Chapter 15. Emotions, Aggression, and Stress
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By Anil Ananthaswamy and Alice Klein Our brain’s defence against invading microbes could cause Alzheimer’s disease – which suggests that vaccination could prevent the condition. Alzheimer’s disease has long been linked to the accumulation of sticky plaques of beta-amyloid proteins in the brain, but the function of plaques has remained unclear. “Does it play a role in the brain, or is it just garbage that accumulates,” asks Rudolph Tanzi of Harvard Medical School. Now he has shown that these plaques could be defences for trapping invading pathogens. Working with Robert Moir at the Massachusetts General Hospital in Boston, Tanzi’s team has shown that beta-amyloid can act as an anti-microbial compound, and may form part of our immune system. .. To test whether beta-amyloid defends us against microbes that manage to get into the brain, the team injected bacteria into the brains of mice that had been bred to develop plaques like humans do. Plaques formed straight away. “When you look in the plaques, each one had a single bacterium in it,” says Tanzi. “A single bacterium can induce an entire plaque overnight.” Double-edged sword This suggests that infections could be triggering the formation of plaques. These sticky plaques may trap and kill bacteria, viruses or other pathogens, but if they aren’t cleared away fast enough, they may lead to inflammation and tangles of another protein, called tau, causing neurons to die and the progression towards © Copyright Reed Business Information Ltd.
By Jordana Cepelewicz General consensus among Alzheimer’s researchers has it that the disease’s main culprit, a protein called amyloid beta, is an unfortunate waste product that is not known to play any useful role in the body—and one that can have devastating consequences. When not properly cleared from the brain it builds up into plaques that destroy synapses, the junctions between nerve cells, resulting in cognitive decline and memory loss. The protein has thus become a major drug target in the search for a cure to Alzheimer’s. Now a team of researchers at Harvard Medical School and Massachusetts General Hospital are proposing a very different story. In a study published this week in Science Translational Medicine, neurologists Rudolph Tanzi and Robert Moir report evidence that amyloid beta serves a crucial purpose: protecting the brain from invading microbes. “The original idea goes back to 2010 or so when Rob had a few too many Coronas,” Tanzi jokes. Moir had come across surprising similarities between amyloid beta and LL37, a protein that acts as a foot soldier in the brain’s innate immune system, killing potentially harmful bugs and alerting other cells to their presence. “These types of proteins, although small, are very sophisticated in what they do,” Moir says. “And they’re very ancient, going back to the dawn of multicellular life.” © 2016 Scientific American,
By GINA KOLATA Could it be that Alzheimer’s disease stems from the toxic remnants of the brain’s attempt to fight off infection? Provocative new research by a team of investigators at Harvard leads to this startling hypothesis, which could explain the origins of plaque, the mysterious hard little balls that pockmark the brains of people with Alzheimer’s. It is still early days, but Alzheimer’s experts not associated with the work are captivated by the idea that infections, including ones that are too mild to elicit symptoms, may produce a fierce reaction that leaves debris in the brain, causing Alzheimer’s. The idea is surprising, but it makes sense, and the Harvard group’s data, published Wednesday in the journal Science Translational Medicine, supports it. If it holds up, the hypothesis has major implications for preventing and treating this degenerative brain disease. The Harvard researchers report a scenario seemingly out of science fiction. A virus, fungus or bacterium gets into the brain, passing through a membrane — the blood-brain barrier — that becomes leaky as people age. The brain’s defense system rushes in to stop the invader by making a sticky cage out of proteins, called beta amyloid. The microbe, like a fly in a spider web, becomes trapped in the cage and dies. What is left behind is the cage — a plaque that is the hallmark of Alzheimer’s. So far, the group has confirmed this hypothesis in neurons growing in petri dishes as well as in yeast, roundworms, fruit flies and mice. There is much more work to be done to determine if a similar sequence happens in humans, but plans — and funding — are in place to start those studies, involving a multicenter project that will examine human brains. “It’s interesting and provocative,” said Dr. Michael W. Weiner, a radiology professor at the University of California, San Francisco, and a principal investigator of the Alzheimer’s Disease Neuroimaging Initiative, a large national effort to track the progression of the disease and look for biomarkers like blood proteins and brain imaging to signal the disease’s presence. © 2016 The New York Times Company
Ronald Crystal The goal of antiaddiction vaccines is to prevent addictive molecules from reaching the brain, where they produce their effects and can create chemical dependencies. Vaccines can accomplish this task, in theory, by generating antibodies—proteins produced by the immune system—that bind to addictive particles and essentially stop them in their tracks. But challenges remain. Among them, addictive molecules are often too small to be spotted by the human immune system. Thus, they can circulate in the body undetected. Researchers have developed two basic strategies for overcoming this problem. One invokes so-called active immunity by tethering an addictive molecule to a larger molecule, such as the proteins that encase a common cold virus. This viral shell does not make people sick but does prompt the immune system to produce high levels of antibodies against it and whatever is attached to it. In our laboratory, we have tested this method in animal models and successfully blocked chemical forms of cocaine or nicotine from reaching the brain. Another approach researchers are testing generates what is known as passive immunity against addictive molecules in the body. They have cultured monoclonal antibodies that can bind selectively to addictive molecules. The hurdle with this particular method is that monoclonal antibodies are expensive to produce and need to be administrated frequently to be effective. © 2016 Scientific American
By Andy Coghlan It’s a tear-jerker worthy of Hollywood – and one of the first examples of compassionate care and grief in a wild monkey. The alpha male of a group of snub-nosed monkeys and his dying partner spent a final, tender hour together beneath the tree from which she had fallen minutes earlier, cracking her head on a rock. Before she succumbed, he gently touched and groomed her. And after she was dead he remained by her side for 5 minutes, touching her and pulling gently at her hand, as if to try and revive her (for a full account of what happened, see “A monkey tends to his dying mate – as it unfolded”, below). “The case we’ve reported is particularly important because of the exclusively gentle nature of the interactions, and the special treatment of the dying female shown by the adult male,” says James Anderson of Kyoto University, Japan. “The events suggest that in the case of strongly bonded individuals at least, monkeys may show compassionate behaviour to ailing or dying individuals.” Together, the reports add to evidence that humans may not be the only species to display grieving behaviour following bereavement, or to show respect for dead individuals with whom they have forged ties. They also hint that animals have some recognition of the finality of death. “It seems likely that in long-lived species such as many primates, repeated exposure to death within the group leads to an understanding of the irreversibility of death,” says Anderson. “I believe the adult male and other members of his unit understood the dead female was no longer alive.” © Copyright Reed Business Information Ltd.
By Diana Kwon A number of factors, including elements of the social environment (such as inequality and isolation) and physical stressors (such as pollution and noise) could explain how the city erodes well-being Credit: Thomas Koehler/Getty Images Life in the city can be taxing. City dwellers often face higher rates of crime, pollution, social isolation and other environmental stressors than those living in rural areas. For years studies have consistently linked the risk of developing schizophrenia to urban environments—but researchers are only beginning to understand why this association exists. Addressing the link is increasingly urgent: According to a recent U.N. report, the proportion of people living in cities will rise from 54 percent of the world’s population in 2014 to 66 percent by 2050. Researchers first suggested in the 1930s that urban living might increase schizophrenia risk. Since then many large epidemiological studies have reported an association between the two, primarily in European countries such as Sweden and Denmark. Converging evidence has revealed that growing up in the city doubles the risk of developing psychosis later in life. Studies have also begun to find that urban environments may heighten the risk of other mental health issues such as depression and anxiety. A number of factors, including elements of the social environment (such as inequality and isolation) and physical stressors (such as pollution and noise) could explain how the city erodes well-being. Conversely, people predisposed to mental illness may simply be more likely to move into urban environments. Two studies published this month shed new light on these effects and suggest both scenarios could be involved. © 2016 Scientific American, a Division
By Karen Weintraub There are case reports of people with no previously known risks having a heart attack after a nightmare, though they appear to be quite rare. No studies have been done to determine just how rare nightmare-induced heart attacks might be, and experts do not know whether they may result from the pulse-racing effects of the frightening dream itself. Nightmares are more commonly seen in the rapid eye movement, or REM, phase of sleep, which gets longer as the night progresses. Therefore, nightmares are more likely to occur in the early morning hours. Heart attacks, too, are most common in the early morning hours, when internal body clocks start secreting stress hormones and blood pressure tends to rise, said Dr. Mary Ann McLaughlin, a cardiologist at the Icahn School of Medicine at Mount Sinai in New York. If someone is at risk for a heart attack — because of high blood pressure, diabetes, sleep apnea, smoking or other factors — that attack is more likely to occur in the early morning. But “it’s rare for an otherwise healthy person to have a nightmare that causes a heart attack,” said Dr. McLaughlin. Nightmares can be triggered by alcohol, lack of sleep and medications, including some antidepressants and blood pressure medications, she said. Anxiety and depression have also been linked to increased risk of nightmares. On the flip side, patients with heart disease often have sleep apnea, a form of disordered breathing that can lead to fragmented sleep, and potentially more nightmares, said Dr. Neomi Shah, a sleep specialist, also at Mount Sinai. One 2013 study found that apnea patients with regular nightmares woke up more often than those who didn’t. Nightmares disappeared in more than 90 percent of the patients who used a continuous positive airway pressure, or CPAP, machine to treat their apnea. © 2016 The New York Times Company
Link ID: 22232 - Posted: 05.21.2016
Rae Ellen Bichell For Tim Goliver and Luther Glenn, the worst illness of their lives started in the same way — probably after having a stomach bug. Tim was 21 and a college student at the University of Michigan. He was majoring in English and biology and active in the Lutheran church. "I was a literature geek," says Tim. "I was really looking forward to my senior year and wherever life would take me." Luther was in his 50s. He'd spent most of his career as a U.S. military policeman and was working in security in Washington, D.C. He'd recently separated from his wife and had just moved into a new house with his two daughters, who were in their 20s. Both men recovered from their stomach bugs, but a few days later they started to feel sluggish. "Here we are trying to unpack, prepare ourselves for new life together and I'm flat out, dead tired," says Luther. He fell asleep in the car one morning and never made it out of the garage. Then he fell in the bathroom. For Tim, it started to feel like running a marathon just to lift a spoonful of soup. One morning, he tried to comb his hair and realized he couldn't lift his arm above his shoulder. "At that moment I started to freak out," he says. Both men got so weak that their families had to wheel them into the emergency room in wheelchairs. They got the same diagnosis: Guillain-Barre syndrome, a neurological disorder which can leave people paralyzed for weeks. © 2016 npr
By Geraldine Dawson There’s a popular saying in the autism community: “If you’ve met one person with autism, you’ve met one person with autism.” Although this phrase is meant to convey the remarkable variation in abilities and disabilities among people with autism spectrum disorder (ASD), we’re learning that it also applies to the extraordinary variability in how ASD develops. When I first began doing research on autism decades ago, we thought of it as one condition and aimed to discover its “cause.” Now we know ASD is actually a group of lifelong conditions that can arise from a complex combination of multiple genetic and environmental factors. In the same way that each person with ASD has a unique personality and profile of talents and disabilities, each also has a distinct developmental history shaped by a specific combination of genetic and environmental factors. More evidence of this extraordinary variety will be presented this week in Baltimore, where nearly 2,000 of the world’s leading autism researchers will gather for the International Meeting for Autism Research (IMFAR). As president of the International Society for Autism Research, which sponsors the conference, I am more impressed than ever with the progress we are making. New findings being presented at the conference will highlight the importance of the prenatal period in understanding how various environmental factors such as exposure to alcohol, smoking and certain chemical compounds can increase risk for ASD. The impact of many environmental factors depends, however, on an individual’s genetic background and the timing of the exposure. Other research links inflammation—detected in blood spot tests taken at birth—with a higher likelihood of an ASD diagnosis later on. Researchers suggest that certain factors such as maternal infection and other factors during pregnancy may influence an infant’s immune system and contribute to risk. As our knowledge of these risk factors grows, so do the opportunities for promoting healthy pregnancies and better outcomes. © 2016 Scientific American
By Marta Zaraska Scientists and laypeople alike have historically attributed political beliefs to upbringing and surroundings, yet recent research shows that our political inclinations have a large genetic component. The largest recent study of political beliefs, published in 2014 in Behavior Genetics, looked at a sample of more than 12,000 twin pairs from five countries, including the U.S. Some were identical and some fraternal; all were raised together. The study reveals that the development of political attitudes depends, on average, about 60 percent on the environment in which we grow up and live and 40 percent on our genes. “We inherit some part of how we process information, how we see the world and how we perceive threats—and these are expressed in a modern society as political attitudes,” explains Peter Hatemi, who is a genetic epidemiologist at the University of Sydney and lead author of the study. The genes involved in such complex traits are difficult to pinpoint because they tend to be involved in a huge number of bodily and cognitive processes that each play a minuscule role in shaping our political attitudes. Yet a study published in 2015 in the Proceedings of the Royal Society B managed to do just that, showing that genes encoding certain receptors for the neurotransmitter dopamine are associated with where we fall on the liberal-conservative axis. Among women who were highly liberal, 62 percent were carriers of certain receptor genotypes that have previously been associated with such traits as extroversion and novelty seeking. Meanwhile, among highly conservative women, the proportion was only 37.5 percent. © 2016 Scientific American
By Jessica Lahey Before she became a neuroscientist, Mary Helen Immordino-Yang was a seventh-grade science teacher at a school outside Boston. One year, during a period of significant racial and ethnic tension at the school, she struggled to engage her students in a unit on human evolution. After days of apathy and outright resistance to Ms. Immordino-Yang’s teaching, a student finally asked the question that altered her teaching — and her career path — forever: “Why are early hominids always shown with dark skin?” With that question, one that connected the abstract concepts of human evolution and the very concrete, personal experiences of racial tension in the school, her students’ resistance gave way to interest. As she explained the connection between the effects of equatorial sunlight, melanin and skin color and went on to explain how evolutionary change and geography result in various human characteristics, interest blossomed into engagement, and something magical happened: Her students began to learn. Dr. Immordino-Yang’s eyes light up as she recounts this story in her office at the Brain and Creativity Institute at the University of Southern California. Now an associate professor of education, psychology and neuroscience, she understands the reason behind her students’ shift from apathy to engagement and, finally, to deep, meaningful learning. Her students learned because they became emotionally engaged in material that had personal relevance to them. Emotion is essential to learning, Dr. Immordino-Yang said, and should not be underestimated or misunderstood as a trend, or as merely the “E” in “SEL,” or social-emotional learning. Emotion is where learning begins, or, as is often the case, where it ends. Put simply, “It is literally neurobiologically impossible to think deeply about things that you don’t care about,” she said. © 2016 The New York Times Company
By Sarah Kaplan Scientists have known for a while that stereotypes warp our perceptions of things. Implicit biases — those unconscious assumptions that worm their way into our brains, without our full awareness and sometimes against our better judgment — can influence grading choices from teachers, split-second decisions by police officers and outcomes in online dating. We can't even see the world without filtering it through the lens of our assumptions, scientists say. In a study published Monday in the journal Nature Neuroscience, psychologists report that the neurons that respond to things such as sex, race and emotion are linked by stereotypes, distorting the way we perceive people's faces before that visual information even reaches our conscious brains. "The moment we actually glimpse another person ... [stereotypes] are biasing that processing in a way that conforms to our already existing expectations," said Jonathan Freeman, a psychology professor at New York University and one of the authors of the report. Responsibility lies in two far-flung regions of the brain: the orbital frontal cortex, which rests just above the eyes and is responsible for rapid visual predictions and categorizations, and the fusiform cortex, which sits in the back of the brain and is involved in recognizing faces. When Freeman and his co-author, Ryan Stolier, had 43 participants look at images of faces in a brain scanner, they noticed that neurons seemed to be firing in similar patterns in both parts of the brain, suggesting that information from each part was influencing the other.
Nicola Davis People with a larger circle of friends are better able to tolerate pain, according to research into the pain thresholds and social networks of volunteers. The link is thought to be down a system in the brain that involves endorphins: potent pain-killing chemicals produced by the body that also trigger a sense of wellbeing. “At an equivalent dose, endorphins have been shown to be stronger than morphine,” said Katerina Johnson, a doctoral student at the University of Oxford, who co-authored the research. Writing in the journal Scientific Reports, Johnson and Robin Dunbar, professor of evolutionary psychology at the University of Oxford, sought to probe the theory that the brain’s endorphin system might have evolved to not only handle our response to physical discomfort, but influence our experience of pleasure from social interactions too. “Social behaviour and being attached to other individuals is really important for our survival - whether that is staying close to our parents, or our offspring or cooperating with others to find food or to help defend ourselves,” said Johnson. To test the link, the authors examined both the social networks and pain thresholds of 101 adults aged between 18 and 34. Each participant was asked to complete a questionnaire, designed to quiz them on friends they contacted once a week and those they got in touch with once a month. The personality of each participant was probed, looking at traits such as “agreeableness”; they were also asked to rate their fitness and stress levels. © 2016 Guardian News and Media Limited
Keyword: Pain & Touch
Link ID: 22156 - Posted: 04.28.2016
People who've recovered from depression stave off relapses with mindfulness therapy as well as with antidepressants, a new review finds. Mindfulness-based cognitive therapy (MBCT) is an eight-week group program that helps people become better observers of their own thoughts and emotions and to learn to distance themselves before ruminations spiral downwards. An international team of psychiatry researchers combined data from nine randomized trials of 1,258 patients total with recurrent depression to compare the mindfulness therapy to placebo, treatment as usual and other active treatments including antidepressants. People suffering from depression who received the mindfulness therapy were 31 per cent less likely to suffer a relapse during the next 60 weeks compared with those who did not receive it, Willem Kuyken of the University of Oxford, in England and his co-authors reported in a meta-analysis review in Wednesday's issue of the journal JAMA Psychiatry. "If you compare MBCT against antidepressant medication it basically holds its own, which means it provides protection on par with what people would get from continuing to take to take medications for one, two or three years after they've recovered from depression," said co-author Dr. Zindel Segal, a professor of psychology at the University of Toronto Scarborough. No one reported side-effects associated with participating in the therapy. ©2016 CBC/Radio-Canada.
by Bethany Brookshire Interviewing for a new job is filled with uncertainty, and that uncertainty fuels stress. There’s the uncertainty associated with preparing for the interview — what questions will they ask me? What should I put in my portfolio? And then there’s the ambiguity when you’re left to stew. Did I get the job? Or did someone else? Scientists have recently shown that these two types of uncertainty — the kind we can prepare for, and the kind we’re just stuck with — are not created equal. The uncertainty we can’t do anything about is more stressful than the one we can. The results help show exactly what in our lives freaks us out — and why. But the findings also show a positive side to the stress we feel when not knowing what’s ahead — the closer our stress levels reflect the real ambiguity in the world, the better we perform in it. “There is a bias in the public perception” against stress, says Claus Lamm, a cognitive neuroscientist at the University of Vienna in Austria. But stress “prepares us to deal with environmental challenges,” he notes, preparing us to fight or flee, and it keeps us paying attention to our surroundings. For decades, scientists have been trying to figure out just what makes us stressed and why. It turns out that unpredictability is a great stressor. Studies in the 1960s and 1970s showed that rats and humans who can’t predict a negative effect (such as a small shock) end up more frazzled than those who can predict when a zap is coming. In a 2006 study, people zapped with unpredictable electric shocks to the hand rated the pain as more unpleasant than when they knew what to expect. © Society for Science & the Public 2000 - 2016.
Link ID: 22151 - Posted: 04.27.2016
By Leonard Sax, M.D., Ph.D Why is it that girls tend to be more anxious than boys? It may start with how they feel about how they look. Some research has shown that in adolescence, girls tend to become more dissatisfied with their bodies, whereas boys tend to become more satisfied with their bodies. Another factor has to do with differences in how girls and boys use social media. A girl is much more likely than a boy to post a photo of herself wearing a swimsuit, while the boy is more likely to post a photo where the emphasis is on something he has done rather than on how he looks. If you don’t like Jake’s selfie showing off his big trophy, he may not care. But if you don’t like Sonya’s photo of herself wearing her bikini, she’s more likely to take it personally. Imagine another girl sitting in her bedroom, alone. She’s scrolling through other girls’ Instagram and Snapchat feeds. She sees Sonya showing off her new bikini; Sonya looks awesome. She sees Madison at a party, having a blast. She sees Vanessa with her adorable new puppy. And she thinks: I’m just sitting here in my bedroom, not doing anything. My life sucks. Boys are at lower risk for the toxic effects of social media than girls are, for at least three reasons. First, boys are less likely to be heavily invested in what you think of their selfies. “Does this swimsuit make me look fat?” is a question asked by girls more often than by boys. Second, boys tend to overestimate how interesting their own life is. Third, the average boy is likely to spend more time playing video games than Photoshopping his selfie for Instagram. And in video games, unlike social media, everybody truly can be a winner, eventually. If you play Grand Theft Auto or Call of Duty long enough, you will, sooner or later, complete all the missions, if you just keep at it. © 2016 The New York Times Company
By SABRINA TAVERNISE WASHINGTON — Suicide in the United States has surged to the highest levels in nearly 30 years, a federal data analysis has found, with increases in every age group except older adults. The rise was particularly steep for women. It was also substantial among middle-aged Americans, sending a signal of deep anguish from a group whose suicide rates had been stable or falling since the 1950s. The suicide rate for middle-aged women, ages 45 to 64, jumped by 63 percent over the period of the study, while it rose by 43 percent for men in that age range, the sharpest increase for males of any age. The overall suicide rate rose by 24 percent from 1999 to 2014, according to the National Center for Health Statistics, which released the study on Friday. The increases were so widespread that they lifted the nation’s suicide rate to 13 per 100,000 people, the highest since 1986. The rate rose by 2 percent a year starting in 2006, double the annual rise in the earlier period of the study. In all, 42,773 people died from suicide in 2014, compared with 29,199 in 1999. From 1999 to 2014, suicide rates in the United States rose among most age groups. Men and women from 45 to 64 had a sharp increase. Rates fell among those age 75 and older. “It’s really stunning to see such a large increase in suicide rates affecting virtually every age group,” said Katherine Hempstead, senior adviser for health care at the Robert Wood Johnson Foundation, who has identified a link between suicides in middle age and rising rates of distress about jobs and personal finances. Researchers also found an alarming increase among girls 10 to 14, whose suicide rate, while still very low, had tripled. The number of girls who killed themselves rose to 150 in 2014 from 50 in 1999. “This one certainly jumped out,” said Sally Curtin, a statistician at the center and an author of the report. © 2016 The New York Times Company
Anna Nowogrodzki There’s a little too much wishful thinking about mindfulness, and it is skewing how researchers report their studies of the technique. Researchers at McGill University in Montreal, Canada, analysed 124 published trials of mindfulness as a mental-health treatment, and found that scientists reported positive findings 60% more often than is statistically likely. The team also examined another 21 trials that were registered with databases such as ClinicalTrials.gov; of these, 62% were unpublished 30 months after they finished. The findings — reported in PLoS ONE on 8 April1 — hint that negative results are going unpublished. Mindfulness is the practice of being aware of thoughts and feelings without judging them good or bad. Mental-health treatments that focus on this method include mindfulness-based stress reduction — an 8-week group-based programme that includes yoga and daily meditation — and mindfulness-based cognitive therapy. A bias toward publishing studies that find the technique to be effective withholds important information from mental-health clinicians and patients, says Christopher Ferguson, a psychologist at Stetson University in Florida, who was not involved in the study. “I think this is a very important finding,” he adds. “We’ll invest a lot of social and financial capital in these issues, and a lot of that can be misplaced unless we have good data.” © 2016 Nature Publishing Group
Link ID: 22129 - Posted: 04.23.2016
By Esther Landhuis Peer inside the brain of someone with Alzheimer’s disease, and you’ll see some striking features: shriveled nerve cells and strange protein clumps. According to a leading theory, proteins called amyloid beta and tau build up in the brain and choke nerve cell communication, setting the disease in motion years before people suspect anything is wrong with their recall. Yet the Alzheimer’s brain has another curious aspect. Some of the clusters of toxic amyloid proteins are entangled with octopus-like immune cells called microglia, cells that live in the brain to clear unwanted clutter. By munching on amyloid plaques, microglia are thought to help keep the disease at bay. But these housekeeping cells have an additional role—they switch on inflammatory pathways. Inflammation is critically important when the immune system encounters infection or needs to repair tissue. If left unchecked, however, the inflammatory process churns out toxic substances that can kill surrounding cells, whose death triggers more inflammation and creates a vicious cycle. For years scientists have probed how neuroinflammation contributes to Alzheimer’s disease and other neurodegenerative ailments. Researchers face a number of immediate questions: Is neuroinflammation a driving force? Does it kick in when the disease is already underway and worsen the process? Could it be harnessed for good in the early stages? Those questions are far from settled, but research is starting to reveal a clearer picture. “It may not be the amyloid plaques themselves that directly damage neurons and the connections between them. Rather, it may be the immune reaction to the plaques that does the damage,” says Cynthia Lemere, a neuroscientist at Brigham and Women’s Hospital. Still, it is hard to say if microglia are good guys or bad, making it challenging to create therapeutics that target these cells. © 2016 Scientific American
By Mitch Leslie The worst part of being sick isn’t always the muscle aches and coughing. It’s the foggy head, the crankiness, the apathy, and the fatigue—in short, what researchers call sickness behavior. A new study uncovers a molecular mechanism that explains why we feel so crummy when we’re under the weather. “It’s a nice study that’s covered a lot of ground,” says neuroimmunologist Colm Cunningham of Trinity College in Dublin who wasn’t connected to the research. “What they’ve found is very plausible.” Although sickness behavior is unpleasant, researchers think the symptoms we suffer during a viral or bacterial infection are beneficial, enabling us to divert our energy to fighting the pathogens that have invaded our bodies. For cancer patients and people with autoimmune diseases, however, sickness behavior can be an unwanted side effect of treatment with immune molecules known as interferons, which our cells naturally release when we have an infection. The condition has posed a puzzle for researchers because they assumed the blood-brain barrier, a protective system that excludes most pathogens and immune molecules from the brain, would block signals from the immune system. Although scientists have identified several mechanisms that allow such messages to cross the barrier and influence behavior, the question of how the immune system and brain communicate “has been only partially answered,” says immunophysiologist Keith Kelley of the University of Illinois, Urbana-Champaign, who wasn’t connected to the new study. © 2016 American Association for the Advancement of Science.
Link ID: 22121 - Posted: 04.20.2016