for conception, and is often not experienced by women during sex itself. But scientists in the US have come up with an answer. Human female orgasm, they say, might be a spin-off from our evolutionary past, when the hormonal surges that accompany it were crucial for reproduction. “It is important to stress that it didn’t look like the human female orgasm looks like now,” said Mihaela Pavličev, co-author of the study from Cincinnati children’s hospital. “We think that [the hormonal surge] is the core that was maybe modified further in humans.” Writing in the journal JEZ-Molecular and Developmental Evolution, Pavličev and co-author Günter Wagner from Yale University describe how they delved into the anatomy and behaviour of a host of placental mammals to uncover the evolutionary origin of female orgasm, based on the hormonal surges associated with it. In mammals such as cats and rabbits, these surges occur during sex and play a crucial role in signalling for eggs to be released from the female’s ovaries. By contrast in a variety of other mammals, including humans and other primates, females ovulate spontaneously. © 2016 Guardian News and Media Limited

Keyword: Sexual Behavior; Hormones & Behavior
Link ID: 22498 - Posted: 08.01.2016

Every year, hundreds of human brains are delivered to a network of special research centres. Why do these "brain banks" exist and what do they do? Rachael Buchanan was given rare access. A neuroscientist once told me with great insistence that brains are beautiful. His words came back to me as I watched a technician at the Bristol brain bank carefully dissect one of the facility's freshly donated specimens. The intricate folds and switchbacks of its surface and its delicate branching structures, revealed by her cuts, were entrancing. They seem only faintly to echo the complexity and power that tissue had held in life. The brain being methodically portioned up for storage was one of around 40 donations the South West Dementia Brain Bank receives each year. This bank in Bristol is one of 10 centres that make up the Medical Research Council's Brain Bank Network. Between them annually they supply hundreds of samples of research tissue to scientists in the UK and abroad. One of the thousand brains already fixed and frozen in the store rooms at Bristol is that of Angela Carlson. Written into that 3lb (1.4kg) of dissected tissue are the experiences, memories and knowledge of a very adventurous woman, for her time. She spent her teens in the land army during World War Two, followed by stints as a cook and child minder in the USA, and in what was then Persia. Twice widowed and without children, she eventually settled in Dorset to be near her niece Susan Jonas. She died there from dementia, aged 89. © 2016 BBC

Keyword: Brain imaging; Alzheimers
Link ID: 22497 - Posted: 08.01.2016

By BENEDICT CAREY Solving a hairy math problem might send a shudder of exultation along your spinal cord. But scientists have historically struggled to deconstruct the exact mental alchemy that occurs when the brain successfully leaps the gap from “Say what?” to “Aha!” Now, using an innovative combination of brain-imaging analyses, researchers have captured four fleeting stages of creative thinking in math. In a paper published in Psychological Science, a team led by John R. Anderson, a professor of psychology and computer science at Carnegie Mellon University, demonstrated a method for reconstructing how the brain moves from understanding a problem to solving it, including the time the brain spends in each stage. The imaging analysis found four stages in all: encoding (downloading), planning (strategizing), solving (performing the math), and responding (typing out an answer). “I’m very happy with the way the study worked out, and I think this precision is about the limit of what we can do” with the brain imaging tools available, said Dr. Anderson, who wrote the report with Aryn A. Pyke and Jon M. Fincham, both also at Carnegie Mellon. To capture these quicksilver mental operations, the team first taught 80 men and women how to interpret a set of math symbols and equations they had not seen before. The underlying math itself wasn’t difficult, mostly addition and subtraction, but manipulating the newly learned symbols required some thinking. The research team could vary the problems to burden specific stages of the thinking process — some were hard to encode, for instance, while others extended the length of the planning stage. The scientists used two techniques of M.R.I. data analysis to sort through what the participants’ brains were doing. One technique tracked the neural firing patterns during the solving of each problem; the other identified significant shifts from one kind of mental state to another. The subjects solved 88 problems each, and the research team analyzed the imaging data from those solved successfully. © 2016 The New York Times Company

Keyword: Attention; Brain imaging
Link ID: 22496 - Posted: 07.30.2016

By NICHOLAS ST. FLEUR Orangutan hear, orangutan do. Researchers at the Indianapolis Zoo observed an orangutan mimic the pitch and tone of human sounds, for the first time. The finding, which was published Wednesday, provides insight into the evolutionary origin of human speech, the team said. “It really redefines for us what we know about the capabilities of orangutans,” said Rob Shumaker, director of the zoo and an author on the paper. “What we have to consider now is the possibility that the origins of spoken language are not exclusively human, and that they may have come from great apes.” Rocky, an 11-year-old orangutan at the zoo, has a special ability. He can make sounds using his vocal folds, or voice box, that resemble the vowel “A,” and sound like “Ah.” The noises, or “wookies” as the researchers called them, are variations of the same vocalization. Sometimes the great ape would say high-pitched “wookies” and sometimes he would say his “Ahs” in a lower pitch. The researchers note that the sounds are specific to Rocky and ones that he used everyday. No other orangutan, captive or wild, made these noises. Rocky, who had never lived in the rain forest, apparently learned the skill during his time as an entertainment orangutan before coming to the zoo. He was at one point the most seen orangutan in movies and commercials, according to the zoo. The researchers said that Rocky’s grunts show that great apes have the capacity to learn to control their muscles to deliberately alter their sounds in a “conversational” manner. The findings, which were published in the journal Scientific Reports, challenge the notion that orangutans — an endangered species that shares about 97 percent of it DNA with humans — make noises simply in response to something, sort of like how you might scream when you place your hand on a hot stove. © 2016 The New York Times Company

Keyword: Language; Evolution
Link ID: 22495 - Posted: 07.30.2016

By Richard Kemeny Sleep is essential for memory. Mounting evidence continues to support the notion that the nocturnal brain replays, stabilizes, reorganizes, and strengthens memories while the body is at rest. Recently, one particular facet of this process has piqued the interest of a growing group of neuroscientists: sleep spindles. For years these brief bursts of brain activity have been largely ignored. Now it seems that examining these neuronal pulses could help researchers better understand—perhaps even treat—cognitive impairments. Sleep spindles are a defining characteristic of stage 2 non-rapid eye movement (NREM) sleep. These electrical bursts between 10-16 Hz last only around a second, and are known to occur in the human brain thousands of times per night. Generated by a thin net of neurons enveloping the thalamus, spindles appear across several regions of the brain, and are thought to perform various functions, including maintaining sleep in the face of disturbances in the environment. It appears they are also a fundamental part of the process by which the human brain consolidates memories during sleep. A memory formed during the day is stored temporarily in the hippocampus, before being spontaneously replayed during the night. Information about the memory is distributed out and integrated into the neocortex through an orchestra of slow-waves, spindles, and rapid hippocampal ripples. Spindles, it seems, could be a guiding force—providing the plasticity and coordination needed for this delicate, interregional transfer of information. © 1986-2016 The Scientist

Keyword: Sleep; Learning & Memory
Link ID: 22494 - Posted: 07.30.2016

By ERICA GOODE You are getting sleepy. Very sleepy. You will forget everything you read in this article. Hypnosis has become a common medical tool, used to reduce pain, help people stop smoking and cure them of phobias. But scientists have long argued about whether the hypnotic “trance” is a separate neurophysiological state or simply a product of a hypnotized person’s expectations. A study published on Thursday by Stanford researchers offers some evidence for the first explanation, finding that some parts of the brain function differently under hypnosis than during normal consciousness. The study was conducted with functional magnetic resonance imaging, a scanning method that measures blood flow in the brain. It found changes in activity in brain areas that are thought to be involved in focused attention, the monitoring and control of the body’s functioning, and the awareness and evaluation of a person’s internal and external environments. “I think we have pretty definitive evidence here that the brain is working differently when a person is in hypnosis,” said Dr. David Spiegel, a professor of psychiatry and behavioral sciences at Stanford who has studied the effectiveness of hypnosis. Functional imaging is a blunt instrument and the findings can be difficult to interpret, especially when a study is looking at activity levels in many brain areas. Still, Dr. Spiegel said, the findings might help explain the intense absorption, lack of self-consciousness and suggestibility that characterize the hypnotic state. © 2016 The New York Times Company

Keyword: Attention; Brain imaging
Link ID: 22493 - Posted: 07.30.2016

By Tanya Lewis The tangled buildup of tau protein in brain cells is a hallmark of the cognitive decline linked with Alzheimer’s disease. Antibodies have been shown to block tau’s spread, but some scientists worry it could also fuel inflammation. Now, researchers from Genentech in San Francisco and colleagues have found that an antibody’s ability to recruit immune cells—known as its effector function—is not necessary for stopping tau’s spread, the team reported today (July 28) in Cell Reports. “Our results suggest that, given that effector function is not required for efficacy [in treating tau accumulation], going without it could offer a safer approach for immunotherapy,” study coauthor Gai Ayalon of Genentech told The Scientist. Alzheimer’s disease causes a characteristic constellation of pathologies: accumulation of amyloid-β plaques outside neurons, neurofibrillary tangles of tau inside brain cells, and chronic inflammation. Clinical research has mostly focused on targeting amyloid-β with antibody therapies, and several treatments based on this approach are currently in clinical trials. But recent efforts have zeroed in on tau as a new potential target. Antibodies are known to spur the brain’s defense system, microglia, to absorb and degrade tau, but their recruitment of immune cells may also worsen inflammation. Ayalon and colleagues wondered whether effector function was necessary for stopping tau’s spread. © 1986-2016 The Scientist

Keyword: Alzheimers; Neuroimmunology
Link ID: 22492 - Posted: 07.30.2016

Laura Sanders Under duress, nerve cells get a little help from their friends. Brain cells called astrocytes send their own energy-producing mitochondria to struggling nerve cells. Those gifts may help the neurons rebound after injuries such as strokes, scientists propose in the July 28 Nature. It was known that astrocytes — star-shaped glial cells that, among other jobs, support neurons — take in and dispose of neurons’ discarded mitochondria. Now it turns out that mitochondria can move the other way, too. This astrocyte-to-neuron transfer is surprising, says neuroscientist Jarek Aronowski of the University of Texas Health Science Center at Houston. “Bottom line: It’s sort of shocking.” Study coauthor Eng Lo of Massachusetts General Hospital and Harvard Medical School cautions that the work is at a very early stage. But he hopes that a deeper understanding of this process might ultimately point out new ways to protect the brain from damage. Mitochondria produce the energy that powers cells in the body. Scientists have spotted the organelles moving into damaged cells in other parts of the body, including the lungs, heart and liver. The new study turns up signs of this mitochondrial generosity in the brain. Astrocytes produce mitochondria and shunt them out into the soup that surrounds cells, Lo and colleagues found. The researchers then put neurons into this mitochondria-rich broth. When starved of glucose and oxygen — a situation that approximates a stroke — the neurons took in the astrocyte-made organelles. |© Society for Science & the Public 2000 - 2016

Keyword: Stroke; Glia
Link ID: 22491 - Posted: 07.30.2016

Janet Raloff Over the last three years, growing evidence has shown that electronic cigarettes are not the harmless alternative to smoking that many proponents have argued. Now, a new study traces a large share of e-cigs’ toxic gases to a heat-triggered breakdown of the liquids used to create the vapors. And the hotter an e-cig gets — and the more it’s used — the more toxic compounds it emits, the study shows. “There is this image that e-cigarettes are a lot better than regular cigarettes, if not harmless,” says Hugo Destaillats, a chemist at Lawrence Berkeley National Laboratory in California. But after his team’s new analyses, published July 27 in Environmental Science & Technology, “we are now definitely convinced that they are far from harmless.” Electronic cigarettes draw liquids over one or more hot metal coils to transform them into vapors. Those liquids — polyethylene glycol, glycerin or a mix of the two — are food-grade solvents laced with flavorings and usually nicotine. The Berkeley team used two current models of e-cigs and three different commercially available e-liquids. The experimental setup mechanically drew air through the devices to create the vapors that a user would normally inhale. Heating up The higher an e-cigarette’s voltage, the more toxic aldehydes it produces in each puff of vapor. Once a certain threshold is hit, each voltage increase produces a disproportionate increase (see last bar) in acrolein, acetaldehyde and formaldehyde, three of the most harmful compounds in the vapor. |© Society for Science & the Public 2000 - 2016

Keyword: Drug Abuse
Link ID: 22490 - Posted: 07.28.2016

By Emily Underwood If your car’s battery dies, you might call on roadside assistance—or a benevolent bystander—for a jump. When damaged neurons lose their “batteries,” energy-generating mitochondria, they call on a different class of brain cells, astrocytes, for a boost, a new study suggests. These cells respond by donating extra mitochondria to the floundering neurons. The finding, still preliminary, might lead to novel ways to help people recover from stroke or other brain injuries, scientists say. “This is a very interesting and important study because it describes a new mechanism whereby astrocytes may protect neurons,” says Reuven Stein, a neurobiologist at The Rabin Institute of Neurobiology in Tel Aviv, Israel, who was not involved in the study. To keep up with the energy-intensive work of transmitting information throughout the brain, neurons need a lot of mitochondria, the power plants that produce the molecular fuel—ATP—that keeps cells alive and working. Mitochondria must be replaced often in neurons, in a process of self-replication called fission—the organelles were originally microbes captured inside a cell as part of a symbiosis. But if mitochondria are damaged or if they can’t keep up with a cell’s needs, energy supplies can run out, killing the cell. In 2014, researchers published the first evidence that cells can transfer mitochondria in the brain—but it seemed more a matter of throwing out the trash. When neurons expel damaged mitochondria, astrocytes swallow them and break them down. Eng Lo and Kazuhide Hayakawa, both neuroscientsists at Massachusetts General Hospital in Charlestown, wondered whether the transfer could go the other way as well—perhaps astrocytes donated working mitochondria to neurons in distress. Research by other groups supported that idea: A 2012 study, for example, found that stem cells from bone marrow can donate mitochondria to lung cells after severe injury. © 2016 American Association for the Advancement of Science

Keyword: Stroke; Glia
Link ID: 22489 - Posted: 07.28.2016

By ANDREW POLLACK A new type of drug for Alzheimer’s disease failed to slow the rate of decline in mental ability and daily functioning in its first large clinical trial. There was a hint, though, that it might be effective for certain patients. The drug, called LMTX, is the first one with its mode of action — trying to undo so-called tau tangles in the brain — to reach the final stage of clinical trials. So the results of the study were eagerly awaited. The initial reaction to the outcome was disappointment, with perhaps a glimmer of hopefulness. Over all, the patients who received LMTX, which was developed by TauRx Therapeutics, did not have a slower rate of decline in mental ability or daily functioning than those in the control group. However, the drug did seem to work for the subset of patients — about 15 percent of those in the study — who took LMTX as their only therapy. The other 85 percent of patients took an existing Alzheimer’s drug in addition to either LMTX or a placebo. “There were highly significant, clinically meaningful, large effects in patients taking the drug as monotherapy, and no effect in patients taking it as an add-on,” Claude Wischik, a founder and the chief executive of TauRx, said in an interview. He spoke from Toronto, where the results were being presented at the Alzheimer’s Association International Conference. Dr. Wischik said a second clinical trial sponsored by the company, whose results will be announced later, found the same phenomenon. He said the company planned to apply for approval of LMTX to be used by itself. But some experts not involved in the study were skeptical about drawing conclusions from a small subset of patients, especially since there was no obvious explanation why LMTX would be expected to work only in patients not getting other drugs. on © 2016 The New York Times Company

Keyword: Alzheimers
Link ID: 22488 - Posted: 07.28.2016

Ian Sample and Nicky Woolf When Bill Gates pulled on a red and white-striped cord to upturn a bucket of iced water positioned delicately over his head, the most immediate thought for many was not, perhaps, of motor neurone disease. But the ice bucket challenge, the charity campaign that went viral in the summer of 2014 and left scores of notable persons from Gates and Mark Zuckerberg to George W. Bush and Anna Wintour shivering and drenched, has paid off in the most spectacular way. Dismissed by some at the time as “slacktivism” - an exercise that appears to do good while achieving very little - the ice bucket challenge raised more than $115m (£88m) for motor neurone disease in a single month. Now, scientists funded with the proceeds have discovered a gene variant associated with the condition. In the near term the NEK1 gene variant, described in the journal Nature Genetics this week, will help scientists understand how the incurable disorder, known also as Amyotrophic Lateral Sclerosis (ALS) or Lou Gehrig’s disease, takes hold. Once the mechanisms are more clearly elucidated, it may steer researchers on a path towards much-needed treatments. The work may never have happened were it not for the curious appeal of the frozen water drenchings. The research grants that scientists are awarded do not get close to the €4m the study required. Instead, Project MinE, which aims to unravel the genetic basis of the disease and ultimately find a cure, was funded by the ALS Association through ice bucket challenge donations. © 2016 Guardian News and Media Limited

Keyword: ALS-Lou Gehrig's Disease ; Genes & Behavior
Link ID: 22487 - Posted: 07.28.2016

By Gretchen Reynolds Learning requires more than the acquisition of unfamiliar knowledge; that new information or know-how, if it’s to be more than ephemeral, must be consolidated and securely stored in long-term memory. Mental repetition is one way to do that, of course. But mounting scientific evidence suggests that what we do physically also plays an important role in this process. Sleep, for instance, reinforces memory. And recent experiments show that when mice and rats jog on running wheels after acquiring a new skill, they learn much better than sedentary rodents do. Exercise seems to increase the production of biochemicals in the body and brain related to mental function. Researchers at the Donders Institute for Brain, Cognition and Behavior at Radboud University in the Netherlands and the University of Edinburgh have begun to explore this connection. For a study published this month in Current Biology, 72 healthy adult men and women spent about 40 minutes undergoing a standard test of visual and spatial learning. They observed pictures on a computer screen and then were asked to remember their locations. Afterward, the subjects all watched nature documentaries. Two-thirds of them also exercised: Half were first put through interval training on exercise bicycles for 35 minutes immediately after completing the test; the others did the same workout four hours after the test. Two days later, everyone returned to the lab and repeated the original computerized test while an M.R.I. machine scanned their brain activity. Those who exercised four hours after the test recognized and recreated the picture locations most accurately. Their brain activity was subtly different, too, showing a more consistent pattern of neural activity. The study’s authors suggest that their brains might have been functioning more efficiently because they had learned the patterns so fully. But why delaying exercise for four hours was more effective than an immediate workout remains mysterious. By contrast, rodents do better in many experiments if they work out right after learning. © 2016 The New York Times Company

Keyword: Learning & Memory
Link ID: 22486 - Posted: 07.28.2016

Jon Hamilton Two studies released at an international Alzheimer's meeting Tuesday suggest doctors may eventually be able to screen people for this form of dementia by testing the ability to identify familiar odors, like smoke, coffee and raspberry. In both studies, people who were in their 60s and older took a standard odor detection test. And in both cases, those who did poorly on the test were more likely to already have — or go on to develop — problems with memory and thinking. "The whole idea is to create tests that a general clinician can use in an office setting," says Dr. William Kreisl, a neurologist at Columbia University, where both studies were done. The research was presented at the Alzheimer's Association International Conference in Toronto. Currently, any tests that are able to spot people in the earliest stages of Alzheimer's are costly and difficult. They include PET scans, which can detect sticky plaques in the brain, and spinal taps that measure the levels of certain proteins in spinal fluid. The idea of an odor detection test arose, in part, from something doctors have observed for many years in patients with Alzheimer's, Kreisl says. "Patients will tell us that food does not taste as good," he says. The reason is often that these patients have lost the ability to smell what they eat. That's not surprising, Kreisl says, given that odor signals from the nose have to be processed in areas of the brain that are among the first to be affected by Alzheimer's disease. But it's been tricky to develop a reliable screening test using odor detection. © 2016 npr

Keyword: Alzheimers; Chemical Senses (Smell & Taste)
Link ID: 22485 - Posted: 07.27.2016