Chapter 7. Life-Span Development of the Brain and Behavior
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Scientists and clinicians have long dreamed of helping the injured brain repair itself by creating new neurons, and an innovative NIH-funded study published today in Nature Medicine may bring this goal much closer to reality. A team of researchers has developed a therapeutic technique that dramatically increases the production of nerve cells in mice with stroke-induced brain damage. The therapy relies on the combination of two methods that show promise as treatments for stroke-induced neurological injury. The first consists of surgically grafting human neural stem cells into the damaged area, where they mature into neurons and other brain cells. The second involves administering a compound called 3K3A-APC, which the scientists have shown helps neural stem cells grown in a petri dish develop into neurons. However, it was unclear what effect the molecule, derived from a human protein called activated protein-C (APC), would have in live animals. A month after their strokes, mice that had received both the stem cells and 3K3A-APC performed significantly better on tests of motor and sensory functions compared to mice that received neither or only one of the treatments. In addition, many more of the stem cells survived and matured into neurons in the mice given 3K3A-APC. “This USC-led animal study could pave the way for a potential breakthrough in how we treat people who have experienced a stroke,” added Jim Koenig, Ph.D., a program director at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS), which funded the research. “If the therapy works in humans, it could markedly accelerate the recovery of these patients.”
By Clare Wilson Taking a daily vitamin or mineral supplement is widely seen as a common-sense way of looking after yourself – a kind of insurance, like wearing a seat belt. But evidence is growing that it might not be such a healthy habit after all. The latest finding is that calcium supplements, taken by many women after the menopause to strengthen their bones, are linked to dementia. Among women who have had a stroke, taking calcium was associated with a seven-fold rise in the number who went on to have dementia. Calcium was also linked with a smaller, non-statistically significant, rise in dementia in women who had not had a stroke. The finding emerged from a study that was not a randomised trial, so it is not the most robust type of medical evidence. The researchers merely counted dementia cases in people who had chosen whether to take calcium, and so the data could be biased. But the results are striking and come on the heels of a previous study that was a randomised trial, which found a link between calcium supplements and a modestly higher risk of heart attacks – suggesting that caution over calcium is indeed warranted. If future research confirms the association with dementia, women would face a horrible dilemma: should they continue to take calcium, staving off bone weakness that can lead to fatal hip fractures, while running an increased risk of one of the most dreaded illness of ageing? So what’s going on? Team member Silke Kern at the Sahlgrenska Academy Institute of Neuroscience and Physiology in Gothenburg, Sweden, says that taking a calcium pill triggers a rapid surge in the mineral’s levels in the blood, one that you wouldn’t get from calcium in food. © Copyright Reed Business Information Ltd.
Link ID: 22588 - Posted: 08.23.2016
By KATHERINE KINZLER You may not be surprised to learn that food preference is a social matter. What we choose to eat depends on more than just what tastes good or is healthful. People in different cultures eat different things, and within a culture, what you eat can signal something about who you are. More surprising is that the sociality of food selection, it turns out, runs deep in human nature. In research published this month in the Proceedings of the National Academy of Sciences, my colleagues and I showed that even 1-year-old babies understand that people’s food preferences depend on their social or cultural group. Interestingly, we found that babies’ thinking about food preferences isn’t really about food per se. It’s more about the people eating foods, and the relationship between food choice and social groups. While it’s hard to know what babies think before they can talk, developmental psychologists have long capitalized on the fact that babies’ visual gaze is guided by their interest. Babies tend to look longer at something that is novel or surprising. Do something bizarre the next time you meet a baby, and you’ll notice her looking intently. Using this method, the psychologists Zoe Liberman, Amanda Woodward, Kathleen Sullivan and I conducted a series of studies. Led by Professor Liberman, we brought more than 200 1-year-olds (and their parents) into a developmental psychology lab, and showed them videos of people visibly expressing like or dislike of foods. For instance, one group of babies saw a video of a person who ate a food and expressed that she loved it. Next they saw a video of a second person who tried the same food and also loved it. This second event was not terribly surprising to the babies: The two people agreed, after all. Accordingly, the babies did not look for very long at this second video; it was what they expected. © 2016 The New York Times Company
By Virginia Morell Scientists have long worried whether animals can respond to the planet’s changing climate. Now, a new study reports that at least one species of songbird—and likely many more—already knows how to prep its chicks for a warming world. They do so by emitting special calls to the embryos inside their eggs, which can hear and learn external sounds. This is the first time scientists have found animals using sound to affect the growth, development, behavior, and reproductive success of their offspring, and adds to a growing body of research revealing that birds can “doctor” their eggs. “The study is novel, surprising, and fascinating, and is sure to lead to much more work on parent-embryo communication,” says Robert Magrath, a behavioral ecologist at the Australian National University in Canberra who was not involved in the study. The idea that the zebra finch (Taeniopygia guttata) parents were “talking to their eggs” occurred to Mylene Mariette, a behavioral ecologist at Deakin University in Waurn Ponds, Australia, while recording the birds’ sounds at an outdoor aviary. She noticed that sometimes when a parent was alone, it would make a rapid, high-pitched series of calls while sitting on the eggs. Mariette and her co-author, Katherine Buchanan, recorded the incubation calls of 61 female and 61 male finches inside the aviary. They found that parents of both sexes uttered these calls only during the end of the incubation period and when the maximum daily temperature rose above 26°C (78.8°F). © 2016 American Association for the Advancement of Scienc
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.
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
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
Link ID: 22559 - Posted: 08.16.2016
David R. Jacobs, We all know that exercise improves our physical fitness, but staying in shape can also boost our brainpower. We are not entirely sure how, but evidence points to several explanations. First, to maintain normal cognitive function, the brain requires a constant supply of oxygen and other chemicals, delivered via its abundant blood vessels. Physical exercise—and even just simple activities such as washing dishes or vacuuming—helps to circulate nutrient-rich blood efficiently throughout the body and keeps the blood vessels healthy. Exercise increases the creation of mitochondria—the cellular structures that generate and maintain our energy—both in our muscles and in our brain, which may explain the mental edge we often experience after a workout. Studies also show that getting the heart rate up enhances neurogenesis—the ability to grow new brain cells—in adults. Regardless of the mechanism, mounting evidence is revealing a robust relation between physical fitness and cognitive function. In our 2014 study, published in Neurology, we found that physical activity has an extensive, long-lasting influence on cognitive performance. We followed 2,747 healthy people between the ages of 18 and 30 for 25 years. In 1985 we evaluated their physical fitness using a treadmill test: the participants walked up an incline that became increasingly steep every two minutes. On average, they walked for about 10 minutes, reaching 3.4 miles per hour at an 18 percent incline (a fairly steep hill). Low performers lasted for only seven minutes and high performers for about 13 minutes. A second treadmill test in 2005 revealed that our participants' fitness levels had declined with age, as would be expected, but those who were in better shape in 1985 were also more likely to be fit 20 years later. © 2016 Scientific American
Link ID: 22555 - Posted: 08.13.2016
Cassie Martin Understanding sea anemones’ exceptional healing abilities may help scientists figure out how to restore hearing. Proteins that the marine invertebrates use to repair damaged cells can also repair mice’s sound-sensing cells, a new study shows. The findings provide insights into the mechanics of hearing and could lead to future treatments for traumatic hearing loss, researchers report in the Aug. 1 Journal of Experimental Biology. “This is a preliminary step, but it’s a very useful step in looking at restoring the structure and function of these damaged cells,” says Lavinia Sheets, a hearing researcher at Harvard Medical School who was not involved in the study. Tentacles of starlet sea anemones (Nematostella vectensis) are covered in tiny hairlike cells that sense vibrations in the water from prey swimming nearby.The cells are similar to sound-sensing cells found in the ears of humans and other mammals. When loud noises damage or kill these hair cells, the result can range from temporary to permanent hearing loss. Anemones’ repair proteins restore their damaged hairlike cells, but landlubbing creatures aren’t as lucky. Glen Watson, a biologist at the University of Louisiana at Lafayette, wondered if anemones’ proteins — which have previously been shown to mend similar cells in blind cave fish — might also work in mammals. |© Society for Science & the Public 2000 - 2016.
By Andy Coghlan The switching-off of genes in the human brain has been watched live for the first time. By comparing this activity in different people’s brains, researchers are now on the hunt for abnormalities underlying disorders such as Alzheimer’s disease and schizophrenia. To see where genes are most and least active in the brain, Jacob Hooker at Harvard Medical School and his team developed a radioactive tracer chemical that binds to a type of enzyme called an HDAC. This enzyme deactivates genes inside our cells, stopping them from making the proteins they code for. When injected into people, brain scans can detect where this tracer has bound to an enzyme, and thus where the enzyme is switching off genes. Live epigenetics The switching-off of genes by HDACs is a form of epigenetics – physical changes to the structure of DNA that modify how active genes are without altering their code. Until now, the only way to examine such activity in the brain has been by looking at post-mortem brain tissue. In the image above from the study, genes are least active in the red regions, such as the bulb-shaped cerebellum area towards the bottom right. The black and blue areas show the highest levels of gene activity – where barely any HDACs are present – and the yellow and green areas fall in between. © Copyright Reed Business Information Ltd.
Nicola Davis Scientists say that they have discovered a possible explanation for how Alzheimer’s disease spreads in the brain. Alzheimer’s is linked to a buildup of protein plaques and tangles that spread across particular tissues in the brain as the disease progresses. But while the pattern of this spread is well-known, the reason behind the pattern is not. Now scientists say they have uncovered a potential explanation as to why certain tissues of the brain are more vulnerable to Alzheimer’s disease. The vulnerability appears to be linked to variations in the levels of proteins in the brain that protect against the clumping of other proteins - variations that are present decades before the onset of the disease. Hope for Alzheimer's treatment as researchers find licensed drugs halt brain degeneration Read more “Our results indicate that within healthy brains a tell-tale pattern of protein levels predicts the progression of Alzheimer’s disease through the brain [in those that are affected by the disease],” said Rosie Freer, a PhD student at the University of Cambridge and first author of the study. The results could open up the possibility of identifying individuals who are at risk of developing Alzheimer’s long before symptoms appear, as well as offering new insights to those attempting to tackle the disease. Charbel Moussa, director of the Laboratory for Dementia and Parkinsonism at Georgetown University Medical Center said that he agreed with the conclusions of the study. “It is probably true that in cases of diseases like Alzheimer’s and Parkinson’s we may have deficiencies in quality control mechanisms like cleaning out bad proteins that collect in the brain cells,” he said, although he warned that using such findings to predict those more at risk of such disease is likely to be difficult. © 2016 Guardian News and Media Limited
By Robert Lavine Just the briefest eye contact can heighten empathetic feelings, giving people a sense of being drawn together. But patients who suffer from autism, even in its most high-functioning forms, often have trouble establishing this sort of a social connection with other people. Researchers are delving into what’s going on behind the eyes when these magical moments occur, and the hormones and neural substrates involved may offer hope of helping people with autism. University of Cambridge neuroscientist Bonnie Auyeung and colleagues gave oxytocin—a compound commonly referred to as the “love hormone,” as it’s been found to play roles in maternal and romantic bonding—to both normal men and those with a high-functioning form of autism also called Asperger’s syndrome. The scientists then tracked the eye movements of the study subjects and found that, compared with controls, those who received oxytocin via nasal spray showed increases in the number of fixations—pauses of about 300 milliseconds—on the eye region of an interviewer’s face and in the fraction of time spent looking at this region during a brief interview (Translational Psychiatry, doi:10.1038/tp.2014.146, 2015). Oxytocin, a neuropeptide hormone secreted by the pituitary gland, has long been known to activate receptors in the uterus and mammary glands, facilitating labor and milk letdown. But research on the neural effects of oxytocin has been accelerated by the availability of a nasal spray formulation of the hormone, which can deliver it more directly to the brain, also rich with oxytocin receptors. Auyeung adds that her study used a unique experimental setup. “Other studies have shown that [oxytocin] increases looking at the eye region when presented with a picture of a face,” Auyeung says. “The new part is that we are using a live interaction.”
Laura Sanders A busy protein known for its role in aging may also have a hand in depression, a study on mice hints. Under certain circumstances, the aging-related SIRT1 protein seems to make mice despondent, scientists report August 10 in the Journal of Neuroscience. The results are preliminary, but they might ultimately help find new depression treatments. Today’s treatments aren’t always effective, and new approaches are sorely needed. “This is one potential new avenue,” says study coauthor Deveroux Ferguson of the University of Arizona College of Medicine in Phoenix. Ferguson and colleagues subjected mice to 10 days of stressful encounters with other mice. After their demoralizing ordeal, the mice showed signs of depression, such as eschewing sugar water and giving up attempts to swim. Along with these signs of rodent despair, the mice had more SIRT1 gene activity in the nucleus accumbens, a brain area that has been linked to motivation and depression. Resveratrol, a compound found in red grapes, supercharges the SIRT1 protein, making it more efficient at its job. When Ferguson and colleagues delivered resveratrol directly to the nucleus accumbens, mice displayed more signs of depression and anxiety. When the researchers used a different compound to hinder SIRT1 activity, the mice showed the opposite effect, appearing bolder in some tests than mice that didn’t receive the compound. |© Society for Science & the Public 2000 - 2016.
By Ann Griswold, Autism shares genetic roots with obsessive-compulsive disorder (OCD) andattention deficit hyperactivity disorder (ADHD). The three conditions have features in common, such as impulsivity. New findings suggest that they also share a brain signature. The first comparison of brain architecture across these conditions has found that all are associated with disruptions in the structure of the corpus callosum. The corpus callosum is a bundle of nerve fibers that links the brain’s left and right hemispheres. The results appeared July 1 in the American Journal of Psychiatry. Clinicians may find it difficult to distinguish autism from ADHD based on symptoms alone. But if the conditions are marked by similar structural problems in the brain, the same interventions might be useful no matter what the diagnosis is, says lead researcher Stephanie Ameis, assistant professor of psychiatry at the University of Toronto. The unique aspects of each condition might arise from other brain attributes, such as differences in the connections between neurons, says Thomas Frazier, director of research at the Cleveland Clinic Foundation. “A reasonable conclusion is that autism and ADHD don’t differ dramatically in a structural way, but could differ in connectivity,” says Frazier, who was not involved in the study. Ameis’ team examined the brains of 71 children with autism, 31 with ADHD, 36 with OCD and 62 typical children using diffusion tensor imaging. This method provides a picture of the brain’s white matter, the long fibers that connect nerve cells, by measuring the diffusion of water across these fibers. © 2016 Scientific American
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 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
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.