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By Emily Underwood In 2010, neurobiologist Beth Stevens had completed a remarkable rise from laboratory technician to star researcher. Then 40, she was in her second year as a principal investigator at Boston Children’s Hospital with a joint faculty position at Harvard Medical School. She had a sleek, newly built lab and a team of eager postdoctoral investigators. Her credentials were impeccable, with high-profile collaborators and her name on an impressive number of papers in well-respected journals. But like many young researchers, Stevens feared she was on the brink of scientific failure. Rather than choosing a small, manageable project, she had set her sights on tackling an ambitious, unifying hypothesis linking the brain and the immune system to explain both normal brain development and disease. Although the preliminary data she’d gathered as a postdoc at Stanford University in Palo Alto, California, were promising, their implications were still murky. “I thought, ‘What if my model is just a model, and I let all these people down?’” she says. Stevens, along with her mentor at Stanford, Ben Barres, had proposed that brain cells called microglia prune neuronal connections during embryonic and later development in response to a signal from a branch of the immune system known as the classical complement pathway. If a glitch in the complement system causes microglia to prune too many or too few connections, called synapses, they’d hypothesized, it could lead to both developmental and degenerative disorders. © 2016 American Association for the Advancement of Science.

Keyword: Development of the Brain; Glia
Link ID: 22576 - Posted: 08.20.2016

Meghan Rosen Zika may harm grown-up brains. The virus, which can cause brain damage in infants infected in the womb, kills stem cells and stunts their numbers in the brains of adult mice, researchers report August 18 in Cell Stem Cell. Though scientists have considered Zika primarily a threat to unborn babies, the new findings suggest that the virus may cause unknown — and potentially long-term — damage to adults as well. In adults, Zika has been linked to Guillain-Barré syndrome, a rare neurological disorder (SN: 4/2/16, p. 29). But for most people, infection is typically mild: a headache, fever and rash lasting up to a week, or no symptoms at all. In pregnant women, though, the virus can lodge in the brain of a fetus and kill off newly developing cells (SN: 4/13/16). If Zika targets newborn brain cells, adults may be at risk, too, reasoned neuroscientist Joseph Gleeson of Rockefeller University in New York City and colleagues. Parts of the forebrain and the hippocampus, which plays a crucial role in learning and memory, continue to generate nerve cells in adult brains. In mice infected with Zika, the virus hit these brain regions hard. Nerve cells died and the regions generated one-fifth to one-half as many new cells compared with those of uninfected mice. The results might not translate to humans; the mice were genetically engineered to have weak immune systems, making them susceptible to Zika. But Zika could potentially harm immunocompromised people and perhaps even healthy people in a similar way, the authors write. © Society for Science & the Public 2000 - 2016.

Keyword: Development of the Brain
Link ID: 22575 - Posted: 08.20.2016

By Nicholas Bakalar Taking antipsychotic medicines during pregnancy does not increase the risk for birth defects, a large new study has found. Antipsychotics are used to treat schizophrenia, bipolar disorder, depression and other psychiatric disorders. Previous studies of their use during pregnancy have been small and have had mixed results. This study, in JAMA Psychiatry, reviewed records of 1,341,715 pregnant women, of whom 9,258 filled prescriptions for the newer atypical antipsychotics like quetiapine (Seroquel) or aripiprazole (Abilify), and 733 for older typical antipsychotics such as haloperidol (Haldol). All prescriptions were filled in the first trimester of pregnancy. After controlling for race, number of pregnancies, smoking, alcohol use, psychiatric conditions, additional medications and other variables, there was no difference in the risk for birth defects between those who took the drugs and those who did not. One possible exception was a marginal increase in risk with one drug, risperidone (Risperdal), which the authors said will require further study. “These findings suggest that the use of antipsychotics during the first trimester does not seem to increase congenital malformation,” or birth defects, said the lead author, Krista F. Huybrechts, an assistant professor of medicine at Harvard. But, she added, “we only looked at congenital malformation, not other possible negative outcomes for women and their children.” © 2016 The New York Times Company

Keyword: Development of the Brain; Schizophrenia
Link ID: 22574 - Posted: 08.20.2016

SINCE nobody really knows how brains work, those researching them must often resort to analogies. A common one is that a brain is a sort of squishy, imprecise, biological version of a digital computer. But analogies work both ways, and computer scientists have a long history of trying to improve their creations by taking ideas from biology. The trendy and rapidly developing branch of artificial intelligence known as “deep learning”, for instance, takes much of its inspiration from the way biological brains are put together. The general idea of building computers to resemble brains is called neuromorphic computing, a term coined by Carver Mead, a pioneering computer scientist, in the late 1980s. There are many attractions. Brains may be slow and error-prone, but they are also robust, adaptable and frugal. They excel at processing the sort of noisy, uncertain data that are common in the real world but which tend to give conventional electronic computers, with their prescriptive arithmetical approach, indigestion. The latest development in this area came on August 3rd, when a group of researchers led by Evangelos Eleftheriou at IBM’s research laboratory in Zurich announced, in a paper published in Nature Nanotechnology, that they had built a working, artificial version of a neuron. Neurons are the spindly, highly interconnected cells that do most of the heavy lifting in real brains. The idea of making artificial versions of them is not new. Dr Mead himself has experimented with using specially tuned transistors, the tiny electronic switches that form the basis of computers, to mimic some of their behaviour. © The Economist Newspaper Limited 2016.

Keyword: Robotics; Intelligence
Link ID: 22573 - Posted: 08.18.2016

By Jef Akst ANDRZEJ KRAUZEAs a psychiatrist at Western University in London, Ontario, Lena Palaniyappan regularly sees patients with schizophrenia, the chronic mental disorder that drastically affects how a person thinks, feels, and behaves. The disorder can be devastating, often involving hallucinations and delusions. But one thing Palaniyappan and other mental health professionals have noticed is that, unlike those with degenerative neurological disorders such as Alzheimer’s disease, Huntington’s, or Parkinson’s, sometimes schizophrenia patients eventually start to improve. “In the clinic we do actually see patients with schizophrenia having a very relentless progress in early years,” Palaniyappan says. “But a lot of them do get better over the years, or they don’t progress as [quickly].” So far, most research has focused on the neurological decline associated with schizophrenia—typically involving a loss of brain tissue. Palaniyappan and his colleagues wondered whether there might be “something happening in the brain [that] helps them come to a state of stability.” To get at this question, he and his colleagues performed MRI scans to assess the cortical thickness of 98 schizophrenia patients at various stages of illness. Sure enough, the researchers noted that, while patients who were less than two years removed from their diagnosis had significantly thinner tissue than healthy controls, those patients who’d had the disease for longer tended to show less deviation in some brain regions, suggesting some sort of cortical amelioration (Psychol Med, doi:10.1017/S0033291716000994, 2016). “Some brain regions are regaining or normalizing while other brain regions continue to show deficits,” Palaniyappan says. © 1986-2016 The Scientist

Keyword: Schizophrenia; Regeneration
Link ID: 22572 - Posted: 08.18.2016

By Jessica Hamzelou JACK NICHOLSON has a lot to answer for. One of the knock-on effects of hit 1975 movie One Flew Over the Cuckoo’s Nest was a public backlash against electroconvulsive therapy (ECT). The treatment, used since the 1930s for a wide range of mental health conditions, delivers a jolt of electricity to the brain big enough to trigger a seizure. The film’s brutal depiction of ECT and lobbying helped it fall out of favour in the 1980s and 1990s. But ECT may now be undergoing a revival, led by psychiatrists who champion it because of its success rate. “It’s the most effective treatment we have in psychiatry,” says George Kirov at Cardiff University, UK, who oversees ECT treatments in the area. A report from the UK Royal College of Psychiatrists last September showed that three-quarters of people with mental health problems felt improvement after having ECT. And psychiatrists say that a similar percentage of people who have schizophrenia that doesn’t respond to drug treatment find ECT effective. “I’ve never seen an ECT treatment that doesn’t work,” says Helen Farrell, a psychiatrist at the Beth Israel Deaconess Medical Center in Boston. “People have such a skewed view of electroconvulsive therapy. It is seen as primitive and horrific“ Mounting evidence has convinced the US Food and Drug Administration (FDA) to consider reclassifying ECT devices to make the technology more accessible for people with depression or bipolar disorder. The public will still take some convincing, however. In a 2005 survey in Switzerland, for example, 56 per cent were against ECT, while just 1 per cent said they were in favour. © Copyright Reed Business Information Ltd.

Keyword: Depression
Link ID: 22571 - Posted: 08.18.2016

Dean Burnett A lot of people, when they travel by car, ship, plane or whatever, end up feeling sick. They’re fine before they get into the vehicle, they’re typically fine when they get out. But whilst in transit, they feel sick. Particularly, it seems, in self-driving cars. Why? One theory is that it’s due to a weird glitch that means your brain gets confused and thinks it’s being poisoned. This may seem surprising; not even the shoddiest low-budget airline would get away with pumping toxins into the passengers (airline food doesn’t count, and that joke is out of date). So where does the brain get this idea that it’s being poisoned? Despite being a very “mobile” species, humans have evolved for certain types of movement. Specifically, walking, or running. Walking has a specific set of neurological processes tied into it, so we’ve had millions of years to adapt to it. Think of all the things going on in your body when you’re walking, and how the brain would pick up on these. There’s the steady thud-thud-thud and pressure on your feet and lower legs. There’s all the signals from your muscles and the movement of your body, meaning the motor cortex (which controls conscious movement of muscles) and proprioception (the sense of the arrangement of your body in space, hence you can know, for example, where your arm is behind your back without looking at it directly) are all supplying particular signals. © 2016 Guardian News and Media Limited

Keyword: Miscellaneous; Vision
Link ID: 22570 - Posted: 08.18.2016

Angus Chen Once people realized that opioid drugs could cause addiction and deadly overdoses, they tried to use newer forms of opioids to treat the addiction to its parent. Morphine, about 10 times the strength of opium, was used to curb opium cravings in the early 19th century. Codeine, too, was touted as a nonaddictive drug for pain relief, as was heroin. Those attempts were doomed to failure because all opioid drugs interact with the brain in the same way. They dock to a specific neural receptor, the mu-opioid receptor, which controls the effects of pleasure, pain relief and need. Now scientists are trying to create opioid painkillers that give relief from pain without triggering the euphoria, dependence and life-threatening respiratory suppression that causes deadly overdoses. That wasn't thought possible until 2000, when a scientist named Laura Bohn found out something about a protein called beta-arrestin, which sticks to the opioid receptor when something like morphine activates it. When she gave morphine to mice that couldn't make beta-arrestin, they were still numb to pain, but a lot of the negative side effects of the drug were missing. They didn't build tolerance to the drug. At certain dosages, they had less withdrawal. Their breathing was more regular, and they weren't as constipated as normal mice on morphine. Before that experiment, scientists thought the mu-opioid receptor was a simple switch that flicked all the effects of opioids on or off together. Now it seems they could be untied. © 2016 npr

Keyword: Pain & Touch; Drug Abuse
Link ID: 22569 - Posted: 08.18.2016

By Melinda Wenner Moyer The science of sleep is woefully incomplete, not least because research on the topic has long ignored half of the population. For decades, sleep studies mostly enrolled men. Now, as sleep researchers are making a more concerted effort to study women, they are uncovering important differences between the sexes. Hormones are a major factor. Estrogen, progesterone and testosterone can influence the chemical systems in the brain that regulate sleep and arousal. Moreover, recent studies indicate that during times of hormonal change—such as puberty, pregnancy and menopause—women are at an increased risk for sleep disorders such as obstructive sleep apnea, restless legs syndrome and insomnia. Women also tend to report that they have more trouble sleeping before and during their menstrual periods. And when women do sleep poorly, they may have a harder time focusing than sleep-deprived men do. In one recent study, researchers shifted the sleep-wake cycles of 16 men and 18 women for 10 days. Volunteers were put on a 28-hour daily cycle involving nearly 19 hours of awake time followed by a little more than nine hours of sleep. During the sleep-shifted period, the women in the group performed much less accurately than the men on cognitive tests. The findings, published in April of this year in the Proceedings of the National Academy of Sciences USA, may help explain why women are more likely than men to get injured working graveyard shifts. In addition, a study conducted in 2015 in teenagers reported that weekday sleep deprivation affects cognitive ability more in girls than in boys. © 2016 Scientific American

Keyword: Sleep; Sexual Behavior
Link ID: 22568 - Posted: 08.18.2016

By Karen Weintraub There’s been lots of coverage lately about meeting exercise recommendations by completing small chunks of exercise throughout the day rather than one, continuous session. Does the same hold true for meeting sleep recommendations? No. Unfortunately, sleep does not work that way. Substituting periodic naps for one consolidated night of sleep creates severe sleep deprivation, said Dr. Daniel Buysse, a sleep expert and professor of psychiatry at the University of Pittsburgh. He and his colleagues once did an experiment in which volunteers agreed to alternate 30 minutes of sleep with 60 minutes of wakefulness for two and a half days straight. They ended up sleep deprived, he said, because sound sleep is not equally likely at all times of day. People have a better chance of falling quickly into deep, restful sleep at night than midday, even if they feel as though they could fall asleep at any time. “Our biological clocks do not allow us to sleep as well during the day as at night,” he said. “All sleep is not necessarily equal.” That’s why night workers get less sleep on average than people who work other shifts – and suffer health consequences as a result, he said. But it’s always a good idea to make up for lost sleep, regardless of the time of day, said Dr. Ruth Benca, a professor of psychiatry and director of the Center for Sleep Medicine and Sleep Research at the University of Wisconsin-Madison. People used to think that it was better to pull an all-nighter than to break it up with a short nap, but that isn’t true, she said. On the other hand, it may be helpful, she said, to take an afternoon nap to compensate for a short night of sleep, bringing a six-and-a-half hour night up to seven, for instance. “If you have to stay awake for a prolonged period, you can mitigate that a little bit by taking some naps, but you can’t live your life like that,” Dr. Benca said. “Any sleep is better than no sleep, and more sleep is better than less sleep.” © 2016 The New York Times Company

Keyword: Sleep
Link ID: 22567 - Posted: 08.18.2016

By Robin Wylie Scientists have been searching for a genetic explanation for athletic ability for decades. So far their efforts have focused largely on genes related to physical attributes, such as muscular function and aerobic efficiency. But geneticists have also started to investigate the neurologicalbasis behind what makes someone excel in sports—and new findings implicate dopamine, a neurotransmitter responsible for the feelings of reward and pleasure. Dopamine is also involved in a host of other mental functions, including the ability to deal with stress and endure pain. Consequently, the new research supports the idea that the mental—not just the physical—is what sets elite athletes above the rest. In an effort to piece together what makes a great athlete great, researchers at the University of Parma in Italy collected DNA from 50 elite athletes (ones who had achieved top scores at an Olympic Games or other international competition) and 100 nonprofessional athletes (ones who played sports regularly, but below competitive level). They then compared four genes across the two groups that had previously been suggested as linked to athletic ability: one related to muscle development, one involved with transporting dopamine in the brain, another that regulates levels of cerebral serotonin and one involved in breaking down neurotransmitters. The researchers found a significant genetic difference between the two groups in only one of the genes: the one involved in transporting dopamine. Two particular variants of this gene (called the dopamine active transporter, or DAT) were significantly more common among the elite athletes than in the control group. One variant was almost five times more prevalent in the elite group (occurring in 24 percent of the elites versus 5 percent of the rest); the other variant was approximately 1.7 times more prevalent (51 percent versus 30 percent). The results were published in Journal of Biosciences. © 2016 Scientific American

Keyword: Drug Abuse; Genes & Behavior
Link ID: 22566 - Posted: 08.17.2016

By Jessica Hamzelou Feel like you’ve read this before? Most of us have experienced the eerie familiarity of déjà vu, and now the first brain scans of this phenomenon have revealed why – it’s a sign of our brain checking its memory. Déjà vu was thought to be caused by the brain making false memories, but research by Akira O’Connor at the University of St Andrews, UK, and his team now suggests this is wrong. Exactly how déjà vu works has long been a mystery, partly because its fleeting and unpredictable nature makes it difficult to study. To get around this, O’Connor and his colleagues developed a way to trigger the sensation of déjà vu in the lab. The team’s technique uses a standard method to trigger false memories. It involves telling a person a list of related words – such as bed, pillow, night, dream – but not the key word linking them together, in this case, sleep. When the person is later quizzed on the words they’ve heard, they tend to believe they have also heard “sleep” – a false memory. To create the feeling of déjà vu, O’ Connor’s team first asked people if they had heard any words beginning with the letter “s”. The volunteers replied that they hadn’t. This meant that when they were later asked if they had heard the word sleep, they were able to remember that they couldn’t have, but at the same time, the word felt familiar. “They report having this strange experience of déjà vu,” says O’Connor. © Copyright Reed Business Information Ltd.

Keyword: Attention; Learning & Memory
Link ID: 22565 - Posted: 08.17.2016

By Gary Stix In recent decades neuroscience has emerged as a star among the biological disciplines. But its enormous popularity as an academic career choice has been accompanied by a drop in the percentage of trained neuroscientists who actually work in academic research positions—largely because of a lack of funding. In 2014 the National Academies organized a workshop to ponder the question of whether this trend bodes well for the scientists-to-be who are now getting their Ph.D.s. The findings were published this summer in Neuron. Steven Hyman of the Broad Institute of the Massachusetts Institute of Technology and Harvard University, who helped to plan the workshop and was recently president of the Society for Neuroscience (SfN), welcomes the flood of doctoral students choosing the field but warns: “Insofar as talented young people are discouraged from academic careers by funding levels so low that they produce debilitating levels of competition or simply foreclose opportunities, the U.S. and the world are losing an incredibly precious resource.” Because there are not enough academic positions to go around, it is now the responsibility of professors to prepare students for alternative careers, says Huda Akil of the University of Michigan Medical School, lead author of the paper. “It's not just academia and industry” where trained neuroscientists can make contributions to society, says Akil, also a former SfN president: “It's nonprofits. It's social policy. It's science writing. It's man-machine interfaces. It's Big Data, or education, or any area where knowledge of the brain is relevant.” © 2016 Scientific American

Keyword: Miscellaneous
Link ID: 22564 - Posted: 08.17.2016

by Helen Thompson Some guys really know how to kill a moment. Among Mediterranean fish called ocellated wrasse (Symphodus ocellatus), single males sneak up on mating pairs in their nest and release a flood of sperm in an effort to fertilize some of the female’s eggs. But female fish may safeguard against such skullduggery through their ovarian fluid, gooey film that covers fish eggs. Suzanne Alonzo, a biologist at Yale University, and her colleagues exposed sperm from both types of males to ovarian fluid from female ocellated wrasse in the lab. Nesting males release speedier sperm in lower numbers (about a million per spawn), while sneaking males release a lot of slower sperm (about four million per spawn). Experiments showed that ovarian fluid enhanced sperm velocity and motility and favored speed over volume. Thus, the fluid gives a female’s chosen mate an edge in the race to the egg, the researchers report August 16 in Nature Communications. While methods to thwart unwanted sperm are common in species that fertilize within the body, evidence from Chinook salmon previously hinted that external fertilizers don’t have that luxury. However, these new results suggest otherwise: Some female fish retain a level of control over who fathers their offspring even after laying their eggs. Male ocellated wrasse come in three varieties: sneaky males (shown) that surprise mating pairs with sperm but don’t help raise offspring; nesting males that build algae nests and court females; and satellite males, which protect nests from sneakers but staying out of parenting. |© Society for Science & the Public 2000 - 2016

Keyword: Sexual Behavior; Evolution
Link ID: 22563 - Posted: 08.17.2016

Neuroscientists peered into the brains of patients with Parkinson’s disease and two similar conditions to see how their neural responses changed over time. The study, funded by the NIH’s Parkinson’s Disease Biomarkers Program and published in Neurology, may provide a new tool for testing experimental medications aimed at alleviating symptoms and slowing the rate at which the diseases damage the brain. “If you know that in Parkinson’s disease the activity in a specific brain region is decreasing over the course of a year, it opens the door to evaluating a therapeutic to see if it can slow that reduction,” said senior author David Vaillancourt, Ph.D., a professor in the University of Florida’s Department of Applied Physiology and Kinesiology. “It provides a marker for evaluating how treatments alter the chronic changes in brain physiology caused by Parkinson’s.” Parkinson’s disease is a neurodegenerative disorder that destroys neurons in the brain that are essential for controlling movement. While many medications exist that lessen the consequences of this neuronal loss, none can prevent the destruction of those cells. Clinical trials for Parkinson’s disease have long relied on observing whether a therapy improves patients’ symptoms, but such studies reveal little about how the treatment affects the underlying progressive neurodegeneration. As a result, while there are treatments that improve symptoms, they become less effective as the neurodegeneration advances. The new study could remedy this issue by providing researchers with measurable targets, called biomarkers, to assess whether a drug slows or even stops the progression of the disease in the brain. “For decades, the field has been searching for an effective biomarker for Parkinson’s disease,” said Debra Babcock, M.D., Ph.D., program director at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS).

Keyword: Parkinsons; Brain imaging
Link ID: 22562 - Posted: 08.16.2016

By Marlene Cimons Former president Jimmy Carter, 91, told the New Yorker recently that 90 percent of the arguments he has with Rosalynn, his wife of 70 years, are about hearing. “When I tell her, ‘Please speak more loudly,’ she absolutely refuses to speak more loudly, or to look at me when she talks,” he told the magazine. In response, the former first lady, 88, declared that having to repeat things “drives me up the wall.” Yet after both went to the doctor, much to her surprise, “I found out it was me!” she said. “I was the one who was deaf.” Hearing loss is like that. It comes on gradually, often without an individual’s realizing it, and it prompts a range of social and health consequences. “You don’t just wake up with a sudden hearing loss,” says Barbara Kelley, executive director of the Hearing Loss Association of America. “It can be insidious. It can creep up on you. You start coping, or your spouse starts doing things for you, like making telephone calls.” An estimated 25 percent of Americans between ages 60 and 69 have some degree of hearing loss, according to the President’s Council of Advisors on Science and Technology. That percentage grows to more than 50 percent for those age 70 to 79, and to almost 80 percent of individuals older than 80. That’s about 30 million people, a number likely to increase as our population ages. Behind these statistics are disturbing repercussions such as social isolation and the inability to work, travel or be physically active.

Keyword: Hearing
Link ID: 22561 - Posted: 08.16.2016

Are you a giver or a taker? Brain scans have identified a region of the cerebral cortex responsible for generosity – and some of us are kinder than others. The area was identified using a computer game that linked different symbols to cash prizes that either went to the player, or one of the study’s other participants. The volunteers readily learned to score prizes that helped other people, but they tended to learn how to benefit themselves more quickly. Read more: The kindness paradox: Why be generous? MRI scanning revealed that one particular brain area – the subgenual anterior cingulate cortex – seemed to be active when participants chose to be generous, prioritising benefits for someone else over getting rewards for themselves. But Patricia Lockwood, at the University of Oxford, and her team found that this brain area was not equally active in every volunteer. People who rated themselves as having higher levels of empathy learned to benefit others faster, and these people had more activity in this particular brain area, says Lockwood. This finding may lead to new ways to identify and understand anti-social and psychopathic behavior. Journal reference: PNAS, DOI: 10.1073/pnas.1603198113 © Copyright Reed Business Information Ltd.

Keyword: Brain imaging; Emotions
Link ID: 22560 - Posted: 08.16.2016

By Roni Caryn Rabin Dementia is a general term for a set of symptoms that includes severe memory loss, a significant decline in reasoning and severely impaired communication skills; it most commonly strikes elderly people and used to be referred to as “senility.” Alzheimer’s disease is a specific illness that is the most common cause of dementia. Though many diseases can cause dementia, Alzheimer’s accounts for 60 percent to 80 percent of dementia cases, “which is why you’ll often hear the terms used interchangeably,” said Heather Snyder, the senior director of medical and scientific operations for the Alzheimer’s Association. She said the question comes up frequently because patients may receive an initial diagnosis of dementia followed by an evaluation that yields the more specific diagnosis of Alzheimer’s disease, and they may be confused. The second most common form of dementia is vascular dementia, which is caused by a stroke or poor blood flow to the brain. Other diseases that can lead to dementia include Huntington’s disease, Parkinson’s disease and Creutzfeldt-Jakob disease. Some patients may have more than one form of dementia. Dementia is caused by damage to brain cells. In the case of Alzheimer’s disease, that damage is characterized by telltale protein fragments or plaques that accumulate in the space between nerve cells and twisted tangles of another protein that build up inside cells. In Alzheimer’s disease, dementia gets progressively worse to the point where patients cannot carry out daily activities and cannot speak, respond to their environment, swallow or walk. Although some treatments may temporarily ease symptoms, the downward progression of disease continues and it is not curable. © 2016 The New York Times Company

Keyword: Alzheimers
Link ID: 22559 - Posted: 08.16.2016

By Anna Azvolinsky Sets of neurons in the brain that behave together—firing synchronously in response to sensory or motor stimuli—are thought to be functionally and physiologically connected. These naturally occurring ensembles of neurons are one of the ways memories may be programmed in the brain. Now, in a paper published today (August 11) in Science, researchers at Columbia University and their colleagues show that it is possible to stimulate visual cortex neurons in living, awake mice and induce a new ensemble of neurons that behave as a group and maintain their concerted firing for several days. “This work takes the concept of correlated [neuronal] firing patterns in a new and important causal direction,” David Kleinfeld, a neurophysicist at the University of California, San Diego, who was not involved in the work told The Scientist. “In a sense, [the researchers] created a memory for a visual feature that does not exist in the physical world as a proof of principal of how real visual memories are formed.” “Researchers have previously related optogenetic stimulation to behavior [in animals], but this study breaks new ground by investigating the dynamics of neural activity in relation to the ensemble to which these neurons belong,” said Sebastian Seung, a computational neuroscientist at the Princeton Neuroscience Institute in New Jersey who also was not involved in the study. Columbia’s Rafael Yuste and colleagues stimulated randomly selected sets of individual neurons in the visual cortices of living mice using two-photon stimulation while the animals ran on a treadmill. © 1986-2016 The Scientist

Keyword: Learning & Memory; Vision
Link ID: 22558 - Posted: 08.13.2016

By Helen Thomson Take a walk while I look inside your brain. Scientists have developed the first wearable PET scanner – allowing them to capture the inner workings of the brain while a person is on the move. The team plans to use it to investigate the exceptional talents of savants, such as perfect memory or exceptional mathematical skill. All available techniques for scanning the deeper regions of our brains require a person to be perfectly still. This limits the kinds of activities we can observe the brain doing, but the new scanner will enable researchers to study brain behaviour in normal life, as well providing a better understanding of the tremors of Parkinson’s disease, and the effectiveness of treatments for stroke. Positron emission tomography scanners track radioactive tracers, injected into the blood, that typically bind to glucose, the molecule that our cells use for energy. In this way, the scanners build 3D images of our bodies, enabling us to see which brain areas are particularly active, or where tumours are guzzling glucose in the body. To adapt this technique for people who are moving around, Stan Majewski at West Virginia University in Morgantown and his colleagues have constructed a ring of 12 radiation detectors that can be placed around a person’s head. This scanner is attached to the ceiling by a bungee-cord contraption, so that the wearer doesn’t feel the extra weight of the scanner. © Copyright Reed Business Information Ltd

Keyword: Brain imaging
Link ID: 22557 - Posted: 08.13.2016