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By Roxanne Khamsi, What if controlling the appetite were as easy as flipping a switch? It sounds like the stuff of science fiction, but Jeffrey Friedman of Rockefeller University and his colleagues did exactly this in genetically engineered mice to try to shed light on how the brain influences appetite. Friedman and his colleagues used magnetic stimulation to switch on neurons in a region of the brain called the ventromedial hypothalamus and found that doing so increased the rodents' blood sugar levels and decreased levels of the hormone insulin. Turning on the neurons also caused the mice to eat more than their control counterparts. The ultimate confirmation came when they inhibited these neurons and saw the opposite effects: it drove blood sugar down, elevated insulin levels and suppressed the animals' urge to consume their chow. That the brain influences hunger is not an unexpected finding, but scientists have recently narrowed in on how it has sway on what ends up in the gut—and how the gut talks to the mind. This two-way communication, defined as the 'gut–brain axis', happens not only through nerve connections between the organs, but also through biochemical signals, such as hormones, that circulate in the body. “The idea that there is bidirectional communication between the gastrointestinal tract and brain that affects metabolism traces back more than a century,” Friedman says, referring to the work of the nineteenth-century French scientist Claude Bernard, who made seminal discoveries into how the body maintains physiological equilibrium. “Our new findings that insulin-producing cells in the pancreas can be controlled by certain neurons in the brain that sense blood sugar provides further experimental evidence supporting this notion.” © 2016 Scientific American,
Link ID: 22522 - Posted: 08.06.2016
Tina Hesman Saey Alcoholism may stem from using genes incorrectly, a study of hard-drinking rats suggests. Rats bred either to drink heavily or to shun alcohol have revealed 930 genes linked to a preference for drinking alcohol, researchers in Indiana report August 4 in PLOS Genetics. Human genetic studies have not found most of the genetic variants that put people at risk for alcoholism, says Michael Miles, a neurogenomicist at Virginia Commonwealth University in Richmond. The new study takes a “significant and somewhat novel approach” to find the genetic differences that separate those who will become addicted to alcohol from those who drink in moderation. It took decades to craft the experiment, says study coauthor William Muir, a population geneticist at Purdue University in West Lafayette, Ind. Starting in the 1980s, rats bred at Indiana University School of Medicine in Indianapolis were given a choice to drink pure water or water mixed with 10 percent ethanol, about the same amount of alcohol as in a weak wine. For more than 40 generations, researchers selected rats from each generation that voluntarily drank the most alcohol and bred them to create a line of rats that consume the rat equivalent of 25 cans of beer a day. Simultaneously, the researchers also selected rats that drank the least alcohol and bred them to make a line of low-drinking rats. A concurrent breeding program produced another line of high-drinking and teetotaling rats. For the new study, Muir and colleagues collected DNA from 10 rats from each of the high- and low-drinking lines. Comparing complete sets of genetic instructions from all the rats identified 930 genes that differ between the two lines. |© Society for Science & the Public 2000 - 2016.
By Nicholas Bakalar A drug used to treat rheumatoid arthritis may have benefits against Alzheimer’s disease, researchers report. Rheumatoid arthritis is an autoimmune disease believed to be driven in part by tumor necrosis factor, or T.N.F., a protein that promotes inflammation. Drugs that block T.N.F., including an injectable drug called etanercept, have been used to treat rheumatoid arthritis for many years. T.N.F. is also elevated in the cerebrospinal fluid of Alzheimer’s patients. Researchers identified 41,109 men and women with a diagnosis of rheumatoid arthritis and 325 with both rheumatoid arthritis and Alzheimer’s disease. In people over 65, the prevalence of Alzheimer’s disease was more than twice as high in people with rheumatoid arthritis as in those without it. The study is in CNS Drugs. But unlike patients treated with five other rheumatoid arthritis drugs, those who had been treated with etanercept showed a significantly reduced risk for Alzheimer’s disease. Still, the lead author, Dr. Richard C. Chou, an assistant professor of medicine at Dartmouth, said that it is too early to think of using etanercept as a treatment for Alzheimer’s. “We’ve identified a process in the brain, and if you can control this process with etanercept, you may be able to control Alzheimer’s,” he said. “But we need clinical trials to prove and confirm it.” © 2016 The New York Times Company
Link ID: 22520 - Posted: 08.06.2016
By LUKE DITTRICH ‘Can you tell me who the president of the United States is at the moment?” A man and a woman sat in an office in the Clinical Research Center at the Massachusetts Institute of Technology. It was 1986, and the man, Henry Molaison, was about to turn 60. He was wearing sweatpants and a checkered shirt and had thick glasses and thick hair. He pondered the question for a moment. “No,” he said. “I can’t.” The woman, Jenni Ogden, was a visiting postdoctoral research fellow from the University of Auckland, in New Zealand. One of the greatest thrills of her time at M.I.T. was the chance to have sit-down sessions with Henry. In her field — neuropsychology — he was a legendary figure, something between a rock star and a saint. “Who’s the last president you remember?” “I don’t. ... ” He paused for a second, mulling over the question. He had a soft, tentative voice, a warm New England accent. “Ike,” he said finally. Dwight D. Eisenhower’s inauguration took place in 1953. Our world had spun around the sun more than 30 times since, though Henry’s world had stayed still, frozen in orbit. This is because 1953 was the year he received an experimental operation, one that destroyed most of several deep-seated structures in his brain, including his hippocampus, his amygdala and his entorhinal cortex. The operation, performed on both sides of his brain and intended to treat Henry’s epilepsy, rendered him profoundly amnesiac, unable to hold on to the present moment for more than 30 seconds or so. That outcome, devastating to Henry, was a boon to science: By 1986, Patient H.M. — as he was called in countless journal articles and textbooks — had become arguably the most important human research subject of all time, revolutionizing our understanding of how memory works. © 2016 The New York Times Company
Keyword: Learning & Memory
Link ID: 22519 - Posted: 08.04.2016
By Jonathan Webb Science reporter, BBC News Scientists have glimpsed activity deep in the mouse brain which can explain why we get thirsty when we eat, and why cold water is more thirst-quenching. A specific "thirst circuit" was rapidly activated by food and quietened by cooling down the animals' mouths. The same brain cells were already known to stimulate drinking, for example when dehydration concentrates the blood. But the new findings describe a much faster response, which predicts the body's future demand for water. The researchers went looking for this type of system because they were puzzled by the fact that drinking behaviour, in humans as well as animals, seems to be regulated very quickly. "There's this textbook model for homeostatic regulation of thirst, that's been around for almost 100 years, that's based on the blood," said the study's senior author Zachary Knight, from the University of California, San Francisco. "There are these neurons in the brain that… generate thirst when the blood becomes too salty or the blood volume falls too low. But lots of aspects of everyday drinking can't possibly be explained by that homeostatic model because they occur much too quickly." Take the "prandial thirst" that comes while we consume a big, salty meal - or the fact that we feel quenched almost as soon as we take a drink. © 2016 BBC.
Link ID: 22518 - Posted: 08.04.2016
By Alice Klein Rise and shine! Neuronal switches have been discovered that can suddenly rouse flies from slumber – or send them into a doze. There are several parallels between sleep in flies and mammals, making fruit flies a good choice for investigating how we sleep. One way to do this is to use optogenetics to activate specific neurons to see what they do. This works by using light to turn on cells genetically modified to respond to certain wavelengths. Gero Miesenböck at the University of Oxford and his team have discovered how to wake flies up. Using light as the trigger the team stimulated neurons that release a molecule called dopamine. The dopamine then switched off sleep-promoting neurons in what’s called the dorsal fan-shaped body, waking the flies. Meanwhile, Fang Guo at Brandeis University in Waltham, Massachusetts, and his team have found that activating neurons that form part of a fly’s internal clock will send it to sleep. When stimulated, these neurons released glutamate, which turned off activity-promoting neurons in the master pacemaker area of the brain. While human and fly brains are obviously very different in structure, being asleep or awake are similar states regardless of the kind of brain an animal has, says Bruno van Swinderen at the University of Queensland, Australia. © Copyright Reed Business Information Ltd.
By Sarah Kaplan Sleep just doesn't make sense. "Think about it," said Gero Miesenböck, a neuroscientist at the University of Oxford. "We do it. Every animal with a brain does it. But obviously it has considerable risks." Sleeping animals are incredibly vulnerable to attacks, with no obvious benefit to make up for it — at best, they waste precious hours that could be used finding food or seducing a mate; at worst, they could get eaten. "If evolution had managed to invent an animal that doesn’t need to sleep ... the selective advantage for it would be immense," Miesenböck said. "The fact that no such animal exists indicates that sleep is really vital, but we don't know why." But Miesenböck is part of team of sleep researchers who believe they are inching closer to to an answer. In a paper published in the journal Nature on Wednesday, they describe a cluster of two dozen brain cells in fruit flies that operate as a homeostatic sleep switch, turning on when the body needs rest and off again when it's time to wake up. "It's like a thermostat," Miesenböck said of the switch, "But instead of responding to temperature it responds to something else." If he and his colleagues could find out what that "something" is, "we might have the answer to the mystery of sleep."
By Megan Scudellari In late 2013, psychologist Raphael Bernier welcomed a 12-year-old girl and her parents into his office at the University of Washington (UW) in Seattle. The girl had been diagnosed with autism spectrum disorder, and Bernier had invited the family in to discuss the results of a genetic analysis his collaborator, geneticist Evan Eichler, had performed in search of the cause. As they chatted, Bernier noticed the girl’s wide-set eyes, which had a slight downward slant. Her head was unusually large, featuring a prominent forehead. The mother described how her daughter had gastrointestinal issues and sometimes wouldn’t sleep for two to three days at a time. The girl’s presentation was interesting, Bernier recalls, but he didn’t think too much of it—until a week later, when he met an eight-year-old boy with similarly wide-set eyes and a large head. Bernier did a double take. The “kiddos,” as he calls children who come to see him, could have been siblings. According to the boy’s parents, he also suffered from gastrointestinal and sleep problems. The similarities between the unrelated children were remarkable, especially for a disorder so notoriously complex that it has been said, “If you’ve met one child with autism, you’ve met one child with autism.” But Bernier knew that the patients shared another similarity that might explain the apparent coincidence: both harbored a mutation in a gene known as chromodomain helicase DNA binding protein 8 (CHD8). © 1986-2016 The Scientist
By JoAnna Klein I expected a bumpy ride on a whitewater trip, so when I fell off my raft and coughed up the water I’d inhaled, I wasn’t afraid. But at the time I didn’t know I was swimming with a deadly parasite. I’d been at a bachelorette party at the U.S. National Whitewater Center in Charlotte, N.C., but after returning home I learned that I had shared the churning rapids with Naegleria fowleri, a single-celled amoeba found mostly in soil and warm freshwater lakes, rivers and hot springs. An Ohio teenager had contracted the amoeba infection after visiting the center around the same time I did, and some of the waters and sediment at and around the center had tested positive for the bug. News that my friends and I had all been at risk of exposure triggered a few days of worry. The illness is rare and, if infected, symptoms show up between one and 10 days after exposure. Chances were that we were fine (we were), but the experience prompted me to learn more about the parasite. Naegleria fowleri lives in fresh water, but not in salt water. If forced up the nose, it can enter the brain and feed on its tissue, resulting in an infection known as primary amebic meningoencephalitis. Death occurs in nearly all of those infected with the parasite, usually within five days after infection. The 18-year-old Ohio woman who died most likely contracted the parasite when she sucked water through her nose after falling from a raft during a church trip. Samples from a channel at the rafting center, collected by the Centers for Disease Control and Prevention, tested positive for the bug. The center’s channels are man-made, and it gets its water from the Charlotte-Mecklenburg Utilities Department and two wells on its property. The center has announced that it disinfects all water with ultraviolet radiation and chlorine, and it added more after the water tests. © 2016 The New York Times Company
Link ID: 22514 - Posted: 08.04.2016
By Anna Vlasits A small corner of the neuroscience world was in a frenzy. It was mid-June and a scientific paper had just been published claiming that years worth of results were riddled with errors. The study had dug into the software used to analyze one kind of brain scan, called functional MRI. The software’s approach was wrong, the researchers wrote, calling into doubt “the validity of some 40,000 fMRI studies”—in other words, all of them. The reaction was swift. Twitter lit up with panicked neuroscientists. Bloggers and reporters rained down headlines citing “seriously flawed” “glitches” and “bugs.” Other scientists thundered out essays defending their studies. Finally, one of the authors of the paper, published in Proceedings of the National Academy of Sciences, stepped into the fray. In a blog post, Thomas Nichols wrote, “There is one number I regret: 40,000.” Their finding, Nichols went on to write, only affects a portion of all fMRI papers—or, some scientists think, possibly none at all. It wasn’t nearly as bad as the hype suggested. The brief kerfuffle could just be dismissed as a tempest in a teapot, science’s self-correcting mechanisms in action. But the study, and its response, heralds a new level of self-scrutiny for fMRI studies, which have been plagued for decades by accusations of shoddy science and pop-culture pandering. fMRI, in other words, is growing up, but not without some pains along the way. A bumpy start for brain scanning © 2016 Scientific American,
Keyword: Brain imaging
Link ID: 22513 - Posted: 08.04.2016
The brains of overweight middle-aged people resemble brains that are a decade older in healthier people. A study of 473 adults has found that people who are overweight have less white matter, which connects different brain areas and enables signaling between them. The volume of white matter in the brains of overweight people at 50 were similar to that seen in the brains of lean people at 60. Human brains naturally shrink with age, but previous research has shown that this seems to happen more quickly in obese people. “As our brains age, they naturally shrink in size, but it isn’t clear why people who are overweight have a greater reduction in the amount of white matter,” says Lisa Ronan, at the University of Cambridge, a member of the research team. “We can only speculate on whether obesity might in some way cause these changes or whether obesity is a consequence of brain changes.” Intriguingly, the difference between lean and overweight people’s brains was only apparent from middle age onwards. It’s possible that this is because we are particularly vulnerable in some way at this time, says team-member Paul Fletcher, also at the University of Cambridge. However, despite this reduction in white matter, cognitive tests did not find any evidence that being overweight was linked to reduced brain function. “We don’t yet know the implications of these changes in brain structure,” says Sadaf Farooqi, at the University of Cambridge, who was also involved in the research. © Copyright Reed Business Information Ltd.
Link ID: 22512 - Posted: 08.04.2016
by Helen Thompson Pinky and The Brain's smarts might not be so far-fetched. Some mice are quicker on the uptake than others. While it might not lead to world domination, wits have their upside: a better shot at staying alive. Biologists Audrey Maille and Carsten Schradin of the University of Strasbourg in France tested reaction time and spatial memory in 90 African striped mice (Rhabdomys pumilio) over the course of a summer. For this particular wild rodent, surviving harsh summer droughts means making it to mating season in the early fall. The team saw some overall trends: Females were more likely to survive if they had quick reflexes, and males were more likely to survive if they had good spatial memory. Cognitive traits like reacting quickly and remembering the best places to hide are key to eluding predators during these tough times but may come with trade-offs for males and females. The results show that an individual mouse’s cognitive strengths are linked to its survival odds, suggesting that the pressure to survive can shape basic cognition, Maille and Schradin write August 3 in Biology Letters. |© Society for Science & the Public 2000 - 2016
Meghan Rosen Exercise may not erase old memories, as some studies in animals have previously suggested. Running on an exercise wheel doesn’t make rats forgetprevious trips through an underwater maze, Ashok Shetty and colleagues report August 2 in the Journal of Neuroscience. Exercise or not, four weeks after learning how to find a hidden platform, rats seem to remember the location just fine, the team found. The results conflict with two earlier papers that show that running triggers memory loss in some rodents by boosting the birth of new brain cells. Making new brain cells rejiggers memory circuits, and that can make it hard for animals to remember what they’ve learned, says Paul Frankland, a neuroscientist at the Hospital for Sick Children in Toronto. He has reported this phenomenon in mice, guinea pigs and degus (SN: 6/14/14, p. 7). Maybe rats are the exception, he says, “but I’m not convinced.” In 2014, Frankland and colleagues reported that brain cell genesis clears out fearful memories in three different kinds of rodents. Two years later, Frankland’s team found similar results with spatial memories. After exercising, mice had trouble remembering the location of a hidden platform in a water maze, the team reported in February in Nature Communications. Again, Frankland and colleagues pinned the memory wipeout on brain cell creation — like a chalkboard eraser that brushes away old information. The wipe seemed to clear the way for new memories to form. Shetty, a neuroscientist at Texas A&M Health Science Center in Temple, wondered if the results held true in rats, too. “Rats are quite different from mice,” he says. “Their biology is similar to humans.” |© Society for Science & the Public 2000 - 2016. All rights reserved.
Keyword: Learning & Memory
Link ID: 22510 - Posted: 08.03.2016
By Alice Klein The debate has finally been put to bed. Wearable brainwave recorders confirm that birds do indeed sleep while flying, but only for brief periods and usually with one half of their brain. We know several bird species can travel vast distances non-stop, prompting speculation that they must nap mid-flight. Great frigatebirds, for example, can fly continuously for up to two months. On the other hand, the male sandpiper, for one, can largely forgo sleep during the breeding season, hinting that it may also be possible for birds to stay awake during prolonged trips. To settle this question, Niels Rattenborg at the Max Planck Institute for Ornithology in Seewiesen, Germany, and his colleagues fitted small brain activity monitors and movement trackers to 14 great frigatebirds. During long flights, the birds slept for an average of 41 minutes per day, in short episodes of about 12 seconds each. By contrast, they slept for more than 12 hours per day on land. Frigatebirds in flight tend to use one hemisphere at a time to sleep, as do ducks and dolphins, but sometimes they used both. “Some people thought that all their sleep would have to be unihemispheric otherwise they would drop from the sky,” says Rattenborg. “But that’s not the case – they can sleep with both hemispheres and they just continue soaring.” Sleep typically took place as the birds were circling in rising air currents, when they did not need to flap their wings. © Copyright Reed Business Information Ltd.
By Libby Copeland Don’t get him wrong: Dean Burnett loves the brain as much as the next neuroscientist. But if he’s being honest, it’s “really quite rubbish in a lot of ways,” he says. In his new book, Idiot Brain, Burnett aims to take our most prized organ down a peg or two. Burnett is most fascinated by the brain’s tendency to trip us up when it’s just trying to help. His book explores many of these quirks: How we edit our own memories to make ourselves look better without knowing it; how anger persuades us we can take on a bully twice our size; and what may cause us to feel like we’re falling and jerk awake just as we’re falling asleep. (It could have something to do with our ancestors sleeping in trees.) We caught up with Burnett, who is also a science blogger for The Guardian and a stand-up comic, to ask him some of our everyday questions and frustrations with neuroscience. Why is it that we get motion sickness when we’re traveling in a plane or a car? We haven’t evolved, obviously, to ride in vehicles; that’s a very new thing in evolutionary terms. So the main theory as to why we get motion sickness is that it’s essentially a conflict in the senses that are being relayed to the subcortical part of the brain where the senses are integrated together. The body and the muscles are saying we are still. Your eyes are saying the environment is still. The balance sense in the ears are detecting movement. The brain is getting conflicting messages from the fundamental senses, and in evolutionary terms there’s only one thing that can cause that, which is a neurotoxin. And as a result the brain thinks it’s been poisoned and what do you do when you’ve been poisoned? Throw up.
Link ID: 22508 - Posted: 08.03.2016
By James Gallagher Controlling human nerve cells with electricity could treat a range of diseases including arthritis, asthma and diabetes, a new company says. Galvani Bioelectronics hopes to bring a new treatment based on the technique before regulators within seven years. GlaxoSmithKline and Verily, formerly Google, Life Sciences, are behind it. Animal experiments have attached tiny silicone cuffs, containing electrodes, around a nerve and then used a power supply to control the nerve's messages. One set of tests suggested the approach could help treat type-2 diabetes, in which the body ignores the hormone insulin. They focused on a cluster of chemical sensors near the main artery in the neck that check levels of sugar and the hormone insulin. The sensors send their findings back to the brain, via a nerve, so the organ can coordinate the body's response to sugar in the bloodstream. GSK vice-president of bioelectronics Kris Famm told the BBC News website: "The neural signatures in the nerve increase in type 2-diabetes. "By blocking those neural signals in diabetic rats, you see the sensitivity of the body to insulin is restored." And early work suggested it could work in other diseases too. "It isn't just a one-trick-pony, it is something that if we get it right could have a new class of therapies on our hands," Mr Famm said. But he said the field was only "scratching the surface" when it came to understanding which nerve signals have what effect in the body. Both the volume and rhythm of the nerve signals could be having an effect rather than it being a simple case of turning the nerve on or off. © 2016 BBC
Link ID: 22507 - Posted: 08.03.2016
By Colby Itkowitz On any given day people face any number of minor annoyances such as being stuck in traffic or spilling coffee on their shirts or forgetting their keys. Then there’s the persistent stressors that come from work, relationships and finances. And there’s the uncontrollable anxieties of global terrorism, mass shootings and Zika-carrying mosquitoes. But why are some people able to deal with it all so calmly, while others freak out? A team of researchers at Yale University may have found the answer in the brain. The scientists studied the brains of 30 adult volunteers with no history of mental or physical health issues as they watched a slideshow of gruesome and terrifying images for six minutes. To compare brain activity, they then showed the participants benign images that would evoke little emotion, such as a photo of a chair. They located three areas of the brain that responded to the stress of seeing photos of people mutilated or at gunpoint or in other harrowing scenarios. But what the researchers found most interesting was how the ventromedial prefrontal cortex (vmPFC), which processes risk and emotional response, adapted while viewing the photos. In everyone, activity in that region decreased initially in response to the images, as though their guard was down, but then in some people, it became hyperactive, as if working overtime to control the emotional response, or in other words, to cope. “We have not had a way of breaking that apart to see what the brain is doing,” said Rajita Sinha, director of the Yale Stress Center and lead author of the study. “How do we cope in the moment? Here, we said, in the moment under acute threat how does the brain cope and regain control?” © 1996-2016 The Washington Post
Link ID: 22506 - Posted: 08.03.2016
Nisha Gaind Most people in the United States are more worried than enthusiastic about the prospect of scientific advances such as gene editing and brain-chip implants, a survey of thousands suggests. The Pew Research Center in Washington DC asked 4,726 US people about the potential uses of three biomedical technologies that it classified as ‘potential human enhancement’: gene editing to reduce disease risk in babies; brain implants to enhance concentration and brain processes, and transfusions of synthetic blood to improve strength and stamina. (None of these procedures are a reality, but the underlying technologies are being researched.) Those who took the survey were overwhelmingly wary about all of the ideas. In each case, more than 60% said that they would be worried about the technologies, and fewer than half expressed enthusiasm about them — with the prospect of brain implants prompting the most concern and least excitement. More than 70% thought that the procedures would become available before they were well understood or officially deemed safe. Around one-third thought the technologies were morally unacceptable, and about 70% were concerned that such enhancements would widen social divides — for instance, because initially only wealthy people would be able to afford them. © 2016 Macmillan Publishers Limited
Link ID: 22505 - Posted: 08.02.2016
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
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.