Chapter 7. Life-Span Development of the Brain and Behavior
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A study suggests that a chemical in dark chocolate and red wine can slow the progression of Alzheimer’s disease. But how conclusive is the data, and does this mean we should all drink more wine? New Scientist looks at the evidence. What is resveratrol? Found in grapes, red wine and dark chocolate, many claims have been made about resveratrol. It has been touted as a potential panacea for a range of age-related disorders, including cancer, diabetes and neurological problems, but so far most of the data supporting these claims has come from lab studies and work in animals. There have been only a few, small studies in humans. How might resveratrol protect us from age-related illness? Extremely calorie-restricted diets greatly reduce age-related diseases in lab animals. This is thought to happen through the activation of a group of enzymes called sirtuins, which seem to affect gene expression and protect against the effects of stress, including a poor diet. The hope is that resveratrol activates sirtuins to get the same benefits – like preventing the onset of age-related diseases, including Alzheimer’s – without having to stick to such a low-energy diet. But some experiments have suggested slowed ageing from caloric restriction may not be down to sirtuins after all. What does the latest study show? To see if resveratrol could delay the progression of Alzheimer’s disease in people , Scott Turner at Georgetown University Medical Centre in Washington DC and his team gave 119 people with mild to moderate symptoms of the disease either a gram of synthesised resveratrol twice a day in pills for a year, or a placebo. © Copyright Reed Business Information Ltd.
Link ID: 21404 - Posted: 09.14.2015
By Elizabeth Landau Ask a physician what the hormone vasopressin is good for, and she will explain that it regulates the volume of water in your body and also affects blood pressure. But since the 1990s, vasopressin has been a hot topic in a very different field: social behavior. And recently it has emerged as a possible target for treating autism spectrum disorders (ASD), which are characterized by social, behavioral and communication impairments. The research is still in early stages, however, and has yielded more questions than answers. Given that one out of 68 children in the U.S. has an autism spectrum disorder, researchers are scrambling to figure out what in the brain might be related to the symptoms, and how they might design an effective treatment. Vasopressin may be a key player in the disorder. But scientists do not yet know whether too much or too little of the hormone—or perhaps some combination of both—is tied to autism. New clinical trials may yield insights. “I think that the work is exciting and important” says Suma Jacob, who leads an autism research laboratory at the University of Minnesota. “I also think we still have a lot more work to do in this field as a whole.” Previous research has shown that vasopressin, like the hormone oxytocin, is associated with parenting behavior and social bonding, including falling in love. In fact, the two hormones are structurally very similar, and there are receptors in the brain that interact with both of them. But high levels of vasopressin are also associated with anxiety and aggression. Intriguingly, some animal studies have found that higher levels of vasopressin increased aggression specifically in males. © 2015 Scientific American
Alison Abbott Only a decade ago, the idea that Alzheimer’s disease might be transmissible between people would have been laughed off the stage. But scientists have since shown that tissues can transmit symptoms of the disease between animals — and new results imply that humans, at least in one unusual circumstance, may not be an exception. The findings, published in this issue of Nature, emerged during autopsy studies of the brains of eight people who had died of the rare but deadly Creutzfeldt–Jakob disease (CJD; Z. Jaunmuktane et al. Nature 525, 247–250; 2015). They contracted it decades after treatment with contaminated batches of growth hormone that had been extracted from the pituitary glands of human cadavers. Six of the brains, in addition to the damage caused by CJD, harboured the tell-tale amyloid pathology that is associated with Alzheimer’s disease. “This is the first evidence of real-world transmission of amyloid pathology,” says molecular neuroscientist John Hardy of University College London (UCL). “It is potentially concerning.” If confirmed, the findings raise the spectre that tens of thousands of other people treated with the human growth-hormone (hGH) extracts might be at risk of Alzheimer’s. And although there is no suggestion that Alzheimer’s could be contracted through normal contact with patients, some scientists worry that the findings may have broader implications: that Alzheimer’s could be passed on by other routes through which CJD can be transmitted, such as blood transfusions or contaminated surgical instruments. © 2015 Nature Publishing Group
By Siri Carpenter Alex, age 10, bounds onto his bed to pose with his Aaron Rodgers poster, grinning as proudly as if he had recruited the Green Bay Packers’ quarterback himself. Continuing the tour of his suburban New York bedroom, he points out his Packers-themed alarm clock, his soccer trophy, his Boy Scout trophy, and then the big reveal: a homemade foam box in Packers green and gold. “Mmm, very nice,” I say. Alex grins—part shy, part sly—as he turns it around to show me the message on the back: “Jets stink.” Even though he seems to be an entirely ordinary boy, there’s something unusual about Alex: He once had autism, and now he does not. There was a time when Alex’s parents didn’t know if he would ever speak in full sentences, let alone joke around with a stranger. His autism, they suspected, might prevent any such future. Alex’s parents began to worry about him before he was even a year old. He wasn’t learning to sit, crawl, or stand as his fraternal twin brother was. Even more striking was how much less social he was than his brother. “Alex was an expressionless child,” says his mother, Amy. (Alex’s and Amy’s names have been changed to protect their privacy.) She remembers a friend trying in vain to get Alex to laugh—jumping up and down, gesturing wildly, making silly faces. “His brother would be in belly laughs, and Alex would be just glazed over,” Amy says. © 2015 The Slate Group LLC.
Link ID: 21393 - Posted: 09.10.2015
By Nicholas Bakalar Being obese at age 50 may be tied to an increased risk of developing Alzheimer’s disease at a younger age. Previous studies have shown that being overweight at midlife is associated with an increased risk of developing Alzheimer’s. Now researchers have found that it also predicts occurrence at a younger age. Scientists studied 1,394 cognitively normal people, average age around 60, following them for an average of 14 years. During the study, 142 developed Alzheimer’s. After controlling for age, race, level of education and cardiovascular risk factors, they found that each unit increase in B.M.I., or body mass index, at age 50 was associated with a 6.7-month decrease in the age of onset of Alzheimer’s. The study, in Molecular Psychiatry, also found an association of higher B.M.I. with larger deposits of neurofibrillary tangles on autopsy, one of the characteristics of brain damage in Alzheimer’s disease. “Age of onset is not as well studied as risk,” said the senior author, Dr. Madhav Thambisetty, a neurologist at the National Institute on Aging. “As we try to cure Alzheimer’s disease, we also want to delay the onset of symptoms. Until we know what factors accelerate onset, we won’t be able to test any potential interventions. And that is perhaps as important as the search for treatment.” © 2015 The New York Times Company
By Melinda Wenner Moyer A worrisome new study caught my eye last week as I perused the website of the journal Pediatrics. It was titled “Cognition and Brain Structure Following Early Childhood Surgery With Anesthesia.” Considering that my now 4-year-old underwent general anesthesia for a minor procedure when he was 2 and that my 14-month-old may be a candidate for ear tube surgery, my interest was immediately piqued. I clicked through and came face to face with a whole lot of yuck. The first sentence alone made me gasp: “Anesthetics induce widespread cell death, permanent neuronal deletion, and neurocognitive impairment in immature animals, raising substantial concerns about similar effects occurring in young children.” Wait, so anesthesia causes brain damage? Why didn’t anyone tell me? I thought. Obviously, I needed to know more. Considering that 6 million American children—including 1.5 million babies under the age of 1—undergo general anesthesia each year, this seemed like a pretty serious issue to delve into. Twenty studies and several phone calls later, I’m feeling a lot better about my kids’ brains. There are still many things scientists don’t know about how anesthesia affects the nervous system, in part because they can’t ethically do the types of experiments that would provide clear answers, like unnecessarily exposing kids to anesthesia. But based on the research that does exist, there’s really no need for parents to freak out. If “going under” has an effect on the developing brain, it’s likely to be very small. Even Andreas Loepke, the pediatric anesthesiologist at Cincinnati Children’s Hospital Medical Center who co-authored the Pediatrics paper, was reassuring to me over the phone. “These are theoretical concerns,” he said. © 2015 The Slate Group LLC.
In 1938, an Austrian pediatrician named Hans Asperger gave the first public talk on autism in history. Asperger was speaking to an audience of Nazis, and he feared that his patients — children who fell onto what we now call the autism spectrum — were in danger of being sent to Nazi extermination camps. As Asperger spoke, he highlighted his "most promising" patients, a notion that would stick with the autistic spectrum for decades to come. "That is where the idea of so-called high-functioning versus low-functioning autistic people comes from really — it comes from Asperger's attempt to save the lives of the children in his clinic," science writer Steve Silberman tells Fresh Air's Terry Gross. Silberman chronicles the history of autism and examines some of the myths surrounding our current understanding of the condition in his new book, NeuroTribes. Along the way, he revisits Asperger's calculated efforts to save his patients. Steve Silberman's articles have been published in Wired, The New Yorker, Nature and Salon. Silberman shies away from using the terms high-functioning and low-functioning, because "both of those terms can be off base," he says. But he praises Asperger's courage in speaking to the Nazis. "I would literally weep while I was writing that chapter," he says. NeuroTribes also explores how a 1987 expansion of the medical definition of autism (which was previously much narrower and led to less frequent diagnoses) contributed to the perception that there was an autism epidemic. © 2015 NPR
Link ID: 21378 - Posted: 09.03.2015
By Jennifer Couzin-Frankel Some rare diseases pull researchers in and don’t let them go, and the unusual bone condition called fibrodysplasia ossificans progressiva (FOP) has long had its hooks in Aris Economides. “The minute you experience it it’s impossible to step back and forget it,” says the functional geneticist who runs the skeletal disease program at Regeneron Pharmaceuticals in Tarrytown, New York. “It’s devastating in the most profound way.” The few thousand or so people with FOP worldwide live with grueling uncertainty: Some of their muscles or other soft tissues periodically, and abruptly, transform into new bone that permanently immobilizes parts of their bodies. Joints such as elbows or ankles may become frozen in place; jaw motion can be impeded and the rib cage fixed, making eating or even breathing difficult. Twenty years after he first stumbled on FOP, Economides and his colleagues report today that the gene mutation shared by 97% of people with the disease can trigger its symptoms in a manner different than had been assumed—through a single molecule not previously eyed as a suspect. And by sheer chance, Regeneron had a treatment for this particular target in its freezers. The company tested that potential therapy, a type of protein known as a monoclonal antibody, on mice with their own form of FOP and lo and behold, they stopped growing unwelcome new bone. © 2015 American Association for the Advancement of Science.
Aftab Ali People who were born prematurely are less intelligent later on in life and earn less money as a result, according to a new study by the University of Warwick. Researchers at the Coventry-based institution said they found a link which connects pre-term birth with low reading and, in particular, maths skills which affect the amount of wealth accumulated as adults. Funded by the Nuffield Foundation, the researchers examined data from two other large studies, following children born more than a decade apart, with one group from 1958 and the other from 1970. In total, more than 15,000 individuals were surveyed – which recruited all children born in a single week in England, Scotland, and Wales. Data were examined for all individuals who were born at between 28 and 42 weeks gestational age, and who had available wealth information at the age of 42. Those participants who were born pre-term – at less than 37 weeks – were compared with those who were born full-term to find both groups’ mathematical ability in childhood had a direct effect on how much they earned as an adult, regardless of later educational qualifications. In order to measure adult wealth, the researchers looked at factors including: family income and social class, housing and employment status, and their own perceptions of their financial situation. In regards to academic abilities, they examined: validated measures for mathematics, reading, and intelligence, along with ratings from teachers and parents. © independent.co.uk
By Gretchen Reynolds At the age of 93, Olga Kotelko — one of the most successful and acclaimed nonagenarian track-and-field athletes in history — traveled to the University of Illinois to let scientists study her brain. Ms. Kotelko held a number of world records and had won hundreds of gold medals in masters events. But she was of particular interest to the scientific community because she hadn’t begun serious athletic training until age 77. So scanning her brain could potentially show scientists what late-life exercise might do for brains. Ms. Kotelko died last year at the age of 95, but the results of that summer brain scan were published last month in Neurocase. And indeed, Ms. Kotelko’s brain looked quite different from those of other volunteers aged 90-plus who participated in the study, the scans showed. The white matter of her brain — the cells that connect neurons and help to transmit messages from one part of the brain to another — showed fewer abnormalities than the brains of other people her age. And her hippocampus, a portion of the brain involved in memory, was larger than that of similarly aged volunteers (although it was somewhat shrunken in comparison to the brains of volunteers decades younger than her). Over all, her brain seemed younger than her age. But because the scientists didn’t have a scan showing Ms. Kotelko’s brain before she began training, it’s impossible to know whether becoming an athlete late in life improved her brain’s health or whether her naturally healthy brain allowed her to become a stellar masters athlete. © 2015 The New York Times Company
An experimental gene therapy reduces the rate at which nerve cells in the brains of Alzheimer’s patients degenerate and die, according to new results from a small clinical trial, published in the current issue of the journal JAMA Neurology. Targeted injection of the Nerve Growth Factor gene into the patients’ brains rescued dying cells around the injection site, enhancing their growth and inducing them to sprout new fibres. In some cases, these beneficial effects persisted for 10 years after the therapy was first delivered. Alzheimer’s is the world’s leading form of dementia, affecting an estimated 47 million people worldwide. This figure is predicted to almost double every 20 years, with much of this increase is likely to be in the developing world. And despite the huge amounts of time, effort, and money devoted to developing an effective cure, the vast majority of new drugs have failed in clinical trials. The new results are preliminary findings from the very first human trials designed to test the potential benefits of nerve growth factor (NGF) gene therapy for Alzheimer’s patients. NGF was discovered in the 1940s by Rita Levi-Montalcini, who convincingly demonstrated that the small protein promotes the survival of certain sub-types of sensory neurons during development of the nervous system. Since then, others have shown that it also promotes the survival of acetylcholine-producing cells in the basal forebrain, which die off in Alzheimer’s. © 2015 Guardian News and Media Limited
By Dina Fine Maron Whenever the fictional character Popeye the Sailor Man managed to down a can of spinach, the results were almost instantaneous: he gained superhuman strength. Devouring any solid object similarly did the trick for one of the X-Men. As we age and begin to struggle with memory problems, many of us would love to reach for an edible mental fix. Sadly, such supernatural effects remain fantastical. Yet making the right food choices may well yield more modest gains. A growing body of evidence suggests that adopting the Mediterranean diet, or one much like it, can help slow memory loss as people age. The diet's hallmarks include lots of fruits and vegetables and whole grains (as opposed to ultrarefined ones) and a moderate intake of fish, poultry and red wine. Dining mainly on single ingredients, such as pumpkin seeds or blueberries, however, will not do the trick. What is more, this diet approach appears to reap brain benefits even when adopted later in life—sometimes aiding cognition in as little as two years. “You will not be Superman or Superwoman,” says Miguel A. Martínez González, chair of the department of preventive medicine at the University of Navarra in Barcelona. “You can keep your cognitive abilities or even improve them slightly, but diet is not magic.” Those small gains, however, can be meaningful in day-to-day life. Scientists long believed that altering diet could not improve memory. But evidence to the contrary started to emerge about 10 years ago. © 2015 Scientific American
Link ID: 21350 - Posted: 08.28.2015
By Emily Underwood It is famous for robbing Lou Gehrig of his life and Stephen Hawking of his mobility and voice, but just how amyotrophic lateral sclerosis (ALS) destroys motor neurons in the brain and spinal cord remains a mystery. Now, scientists are converging on an explanation, at least for a fraction of the ALS cases caused by a specific mutation. In cells with the mutation, the new work shows, pores in the membrane separating the nucleus and cytoplasm become clogged, preventing vital molecules from passing through and creating a fatal cellular traffic jam. For now, the work applies only to the mutation dubbed C9orf72—a DNA stutter in which a short nucleotide sequence, GGGGCC, is repeated hundreds to thousands of times in a gene on chromosome 9. Nor do the multiple labs reporting results this week agree on exactly what plugs those nuclear pores and how the cells die. Still, the work is “a major breakthrough” in ALS research, says Amelie Gubitz, program director of the neurodegeneration division at the National Institute of Neurological Disorders in Bethesda, Maryland. The groups worked independently, starting with different hypotheses and experimental designs, yet reached similar conclusions, making the finding more convincing. And it suggests that boosting traffic through nuclear pores could be a new strategy for treating some cases of ALS and frontotemporal dementia (FTD), another neurodegenerative condition C9orf72 can cause. Based on past work by their own and other groups, neuroscientists Jeff Rothstein and Tom Lloyd at Johns Hopkins University in Baltimore, Maryland, suspected that the long strands of excess RNA produced by C9orf72 cause neurodegeneration by binding to, and thus sequestering, key cellular proteins. The team tested the idea in fruit flies with the mutation, which display damage in the nerve cells of their eyes and in motor neurons. © 2015 American Association for the Advancement of Science
By Elizabeth Kolbert C57BL/6J mice are black, with pink ears and long pink tails. Inbred for the purposes of experimentation, they exhibit a number of infelicitous traits, including a susceptibility to obesity, a taste for morphine, and a tendency to nibble off their cage mates’ hair. They’re also tipplers. Given access to ethanol, C57BL/6J mice routinely suck away until the point that, were they to get behind the wheel of a Stuart Little-size roadster, they’d get pulled over for D.U.I. Not long ago, a team of researchers at Temple University decided to take advantage of C57BL/6Js’ bad habits to test a hunch. They gathered eighty-six mice and placed them in Plexiglas cages, either singly or in groups of three. Then they spiked the water with ethanol and videotaped the results. Half of the test mice were four weeks old, which, in murine terms, qualifies them as adolescents. The other half were twelve-week-old adults. When the researchers watched the videos, they found that the youngsters had, on average, outdrunk their elders. More striking still was the pattern of consumption. Young male C57BL/6Js who were alone drank roughly the same amount as adult males. But adolescent males with cage mates went on a bender; they spent, on average, twice as much time drinking as solo boy mice and about thirty per cent more time than solo girls. The researchers published the results in the journal Developmental Science. In their paper, they noted that it was “not possible” to conduct a similar study on human adolescents, owing to the obvious ethical concerns. But, of course, similar experiments are performed all the time, under far less controlled circumstances. Just ask any college dean. Or ask a teen-ager.
While some research suggests that a diet high in omega-3 fatty acids can protect brain health, a large clinical trial by researchers at the National Institutes of Health found that omega-3 supplements did not slow cognitive decline in older persons. With 4,000 patients followed over a five-year period, the study is one of the largest and longest of its kind. It was published today in the Journal of the American Medical Association. “Contrary to popular belief, we didn’t see any benefit of omega-3 supplements for stopping cognitive decline,” said Emily Chew, M.D., . Dr. Chew leads the Age-Related Eye Disease Study (AREDS), which was designed to investigate a combination of nutritional supplements for slowing age-related macular degeneration (AMD), a major cause of vision loss among older Americans. That study established that daily high doses of certain antioxidants and minerals — called the AREDS formulation — can help slow the progression to advanced AMD. A later study, called AREDS2, tested the addition of omega-3 fatty acids to the AREDS formula. But the omega-3’s made no difference. Omega-3 fatty acids are made by marine algae and are concentrated in fish oils; they are believed to be responsible for the health benefits associated with regularly eating fish, such as salmon, tuna, and halibut.*Where studies have surveyed people on their dietary habits and health, they’ve found that regular consumption of fish is associated with lower rates of AMD, cardiovascular disease, and possibly dementia. “We’ve seen data that eating foods with omega-3 may have a benefit for eye, brain, and heart health,” Dr. Chew explained.
Link ID: 21340 - Posted: 08.26.2015
Helen Thomson Genetic changes stemming from the trauma suffered by Holocaust survivors are capable of being passed on to their children, the clearest sign yet that one person’s life experience can affect subsequent generations. The conclusion from a research team at New York’s Mount Sinai hospital led by Rachel Yehuda stems from the genetic study of 32 Jewish men and women who had either been interned in a Nazi concentration camp, witnessed or experienced torture or who had had to hide during the second world war. They also analysed the genes of their children, who are known to have increased likelihood of stress disorders, and compared the results with Jewish families who were living outside of Europe during the war. “The gene changes in the children could only be attributed to Holocaust exposure in the parents,” said Yehuda. Her team’s work is the clearest example in humans of the transmission of trauma to a child via what is called “epigenetic inheritance” - the idea that environmental influences such as smoking, diet and stress can affect the genes of your children and possibly even grandchildren. The idea is controversial, as scientific convention states that genes contained in DNA are the only way to transmit biological information between generations. However, our genes are modified by the environment all the time, through chemical tags that attach themselves to our DNA, switching genes on and off. Recent studies suggest that some of these tags might somehow be passed through generations, meaning our environment could have and impact on our children’s health. © 2015 Guardian News and Media Limited
Almost fully-formed brain grown in a lab. Woah: Scientists grow first nearly fully-formed human brain. Boffins raise five-week-old fetal human brain in the lab for experimentation. On Tuesday, all the above appeared as headlines for one particular story. What was it all about? Mini-brains 3 to 4 millimetres across have been grown in the lab before, but if a larger brain had been created – and the press release publicising the claim said it was the size of a pencil eraser – that would be a major breakthrough. New Scientist investigated the claims. The announcement was made by Rene Anand, a neuroscientist at Ohio State University in Columbus, at a military health research meeting in Florida. Anand says he has grown a brain – complete with a cortex, midbrain and brainstem – in a dish, comparable in maturity to that of a fetus aged 5 weeks. Anand and his colleague Susan McKay started with human skin cells, which they turned into induced pluripotent stem cells (iPSCs) using a tried-and-tested method. By applying an undisclosed technique, one that a patent has been applied for, the pair say they were able to encourage these stem cells to form a brain. “We are replicating normal development,” says Anand. He says they hope to be able to create miniature models of brains experiencing a range of diseases, such as Parkinson’s and Alzheimer’s. Inconclusive evidence But not everyone is convinced, especially as Anand hasn’t published his results. Scientists we sent Anand’s poster presentation to said that although the team has indeed grown some kind of miniature collection of cells, or “organoid”, in a dish, the structure isn’t much like a fetal brain. © Copyright Reed Business Information Ltd.
Keyword: Development of the Brain
Link ID: 21322 - Posted: 08.22.2015
Tina Hesman Saey Researchers have discovered a “genetic switch” that determines whether people will burn extra calories or save them as fat. A genetic variant tightly linked to obesity causes fat-producing cells to become energy-storing white fat cells instead of energy-burning beige fat, researchers report online August 19 in the New England Journal of Medicine. Previously scientists thought that the variant, in a gene known as FTO (originally called fatso), worked in the brain to increase appetite. The new work shows that the FTO gene itself has nothing to do with obesity, says coauthor Manolis Kellis, a computational biologist at MIT and the Broad Institute. But the work may point to a new way to control body fat. In humans and many other organisms, genes are interrupted by stretches of DNA known as introns. Kellis and Melina Claussnitzer of Harvard Medical School and colleagues discovered that a genetic variant linked to increased risk of obesity affects one of the introns in the FTO gene. It does not change the protein produced from the FTO gene or change the gene’s activity. Instead, the variant doubles the activity of two genes, IRX3 and IRX5, which are involved in determining which kind of fat cells will be produced. FTO’s intron is an enhancer, a stretch of DNA needed to control activity of far-away genes, the researchers discovered. Normally, a protein called ARID5B squats on the enhancer and prevents it from dialing up activity of the fat-determining genes. In fat cells of people who have the obesity-risk variant, ARID5B can’t do its job and the IRX genes crank up production of energy-storing white fat. © Society for Science & the Public 2000 - 2015.
Helen Thomson An almost fully-formed human brain has been grown in a lab for the first time, claim scientists from Ohio State University. The team behind the feat hope the brain could transform our understanding of neurological disease. Though not conscious the miniature brain, which resembles that of a five-week-old foetus, could potentially be useful for scientists who want to study the progression of developmental diseases. It could also be used to test drugs for conditions such as Alzheimer’s and Parkinson’s, since the regions they affect are in place during an early stage of brain development. The brain, which is about the size of a pencil eraser, is engineered from adult human skin cells and is the most complete human brain model yet developed, claimed Rene Anand of Ohio State University, Columbus, who presented the work today at the Military Health System Research Symposium in Fort Lauderdale, Florida. Previous attempts at growing whole brains have at best achieved mini-organs that resemble those of nine-week-old foetuses, although these “cerebral organoids” were not complete and only contained certain aspects of the brain. “We have grown the entire brain from the get-go,” said Anand. Anand and his colleagues claim to have reproduced 99% of the brain’s diverse cell types and genes. They say their brain also contains a spinal cord, signalling circuitry and even a retina. The ethical concerns were non-existent, said Anand. “We don’t have any sensory stimuli entering the brain. This brain is not thinking in any way.” © 2015 Guardian News and Media Limited
Keyword: Development of the Brain
Link ID: 21316 - Posted: 08.19.2015
—By Chris Mooney It is still considered highly uncool to ascribe a person's political beliefs, even in part, to that person's biology: hormones, physiological responses, even brain structures and genes. And no wonder: Doing so raises all kinds of thorny, non-PC issues involving free will, determinism, toleration, and much else. There's just one problem: Published scientific research keeps going there, with ever increasing audacity (not to mention growing stacks of data). The past two weeks have seen not one but two studies published in scientific journals on the biological underpinnings of political ideology. And these studies go straight at the role of genes and the brain in shaping our views, and even our votes. First, in the American Journal of Political Science, a team of researchers including Peter Hatemi of Penn State University and Rose McDermott of Brown University studied the relationship between our deep-seated tendencies to experience fear—tendencies that vary from person to person, partly for reasons that seem rooted in our genes—and our political beliefs. What they found is that people who have more fearful disposition also tend to be more politically conservative, and less tolerant of immigrants and people of races different from their own. As McDermott carefully emphasizes, that does not mean that every conservative has a high fear disposition. "It's not that conservative people are more fearful, it's that fearful people are more conservative," as she puts it. I interviewed the paper's lead author, Peter Hatemi, about his research for my 2012 book The Republican Brain. Hatemi is both a political scientist and also a microbiologist, and as he stressed to me, "nothing is all genes, or all environment." These forces combine to make us who we are, in incredibly intricate ways. ©2015 Mother Jones