Chapter 7. Life-Span Development of the Brain and Behavior
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by Flora Graham This glowing blue web of neurons is usually what researchers examine when searching for a cure for Parkinson's. But a new study, part-funded by Parkinson's UK, hones in on the tiny yellow dots. These are the connections between brain cells known as synapses, has discovered a killer that targets these links, potentially paving the way for new treatments. Soledad Galli at University College London and her colleagues have found that the death of synapses in mice may be due to malfunctioning proteins called Wnt proteins. "If we confirm that Wnt is involved in the early stages of Parkinson's, this throws up exciting possibilities, not just for new treatment targets, but also for new ways to identify people with Parkinson's early on in their condition," says Galli. Most patients currently depend on the drug levodopa, which is over 50 years old and can have severe side-effects, in addition to becoming less effective over time. Moreover, it only masks the symptoms: there is no cure for Parkinson's and no way to stop its progression. Journal reference: Nature Communications, DOI: 10.1038/ncomms5992 © Copyright Reed Business Information Ltd
2014 by Andy Coghlan Seeing is definitely believing when it comes to stem cell therapy. A blind man has recovered enough sight to ride his horse. A woman who could see no letters at all on a standard eye test chart can now read the letters on the top four lines. Others have recovered the ability to see colour. All have had injections of specialised retinal cells in their eyes to replace ones lost through age or disease. A trial in 18 people with degenerative eye conditions is being hailed as the most promising yet for a treatment based on human embryonic stem cells. "We've been hearing about their potential for more than a decade, but the results have always been in mice and rats, and no one has shown they're safe or effective in humans long term," says Robert Lanza of Advanced Cell Technology in Marlborough, Massachusetts, the company that carried out the stem cell intervention. "Now, we've shown both that they're safe and that there's a real chance these cells can help people." Ten years ago, the team at Advanced Cell Technology announced that it had successfully converted human embryonic stem cells into retinal pigment epithelial cells. These cells help keep the eyes' light-detecting rods and cones healthy. But when retinal pigment epithelial cells deteriorate, blindness can occur. This happens in age-related macular degeneration and Stargardt's macular dystrophy. In a bid to reverse this, Lanza's team injected retinal cells into one of each of the 18 participants' eyes, half of whom had age-related macular degeneration and half had Stargardt's. A year later, 10 people's eyes had improved, and the eyes of the others had stabilised. Untreated eyes had continued to deteriorate. © Copyright Reed Business Information Ltd.
|By Jenni Laidman During the second and third trimester of pregnancy, the outer layer of the embryo's brain, the cortex, assembles itself into six distinct layers. But in autism, according to new research, this organization goes awry—marring parts of the brain associated with the abilities often impaired in the disorder, such as social skills and language development. Eric Courchesne, director of the Autism Center of Excellence at the University of California, San Diego, and his colleagues uncovered this developmental misstep in a small study that compared 11 brains of children with autism who died at ages two through 15 with 11 brains of kids who died without the diagnosis. The study employed a sophisticated genetic technique that looked for signatures of the activity of 25 genes in brain slices taken from the front of the brain—an area called the prefrontal cortex—as well as from the occipital cortex at the back of the brain and the temporal cortex near the temple. The researchers found disorganized patches, roughly a quarter of an inch across, in which gene expression indicated cells were not where they were supposed to be, amid the folds of tissue in the prefrontal cortex in 10 of 11 brains from children with autism. That part of the brain is associated with higher-order communication and social interactions. The team also found messy patches in the temporal cortices of autistic brains but no disorder at the back of the brain, which also matches typical symptom profiles. The patches appeared at seemingly random locations within the frontal and temporal cortices, which may help explain why symptoms can differ dramatically among individuals, says Rich Stoner, then at U.C. San Diego and the first author of the study, which appeared in the New England Journal of Medicine. © 2014 Scientific American
By JOSHUA A. KRISCH An old stucco house stands atop a grassy hill overlooking the Long Island Sound. Less than a mile down the road, the renowned Cold Spring Harbor Laboratory bustles with more than 600 researchers and technicians, regularly producing breakthroughs in genetics, cancer and neuroscience. But that old house, now a private residence on the outskirts of town, once held a facility whose very name evokes dark memories: the Eugenics Record Office. In its heyday, the office was the premier scientific enterprise at Cold Spring Harbor. There, bigoted scientists applied rudimentary genetics to singling out supposedly superior races and degrading minorities. By the mid-1920s, the office had become the center of the eugenics movement in America. Today, all that remains of it are files and photographs — reams of discredited research that once shaped anti-immigration laws, spurred forced-sterilization campaigns and barred refugees from entering Ellis Island. Now, historians and artists at New York University are bringing the eugenics office back into the public eye. “Haunted Files: The Eugenics Record Office,” a new exhibit at the university’s Asian/Pacific/American Institute, transports visitors to 1924, the height of the eugenics movement in the United States. Inside a dimly lit room, the sounds of an old typewriter click and clack, a teakettle whistles and papers shuffle. The office’s original file cabinets loom over reproduced desks and period knickknacks. Creaky cabinets slide open, and visitors are encouraged to thumb through copies of pseudoscientific papers. © 2014 The New York Times Company
Keyword: Genes & Behavior
Link ID: 20204 - Posted: 10.14.2014
By GINA KOLATA For the first time, and to the astonishment of many of their colleagues, researchers created what they call Alzheimer’s in a Dish — a petri dish with human brain cells that develop the telltale structures of Alzheimer’s disease. In doing so, they resolved a longstanding problem of how to study Alzheimer’s and search for drugs to treat it; the best they had until now were mice that developed an imperfect form of the disease. The key to their success, said the lead researcher, Rudolph E. Tanzi of Massachusetts General Hospital in Boston, was a suggestion by his colleague Doo Yeon Kim to grow human brain cells in a gel, where they formed networks as in an actual brain. They gave the neurons genes for Alzheimer’s disease. Within weeks they saw the hard Brillo-like clumps known as plaques and then the twisted spaghetti-like coils known as tangles — the defining features of Alzheimer’s disease. The work, which also offers strong support for an old idea about how the disease progresses, was published in Nature on Sunday. Leading researchers said it should have a big effect. “It is a giant step forward for the field,” said Dr. P. Murali Doraiswamy, an Alzheimer’s researcher at Duke University. “It could dramatically accelerate testing of new drug candidates.” Of course, a petri dish is not a brain, and the petri dish system lacks certain crucial components, like immune system cells, that appear to contribute to the devastation once Alzheimer’s gets started. But it allows researchers to quickly, cheaply and easily test drugs that might stop the process in the first place. The crucial step, of course, will be to see if drugs that work in this system stop Alzheimer’s in patients. © 2014 The New York Times Company
Link ID: 20203 - Posted: 10.13.2014
By David Leonhardt and Amanda Cox Like so many other parts of health care, childbirth has become a more medically intense experience over the last two decades. The use of drugs to induce labor has become far more common, as have cesarean sections. Today, about half of all births in this country are hastened either by drugs or surgery, double the share in 1990. Crucial to the change has been a widely held belief that once fetuses pass a certain set of thresholds — often 39 weeks of gestation and five and a half pounds in weight — they’re as healthy as they can get. More time in the womb doesn’t do them much good, according to this thinking. For parents and doctors, meanwhile, scheduling a birth, rather than waiting for its random arrival, is clearly more convenient. But a huge new set of data, based on every child born in Florida over an 11-year span, is calling into question some of the most basic assumptions of our medicalized approach to childbirth. The results also play into a larger issue: the growing sense among many doctors and other experts that Americans would actually be healthier if our health care system were sometimes less aggressive. The new data suggest that the thresholds to maximize a child’s health seem to be higher, which means that many fetuses might benefit by staying longer in the womb, where they typically add at least a quarter-pound per week. Seven-pound babies appear to be healthier than six-pound babies — and to fare better in school as they age. The same goes for eight-pound babies compared with seven-pound babies, and nine-pound babies compared with eight-pound babies. Weight, of course, may partly be an indicator of broader fetal health, but it seems to be a meaningful one: The chunkier the baby, the better it does on average, all the way up to almost 10 pounds. “Birth weight matters, and it matters for everyone,” says David N. Figlio, a Northwestern University professor and co-author of the study, which will soon be published in the American Economic Review, one of the field’s top journals. © 2014 The New York Times Company
Ann Robinson Neuroscience research got a huge boost last week with news of Professor John O’Keefe’s Nobel prize for work on the “brain’s internal GPS system”. It is an exciting new part of the giant jigsaw puzzle of our brain and how it functions. But how does cutting-edge neuroscience research translate into practical advice about how to pass exams, remember names, tot up household bills and find where the hell you left the car in a crowded car park? O’Keefe’s prize was awarded jointly with Swedish husband and wife team Edvard and May-Britt Moser for their discovery of “place and grid cells” that allow rats to chart where they are. When rats run through a new environment, these cells show increased activity. The same activity happens much faster while the rats are asleep, as they replay the new route. We already knew that the part of the brain known as the hippocampus was involved in spatial awareness in birds and mammals, and this latest work on place cells sheds more light on how we know where we are and where we’re going. In 2000, researchers at University College London led by Dr Eleanor Maguire showed that London taxi drivers develop a pumped-up hippocampus after years of doing the knowledge and navigating the backstreets of the city. MRI scans showed that cabbies start off with bigger hippocampuses than average, and that the area gets bigger the longer they do the job. As driver David Cohen said at the time to BBC News: “I never noticed part of my brain growing – it makes you wonder what happened to the rest of it!” © 2014 Guardian News and Media Limited
For decades, scientists thought that neurons in the brain were born only during the early development period and could not be replenished. More recently, however, they discovered cells with the ability to divide and turn into new neurons in specific brain regions. The function of these neuroprogenitor cells remains an intense area of research. Scientists at the National Institutes of Health (NIH) report that newly formed brain cells in the mouse olfactory system — the area that processes smells — play a critical role in maintaining proper connections. The results were published in the October 8 issue of the Journal of Neuroscience. “This is a surprising new role for brain stem cells and changes the way we view them,” said Leonardo Belluscio, Ph.D., a scientist at NIH’s National Institute of Neurological Disorders and Stroke (NINDS) and lead author of the study. The olfactory bulb is located in the front of the brain and receives information directly from the nose about odors in the environment. Neurons in the olfactory bulb sort that information and relay the signals to the rest of the brain, at which point we become aware of the smells we are experiencing. Olfactory loss is often an early symptom in a variety of neurological disorders, including Alzheimer’s and Parkinson’s diseases. In a process known as neurogenesis, adult-born neuroprogenitor cells are generated in the subventricular zone deep in the brain and migrate to the olfactory bulb where they assume their final positions. Once in place, they form connections with existing cells and are incorporated into the circuitry.
by Andy Coghlan Ten years after the death of everyone's favourite Superman, Christopher Reeve, his son Matthew Reeve is pushing ahead with a spine-tingling clinical trial You're planning a large study of a paralysis treatment that has already helped four young men. What will it entail? This study will include 36 people with spinal cord injuries who will be treated with epidural stimulation – a technique in which a device is used to apply electrical current to the spinal cord. If we see the same results as we did in the first four, this therapy could have a profound impact on thousands of people living with paralysis. It has the potential to become as commonplace as the pacemaker is for cardiac patients. How well has the treatment worked for the four men who have already received it? Prior to epidural stimulation, they had all suffered chronic injuries caused by completely severed spinal cords. All four have seen dramatic improvements, including the ability to voluntarily move their toes, feet, ankles and legs, and even stand at times, when the device is on. One unexpected bonus has been the return of autonomic function, such as bladder and bowel control and sexual function. From a quality-of-life point of view, this is the biggest improvement. Also unexpectedly, these autonomic functions continue in all four men even when the device is switched off, although they still need it to stand, move their legs and do exercises. © Copyright Reed Business Information Ltd.
By Sarah C. P. Williams If you sailed through school with high grades and perfect test scores, you probably did it with traits beyond sheer smarts. A new study of more than 6000 pairs of twins finds that academic achievement is influenced by genes affecting motivation, personality, confidence, and dozens of other traits, in addition to those that shape intelligence. The results may lead to new ways to improve childhood education. “I think this is going to end up being a really classic paper in the literature,” says psychologist Lee Thompson of Case Western Reserve University in Cleveland, Ohio, who has studied the genetics of cognitive skills and who was not involved in the work. “It’s a really firm foundation from which we can build on.” Researchers have previously shown that a person’s IQ is highly influenced by genetic factors, and have even identified certain genes that play a role. They’ve also shown that performance in school has genetic factors. But it’s been unclear whether the same genes that influence IQ also influence grades and test scores. In the new study, researchers at King’s College London turned to a cohort of more than 11,000 pairs of both identical and nonidentical twins born in the United Kingdom between 1994 and 1996. Rather than focus solely on IQ, as many previous studies had, the scientists analyzed 83 different traits, which had been reported on questionnaires that the twins, at age 16, and their parents filled out. The traits ranged from measures of health and overall happiness to ratings of how much each teen liked school and how hard they worked. © 2014 American Association for the Advancement of Science
by Michael Marshall When we search for the seat of humanity, are we looking at the wrong part of the brain? Most neuroscientists assume that the neocortex, the brain's distinctive folded outer layer, is the thing that makes us uniquely human. But a new study suggests that another part of the brain, the cerebellum, grew much faster in our ape ancestors. "Contrary to traditional wisdom, in the human lineage the cerebellum was the part of the brain that accelerated its expansion most rapidly, rather than the neocortex," says Rob Barton of Durham University in the UK. With Chris Venditti of the University of Reading in the UK, Barton examined how the relative sizes of different parts of the brain changed as primates evolved. During the evolution of monkeys, the neocortex and cerebellum grew in tandem, a change in one being swiftly followed by a change in the other. But starting with the first apes around 25 million years ago through to chimpanzees and humans, the cerebellum grew much faster. As a result, the cerebellums of apes and humans contain far more neurons than the cerebellum of a monkey, even if that monkey were scaled up to the size of an ape. "The difference in ape cerebellar volume, relative to a scaled monkey brain, is equal to 16 billion extra neurons," says Barton. "That's the number of neurons in the entire human neocortex." © Copyright Reed Business Information Ltd.
By Fredrick Kunkle Years ago, many scientists assumed that a woman’s heart worked pretty much the same as a man’s. But as more women entered the male-dominated field of cardiology, many such assumptions vanished, opening the way for new approaches to research and treatment. A similar shift is underway in the study of Alzheimer’s disease. It has long been known that more women than men get the deadly neurodegenerative disease, and an emerging body of research is challenging the common wisdom as to why. Although the question is by no means settled, recent findings suggest that biological, genetic and even cultural influences may play heavy roles. Of the more than 5 million people in the United States who have been diagnosed with Alzheimer’s, the leading cause of dementia, two-thirds are women. Because advancing age is considered the biggest risk factor for the disease, researchers largely have attributed that disparity to women’s longer life spans. The average life expectancy for women is 81 years, compared with 76 for men. Yet “even after taking age into account, women are more at risk,” said Richard Lipton, a physician who heads the Einstein Aging Study at Albert Einstein College of Medicine in New York. With the number of Alzheimer’s cases in the United States expected to more than triple by 2050, some researchers are urging a greater focus on understanding the underlying reasons women are more prone to the disease and on developing gender-specific treatments. .
By Smitha Mundasad Health reporter, BBC News Measuring people's sense of smell in later life could help doctors predict how likely they are to be alive in five years' time, a PLOS One study suggests. A survey of 3,000 adults found 39% with the poorest sense of smell were dead within five years - compared to just 10% who identified odours correctly. Scientists say the loss of smell sense does not cause death directly, but may be an early warning sign. They say anyone with long-lasting changes should seek medical advice. Researchers from the University of Chicago asked a representative sample of adults between the ages of 57-85 to take part in a quick smell test. The assessment involved identifying distinct odours encased on the tips of felt-tip pens. The smells included peppermint, fish, orange, rose and leather. Five years later some 39% of adults who had the lowest scores (4-5 errors) had passed away, compared with 19% with moderate smell loss and just 10% with a healthy sense of smell (0-1 errors). And despite taking issues such as age, nutrition, smoking habits, poverty and overall health into account, researchers found those with the poorest sense of smell were still at greatest risk. Lead scientist, Prof Jayant Pinto, said: "We think loss of the sense of smell is like the canary in the coal mine. BBC © 2014
By Fredrick Kunkle Here’s something to worry about: A recent study suggests that middle-age women whose personalities tend toward the neurotic run a higher risk of developing Alzheimer’s disease later in life. The study by researchers at the University of Gothenburg in Sweden followed a group of women in their 40s, whose disposition made them prone to anxiety, moodiness and psychological distress, to see how many developed dementia over the next 38 years. In line with other research, the study suggested that women who were the most easily upset by stress — as determined by a commonly used personality test — were two times more likely to develop Alzheimer’s disease than women who were least prone to neuroticism. In other words, personality really is — in some ways — destiny. “Most Alzheimer’s research has been devoted to factors such as education, heart and blood risk factors, head trauma, family history and genetics,” study author Lena Johansson said in a written statement. “Personality may influence the individual’s risk for dementia through its effect on behavior, lifestyle or reactions to stress.” The researchers cautioned that the results cannot be extrapolated to men because they were not included in the study and that further work is needed to determine possible causes for the link. The study, which appeared Wednesday in the American Academy of Neurology’s journal, Neurology, examined 800 women whose average age in 1968 was 46 years to see whether neuroticism — which involves being easily distressed and subject to excessive worry, jealousy or moodiness — might have a bearing on the risk of dementia.
|By Brian Bienkowski and Environmental Health News Babies born to mothers with high levels of perchlorate during their first trimester are more likely to have lower IQs later in life, according to a new study. The research is the first to link pregnant women's perchlorate levels to their babies’ brain development. It adds to evidence that the drinking water contaminant may disrupt thyroid hormones that are crucial for proper brain development. Perchlorate, which is both naturally occurring and manmade, is used in rocket fuel, fireworks and fertilizers. It has been found in 4 percent of U.S. public water systems serving an estimated 5 to 17 million people, largely near military bases and defense contractors in the U.S. West, particularly around Las Vegas and in Southern California. “We would not recommend action on perchlorate levels from this study alone, although our report highlights a pressing need for larger studies of perchlorate levels from the general pregnant population and those with undetected hypothyroidism,” the authors from the United Kingdom, Italy and Boston wrote in the study published in The Journal of Clinical Endocrinology & Metabolism. The Environmental Protection Agency for decades has debated setting a national drinking water standard for perchlorate. The agency in 2011 announced it would start developing a standard, reversing an earlier decision. In the meantime, two states, California and Massachusetts, have set their own standards. © 2014 Scientific American
By Gary Stix If it’s good for the heart, it could also be good for the neurons, astrocytes and oligodendrocytes, cells that make up the main items on the brain’s parts list. The heart-brain adage comes from epidemiological studies that show that people with cardiovascular risk factors such as high-blood pressure and elevated cholesterol levels, may be more at risk for Alzheimer’s and other dementias. This connection between heart and brain has also led to some disappointments: clinical trials of lipid-lowering statins have not helped patients diagnosed with Alzheimer’s, although epidemiological studies suggest that long-term use of the drugs may help prevent Alzheimer’s and other dementias. The link between head and heart is still being pursued because new Alzheimer’s drugs have failed time and again. One approach that is now drawing some interest looks at the set of proteins that carry around fats in the brain. These lipoproteins could potentially act as molecular sponges that mop up the amyloid-beta peptide that clogs up connections among brain cells in Alzheimer’s. One of these proteins—Apolipoprotein J, also known as clusterin—intrigues researchers because of the way it interacts with amyloid-beta and the status of its gene as a risk factor for Alzheimer’s. A researcher from the University of Minnesota, Ling Li, recently presented preliminary work at the Alzheimer’s Disease Drug Discovery Foundation annual meeting that showed that, at least in a lab dish, a molecule made up of a group of amino acids from APOJ is capable of protecting against the toxicity of the amyloid-beta peptide. It also quelled inflammation and promoted the health of synapses—the junctions where one brain cell encounters another. Earlier work by another group showed that the peptide prevented the development of lesions in the blood vessels of animals.
Link ID: 20135 - Posted: 09.30.2014
By Smitha Mundasad Health reporter, BBC News A spice commonly found in curries may boost the brain's ability to heal itself, according to a report in the journal Stem Cell Research and Therapy. The German study suggests a compound found in turmeric could encourage the growth of nerve cells thought to be part of the brain's repair kit. Scientists say this work, based in rats, may pave the way for future drugs for strokes and Alzheimer's disease. But they say more trials are needed to see whether this applies to humans. Researchers from the Institute of Neuroscience and Medicine in Julich, Germany, studied the effects of aromatic-turmerone - a compound found naturally in turmeric. Rats were injected with the compound and their brains were then scanned. Particular parts of the brain, known to be involved in nerve cell growth, were seen to be more active after the aromatic-turmerone infusion. Scientists say the compound may encourage a proliferation of brain cells. In a separate part of the trial, researchers bathed rodent neural stem cells (NSCs) in different concentrations of aromatic-tumerone extract. NSCs have the ability to transform into any type of brain cell and scientists suggest they could have a role in repair after damage or disease. Dr Maria Adele Rueger, who was part of the research team, said: "In humans and higher developed animals their abilities do not seem to be sufficient to repair the brain but in fish and smaller animals they seem to work well." Picture of the spice turmeric Turmeric belongs to the same plant family as ginger BBC © 2014
by Sarah Zielinski Chimps may be cute and have mannerisms similar to humans, but they are wild animals. A new study finds that chimps raised as pets or entertainers have behavioral problems as adults. There are plenty of good reasons why chimpanzees should not be pets or performers, no matter how cute or humanlike they appear: They are wild animals. They can be violent with each other. And they can be violent toward humans — even humans that have a long history with the chimp. Plus, there’s evidence that seeing an adorable chimp dressed up like a miniature human actually makes us care less about the plight of their species. Now comes evidence that the way that chimps are raised to become pets or entertainers — taking them away from other chimps at a young age and putting them in the care of humans, who may or may not feed and care for them properly — has long-term, negative effects on their behavior. “We now add empirical evidence of the potentially negative welfare effects on the chimpanzees themselves as important considerations in the discussion of privately owned chimpanzees,” Hani Freeman and Stephen Ross of the Lincoln Park Zoo in Chicago write September 23 in PeerJ. Freeman and Ross compiled life history and behavioral data on 60 captive chimps living in zoos. Some of the animals had always lived in zoos and grew up in groups of chimpanzees. Six were raised solely by humans and were later placed in zoos after they became too big or too old for their owners to care for them. Others had a more mixed background. © Society for Science & the Public 2000 - 2014
Jia You In the future, a nurse could determine whether a baby is likely to develop a reading disorder simply by attaching a few electrodes to its scalp and watching its brain waves respond to human speech. Such is the scenario suggested by a new study, which finds a potential biological indicator of how well preschool children perceive rhythm, an ability linked to language development. “It’s really impressive to work with children this young, who are not often looked at,” says Aniruddh Patel, a cognitive neuroscientist at Tufts University in Medford, Massachusetts, who was not involved with the research. Spoken language consists of sound waves occurring over multiple timescales. A syllable, for example, takes place over a quarter of a second, while a sentence unfolds over a few seconds. To make sense of this complex auditory information, humans use rhythmic cues such as stress and pause to discern words and syllables. Adults and school-aged children with reading disorders, however, struggle to pick up on these rhythmic patterns. Scientists estimate that dyslexia and other reading disabilities plague about 5% to 10% of the population. Detecting such impairments early could lead to more effective intervention, but observing telltale signs in younger children who have not learned to read has proven a challenge. So biologist Nina Kraus of Northwestern University in Evanston, Illinois, and her colleagues looked for automatic brain responses that can track language development in preschoolers, who have not learned to read. © 2014 American Association for the Advancement of Science
|By Melinda Wenner Moyer Autism is primarily a disorder of the brain, but research suggests that as many as nine out of 10 individuals with the condition also suffer from gastrointestinal problems such as inflammatory bowel disease and “leaky gut.” The latter condition occurs when the intestines become excessively permeable and leak their contents into the bloodstream. Scientists have long wondered whether the composition of bacteria in the intestines, known as the gut microbiome, might be abnormal in people with autism and drive some of these symptoms. Now a spate of new studies supports this notion and suggests that restoring proper microbial balance could alleviate some of the disorder's behavioral symptoms. At the annual meeting of the American Society for Microbiology held in May in Boston, researchers at Arizona State University reported the results of an experiment in which they measured the levels of various microbial by-products in the feces of children with autism and compared them with those found in healthy children. The levels of 50 of these substances, they found, significantly differed between the two groups. And in a 2013 study published in PLOS ONE, Italian researchers reported that, compared with healthy kids, those with autism had altered levels of several intestinal bacterial species, including fewer Bifidobacterium, a group known to promote good intestinal health. One open question is whether these microbial differences drive the development of the condition or are instead a consequence of it. A study published in December 2013 in Cell supports the former idea. When researchers at the California Institute of Technology incited autismlike symptoms in mice using an established paradigm that involved infecting their mothers with a viruslike molecule during pregnancy, they found that after birth, the mice had altered gut bacteria compared with healthy mice. © 2014 Scientific American,
Link ID: 20104 - Posted: 09.23.2014