Chapter 7. Life-Span Development of the Brain and Behavior
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Ewen Callaway Researchers found 69 genes that correlate with higher educational attainment — and three of those also also appear to have a direct link to slightly better cognitive abilities. Scientists looking for the genes underlying intelligence are in for a slog. One of the largest, most rigorous genetic study of human cognition1 has turned up inconclusive findings, and experts concede that they will probably need to scour the genomes of more than 1 million people to confidently identify even a small genetic influence on intelligence and other behavioural traits. Studies of twins have repeatedly confirmed a genetic basis for intelligence, personality and other aspects of behaviour. But efforts to link IQ to specific variations in DNA have led to a slew of irreproducible results. Critics have alleged that some of these studies' methods were marred by wishful thinking and shoddy statistics. A sobering editorial in the January 2012 issue of Behavior Genetics2 declared that “it now seems likely that many of the published findings of the last decade are wrong or misleading and have not contributed to real advances in knowledge”. In 2011, an international collaboration of researchers launched an effort to bring more rigour to studies of how genes contribute to behaviour. The group, called the Social Sciences Genetic Association Consortium, aimed to do studies using practices borrowed from the medical genetics community, which emphasizes large numbers of participants, rigorous statistics and reproducibility. In a 2013 study3 comparing the genomes of more than 126,000 people, the group identified three gene variants associated with with how many years of schooling a person had gone through or whether they had attended university. But the effect of these variants was small — each variant correlated with roughly one additional month of schooling in people who had it compared with people who did not. © 2014 Nature Publishing Group
By C. CLAIBORNE RAY Q. Is there a difference between alcoholic dementia and “regular” dementia in the elderly? A. Dementia refers to the general category of diseases that cause acquired cognitive loss, usually in later life, said Dr. Mark S. Lachs, director of geriatrics for the NewYork-Presbyterian Healthcare System. Such loss has scores of possible causes, he said, but Alzheimer’s disease is the culprit in a vast majority of cases in the developed world. Alzheimer’s and what doctors call alcohol-related dementia affect parts of the brain cortex that control memory, language and the ability to follow motor commands. Because Alzheimer’s and excessive drinking are relatively common in the older population and can occur at the same time, and because many of their clinical features overlap and affect similar parts of the brain, “it is more accurate to say that each condition potentially exacerbates the other,” Dr. Lachs said. Abstinence is the treatment of choice in alcohol-related dementia, with or without concurrent Alzheimer’s disease or another form of dementia. Even in patients with “pure” Alzheimer’s disease or another kind of dementia, Dr. Lachs said, most experts recommend greatly moderating alcohol consumption or eliminating it, as even occasional drinking “can serve as a brain stress test for a patient with impaired cognition from any cause.” © 2014 The New York Times Company
By Maggie Fox, Erika Edwards and Judy Silverman Here’s how you might be able to turn autism around in a baby: Carefully watch her cues, and push just a little harder with that game of peek-a-boo or “This little piggy.” But don’t push too hard — kids with autism are super-sensitive. That’s what Sally Rogers of the University of California, Davis has found in an intense experiment with the parents of infants who showed clear signs of autism. It’s one of the most hopeful signs yet that if you diagnose autism very early, you can help children rewire their brains and reverse the symptoms. It was a small study, and it’s very hard to find infants who are likely to have autism, which is usually diagnosed in the toddler years. But the findings, published in the Journal of Autism and Developmental Disorders, offer some hope to parents worried about their babies. “With only seven infants in the treatment group, no conclusions can be drawn,” they wrote. However, the effects were striking. Six out of the seven children in the study had normal learning and language skills by the time they were 2 to 3. Isobel was one of them. “She is 3 years old now and she is a 100 percent typical, normally developing child,” her mother, Megan, told NBC News. The family doesn’t want their last name used for privacy reasons. “We don’t have to do the therapy any more. It literally rewired her brain.” Autism is a very common diagnosis for children in the U.S. The latest survey by the Centers for Disease Control and Prevention shows a startling 30 percent jump among 8-year-olds diagnosed with the disorder in a two-year period, to one in every 68 children.
Link ID: 20047 - Posted: 09.09.2014
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. The area of inquiry has been growing in part because of a push by female Alzheimer’s researchers, who have formed a group to advocate for a larger leadership role in the field and more gender-specific research.
By Kate Wong In 1871 Charles Darwin surmised that humans were evolutionarily closer to the African apes than to any other species alive. The recent sequencing of the gorilla, chimpanzee and bonobo genomes confirms that supposition and provides a clearer view of how we are connected: chimps and bonobos in particular take pride of place as our nearest living relatives, sharing approximately 99 percent of our DNA, with gorillas trailing at 98 percent. Yet that tiny portion of unshared DNA makes a world of difference: it gives us, for instance, our bipedal stance and the ability to plan missions to Mars. Scientists do not yet know how most of the DNA that is uniquely ours affects gene function. But they can conduct whole-genome analyses—with intriguing results. For example, comparing the 33 percent of our genome that codes for proteins with our relatives' genomes reveals that although the sum total of our genetic differences is small, the individual differences pervade the genome, affecting each of our chromosomes in numerous ways. © 2014 Scientific American
By RONI CARYN RABIN Pregnant women often go to great lengths to give their babies a healthy start in life. They quit smoking, skip the chardonnay, switch to decaf, forgo aspirin. They say no to swordfish and politely decline Brie. Yet they rarely wean themselves from popular selective serotonin reuptake inhibitor antidepressants like Prozac, Celexa and Zoloft despite an increasing number of studies linking prenatal exposure to birth defects, complications after birth and even developmental delays and autism. Up to 14 percent of pregnant women take antidepressants, and the Food and Drug Administration has issued strong warnings that one of them, paroxetine (Paxil), may cause birth defects. But the prevailing attitude among doctors has been that depression during pregnancy is more dangerous to mother and child than any drug could be. Now a growing number of critics are challenging that assumption. “If antidepressants made such a big difference, and women on them were eating better, sleeping better and taking better care of themselves, then one would expect to see better birth outcomes among the women who took medication than among similar women who did not,” said Barbara Mintzes, an associate professor at the University of British Columbia School of Population and Public Health. “What’s striking is that there’s no research evidence showing that.” On the contrary, she said, “when you look for it, all you find are harms.” S.S.R.I.s are believed to work in part by blocking reabsorption (or reuptake) of serotonin, altering levels of this important neurotransmitter in the brain and elsewhere in the body. Taken by a pregnant woman, the drugs cross the placental barrier, affecting the fetus. © 2014 The New York Times Company
Moheb Costandi Autism can be baffling, appearing in various forms and guises and thwarting our best attempts to understand the minds of people affected by it. Anything we know for sure about the disorder can probably be traced back to the pioneering research of the developmental psychologist Uta Frith. Frith was the first to propose that people with autism lack theory of mind, the ability to attribute beliefs, intentions and desires to others. She also recognized the superior perceptual abilities of many with the disorder — and their tendency to be unable to see the forest for the trees. Frith, now affiliated with the Institute of Cognitive Neuroscience at University College London (UCL), has shaped autism research for an entire generation of investigators. Meanwhile, her husband Chris Frith formulated a new view of schizophrenia, a mental illness marked by hallucinations, disordered thinking and apathy. His work explored how the disorder affects the experience of agency, the sense that we are in control of our bodies and responsible for our actions. And his innovations in brain imaging helped researchers examine the relationship between brain and mind. Independently, husband and wife explored the social and cognitive aspects of these psychiatric disorders. Together, they helped lay the foundations of cognitive neuroscience, the discipline that seeks to understand the biological basis of thought processes. Trevor Robbins, a cognitive neuroscientist at the University of Cambridge in the U.K., calls them “tremendously influential pioneers,” in particular because both brought a social perspective to cognitive neuroscience. © Copyright 2014 Simons Foundation
Link ID: 20019 - Posted: 09.02.2014
By JAMIE EDGIN and FABIAN FERNANDEZ LAST week the biologist Richard Dawkins sparked controversy when, in response to a woman’s hypothetical question about whether to carry to term a child with Down syndrome, he wrote on Twitter: “Abort it and try again. It would be immoral to bring it into the world if you have the choice.” In further statements, Mr. Dawkins suggested that his view was rooted in the moral principle of reducing overall suffering whenever possible — in this case, that of individuals born with Down syndrome and their families. But Mr. Dawkins’s argument is flawed. Not because his moral reasoning is wrong, necessarily (that is a question for another day), but because his understanding of the facts is mistaken. Recent research indicates that individuals with Down syndrome can experience more happiness and potential for success than Mr. Dawkins seems to appreciate. There are, of course, many challenges facing families caring for children with Down syndrome, including a high likelihood that their children will face surgery in infancy and Alzheimer’s disease in adulthood. But at the same time, studies have suggested that families of these children show levels of well-being that are often greater than those of families with children with other developmental disabilities, and sometimes equivalent to those of families with nondisabled children. These effects are prevalent enough to have been coined the “Down syndrome advantage.” In 2010, researchers reported that parents of preschoolers with Down syndrome experienced lower levels of stress than parents of preschoolers with autism. In 2007, researchers found that the divorce rate in families with a child with Down syndrome was lower on average than that in families with a child with other congenital abnormalities and in those with a nondisabled child. © 2014 The New York Times Company
|By Michael Leon I had been working quite happily on the basic biology of the brain when a good friend of mine called for advice about his daughter, who had just been diagnosed with autism. I could hear the anguish and fear in his voice when he asked me whether there was anything that could be done to make her better. I told him about the standard-care therapies, including Intensive Behavioral Intervention, Early Intensive Behavioral Intervention, Applied Behavior Analysis, and the Early Start Denver Model (ESDM). These therapies also are expensive, time-consuming and have variable outcomes, with the best outcomes seen for ESDM. There are, however, few ESDM therapists, and the cost of such intensive therapy can be quite high. Moreover, my friend’s daughter was already past the age of the oldest children in the study that demonstrated the efficacy of ESDM. My feeling was that there was a good chance that there was an effective therapy for her using a simple, inexpensive at-home approach involving daily exposure to a wide variety of sensory stimulation. This is a partial list of the disorders whose symptoms can be greatly reduced, or even completely reversed, with what is known as “environmental enrichment”: Autism Stroke Seizures Brain damage Neuronal death during aging ADHD Prenatal alcohol syndrome Lead exposure Multiple sclerosis Addiction Schizophrenia Memory loss Huntington’s disease Parkinson’s disease Alzheimer’s disease Down syndrome Depression But why haven’t you heard about this? The reason is that all of these disorders that have been successfully treated only in animal models of these neurological problems. However, the effects seen in lab animals can be dramatic. © 2014 Scientific American,
|By Roni Jacobson Children are notoriously unreliable witnesses. Conventional wisdom holds that they frequently “remember” things that never happened. Yet a large body of research indicates that adults actually generate more false memories than children. Now a new study finds that children are just as susceptible to false memories as adults, if not more so. Scientists may simply have been using the wrong test. Traditionally, researchers have explored false memories by presenting test subjects with a list of associated words (for instance, “weep,” “sorrow” and “wet”) thematically related to a word not on the list (in this case, “cry”) and then asking them what words they remember. Adults typically mention the missing related word more often than children do—possibly because their life experiences enable them to draw associations between concepts more readily, says Henry Otgaar, a forensic psychologist at Maastricht University in the Netherlands and co-author of the new paper, published in May in the Journal of Experimental Child Psychology. Instead of using word lists to investigate false memories, Otgaar and his colleagues showed participants pictures of scenes, including a classroom, a funeral and a beach. After a short break, they asked those participants whether they remembered seeing certain objects in each picture. Across three experiments, seven- and eight-year-old children consistently reported seeing more objects that were not in the pictures than adults did. © 2014 Scientific American
By Priyanka Pulla Humans are late bloomers when compared with other primates—they spend almost twice as long in childhood and adolescence as chimps, gibbons, or macaques do. But why? One widely accepted but hard-to-test theory is that children’s brains consume so much energy that they divert glucose from the rest of the body, slowing growth. Now, a clever study of glucose uptake and body growth in children confirms this “expensive tissue” hypothesis. Previous studies have shown that our brains guzzle between 44% and 87% of the total energy consumed by our resting bodies during infancy and childhood. Could that be why we take so long to grow up? One way to find out is with more precise studies of brain metabolism throughout childhood, but those studies don’t exist yet. However, a new study published online today in the Proceedings of the National Academy of Sciences (PNAS) spliced together three older data sets to provide a test of this hypothesis. First, the researchers used a 1987 study of PET scans of 36 people between infancy and 30 years of age to estimate age trends in glucose uptake by three major sections of the brain. Then, to calculate how uptake varied for the entire brain, they combined that data with the brain volumes and ages of 400 individuals between 4.5 years of age and adulthood, gathered from a National Institutes of Health study and others. Finally, to link age and brain glucose uptake to body size, they used an age series of brain and body weights of 1000 individuals from birth to adulthood, gathered in 1978. © 2014 American Association for the Advancement of Science.
By DAVID LEVINE MONTREAL — When twins have similar personalities, is it mainly because they share so much genetic material or because their physical resemblance makes other people treat them alike? Most researchers believe the former, but the proposition has been hard to prove. So Nancy L. Segal, a psychologist who directs the Twin Studies Center at California State University, Fullerton, decided to test it — and enlisted an unlikely ally. He is François Brunelle, a photographer in Montreal who takes pictures of pairs of people who look alike but are not twins. Dr. Segal was sent to Mr. Brunelle’s website by a graduate student who knew of her research with twins. When she saw the photographs, she realized that the unrelated look-alikes would be ideal study subjects: She could compare their similarities and differences to those of actual twins. “I reasoned that if personality resides in the face,” she said, “then unrelated look-alikes should be as similar in behavior as identical twins reared apart. Alternatively, if personality traits are influenced by genetic factors, then unrelated look-alikes should show negligible personality similarity.” For 14 years, Mr. Brunelle, 64, has been working on a project he calls “I’m Not a Look-Alike!”: more than 200 black-and-white portraits of pairs who do, in fact, look startlingly alike. “I originally named the project ‘Look-Alikes,’ but I felt it was boring and some of the subjects did not feel they looked alike,” he said. “The new name gives ownership to the people I photographed and allows viewers of my website to decide for themselves if the people look alike or not.” Most come to him through social media links to his website. “It has taken on a life of its own,” he said. “I have heard from people in China — and even a man who has an uncle in Uzbekistan who is a dead ringer for former President George W. Bush.” © 2014 The New York Times Company
Keyword: Genes & Behavior
Link ID: 19997 - Posted: 08.26.2014
|By Mark Fischetti Parents, students and teachers often argue, with little evidence, about whether U.S. high schools begin too early in the morning. In the past three years, however, scientific studies have piled up, and they all lead to the same conclusion: a later start time improves learning. And the later the start, the better. Biological research shows that circadian rhythms shift during the teen years, pushing boys and girls to stay up later at night and sleep later into the morning. The phase shift, driven by a change in melatonin in the brain, begins around age 13, gets stronger by ages 15 and 16, and peaks at ages 17, 18 or 19. Does that affect learning? It does, according to Kyla Wahlstrom, director of the Center for Applied Research and Educational Improvement at the University of Minnesota. She published a large study in February that tracked more than 9,000 students in eight public high schools in Minnesota, Colorado and Wyoming. After one semester, when school began at 8:35 a.m. or later, grades earned in math, English, science and social studies typically rose a quarter step—for example, up halfway from B to B+. Two journal articles that Wahlstrom has reviewed but have not yet been published reach similar conclusions. So did a controlled experiment completed by the U.S. Air Force Academy, which required different sets of cadets to begin at different times during their freshman year. A 2012 study of North Carolina school districts that varied school times because of transportation problems showed that later start times correlated with higher scores in math and reading. Still other studies indicate that delaying start times raises attendance, lowers depression rates and reduces car crashes among teens, all because they are getting more of the extra sleep they need. © 2014 Scientific American
By PAM BELLUCK As a baby’s brain develops, there is an explosion of synapses, the connections that allow neurons to send and receive signals. But during childhood and adolescence, the brain needs to start pruning those synapses, limiting their number so different brain areas can develop specific functions and are not overloaded with stimuli. Now a new study suggests that in children with autism, something in the process goes awry, leaving an oversupply of synapses in at least some parts of the brain. The finding provides clues to how autism develops from childhood on, and may help explain some symptoms like oversensitivity to noise or social experiences, as well as why many people with autism also have epileptic seizures. It could also help scientists in the search for treatments, if they can develop safe therapies to fix the system the brain uses to clear extra synapses. The study, published Thursday in the journal Neuron, involved tissue from the brains of children and adolescents who had died from ages 2 to 20. About half had autism; the others did not. The researchers, from Columbia University Medical Center, looked closely at an area of the brain’s temporal lobe involved in social behavior and communication. Analyzing tissue from 20 of the brains, they counted spines — the tiny neuron protrusions that receive signals via synapses — and found more spines in children with autism. The scientists found that at younger ages, the number of spines did not differ tremendously between the two groups of children, but adolescents with autism had significantly more than those without autism. Typical 19-year-olds had 41 percent fewer synapses than toddlers, but those in their late teenage years with autism had only 16 percent fewer than young children with autism. © 2014 The New York Times Company
By TARA PARKER-POPE When the antidrug educator Tim Ryan talks to students, he often asks them what they know about marijuana. “It’s a plant,” is a common response. But more recently, the answer has changed. Now they reply, “It’s legal in Colorado.” These are confusing times for middle and high school students, who for most of their young lives have been lectured about the perils of substance abuse, particularly marijuana. Now it seems that the adults in their lives have done an about-face. Recreational marijuana is legal in Colorado and in Washington, and many other states have approved it for medical use. Lawmakers, the news media and even parents are debating the merits of full-scale legalization. “They are growing up in a generation where marijuana used to be bad, and maybe now it’s not bad,” said Mr. Ryan, a senior prevention specialist with FCD Educational Services, an antidrug group that works with students in the classroom. “Their parents are telling them not to do it, but they may be supporting legalization of it at the same time.” Antidrug advocates say efforts to legalize marijuana have created new challenges as they work to educate teenagers and their parents about the unique risks that alcohol, marijuana and other drugs pose to the developing teenage brain. These educators say their goal is not to vilify marijuana or take a stand on legalization; instead, they say their role is to convince young people and their parents that the use of drugs is not just a moral or legal issue, but a significant health issue. “The health risks are real,” said Steve Pasierb, the chief executive of the Partnership for Drug-Free Kids. “Every passing year, science unearths more health risks about why any form of substance use is unhealthy for young people.” © 2014 The New York Times Company
Claudia M. Gold When I hear debate over the association between SSRI’s (selective serotonin re-uptake inhibitors, a class of antidepressant medication) and suicidal behavior in children and adolescents, I am immediately brought back to a night in the early 2000's. As the covering pediatrician I was called to the emergency room to see a young man, a patient of a pediatrician in a neighboring town, who had attempted suicide by taking a nearly lethal overdose. That night, as I watched over him in the intensive care unit, I learned that he was a high achieving student and athlete who, struggling under the pressures of the college application process, had been prescribed an SSRI by his pediatrician. His parents described a transformation in his personality over the months preceding the suicide attempt that was so dramatic that I ordered a CT scan to see if he had a brain tumor. It was normal. When, in the coming years the data emerged about increasing suicidal behavior following use of SSRI's, I recognized in retrospect that his change in behavior was a result of the medication. But at the time I knew nothing of these serious side effects. At that time, coinciding with pharmaceutical industry's aggressive marketing campaign directed at the public as well as a professional audience, these drugs were becoming increasingly popular with pediatricians. As the possible serious side effects of these medications came increasingly in to awareness, the FDA issued the controversial "black box warning" that the drugs carried an increased risk of suicidal behavior. Following the black box warning, pediatricians, myself included, became reluctant to prescribe these medications. We did not have the time or experience to provide the recommended increased monitoring and close follow-up.
by Clare Wilson Figuring out how the brain works is enough to make your head spin. But now we seem to have a handle on how it gets its folded shape. The surface layer of the brain, or cortex, is also referred to as our grey matter. Mammals with larger brains have a more folded cortex, and the human brain is the most wrinkled of all, cramming as much grey matter into our skulls as possible. L. Mahadevan at Harvard University and his colleagues physically modelled how the brain develops in the embryo, using a layer of gel to stand in for the grey matter. This gel adhered to the top of a solid hemisphere of gel representing the white matter beneath. In the embryo, grey matter grows as neurons are created or others migrate to the cortex from the brain's centre. By adding a solvent to make the grey matter gel expand, the team mimicked how the cortex might grow in the developing brain. They didn't model what effect, if any, the skull would have had. Hills and valleys The team varied factors such as the stiffness of the gels and the depth of the upper layer to find a combination that led to similarly shaped wrinkles as those of the human brain, with smooth "hills" and sharply cusped "valleys". There are several theories about how the brain's folds form. These include the possibility that more neurons migrate to the hills, making them rise above the valleys, or that the valleys are pulled down by the axons – fibres that connect neurons to each other – linking highly interconnected parts of the brain together. © Copyright Reed Business Information Ltd.
Keyword: Development of the Brain
Link ID: 19974 - Posted: 08.19.2014
Sara Reardon The National Science Foundation (NSF)’s role in the Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative is starting to take shape. On 18 August, the NSF awarded 36 small grants totalling US$10.8 million to projects studying everything from electrodes that measure chemical and electronic signals to artificial intelligence programs to identify brain structures. The three agencies participating in the BRAIN Initiative have taken markedly different approaches. The Defense Advanced Research Projects Agency, which received $50 million this year for the neuroscience programme, is concentrating on prosthetics and treatments for brain disorders that affect veterans, such as post-traumatic stress disorder. It has already awarded multi-million dollar grants to several teams. The National Institutes of Health, which received $40 million this year, has put together a 146-page plan to map and observe the brain over the next decade, and will announce its first round of grant recipients next month. The NSF, by contrast, has cast a wider net. The agency sent an request in March for informal, two-page project ideas. The only criterion was that the projects somehow address the properties of neural circuits. The response was overwhelming, says James Deshler, deputy director of the NSF’s Division of Biological Infrastructure. The agency had expected to fund about 12 grants, but decided to triple that number after receiving nearly 600 applications. “People started finding money in different pockets,” Deshler says. The wide-ranging list of winning projects includes mathematical models that help computers recognize different parts and patterns in the brain, physical tools such as new types of electrodes, and other tools that integrate and link neural activity to behaviour. © 2014 Nature Publishing Group
Helen Shen For most adults, adding small numbers requires little effort, but for some children, it can take all ten fingers and a lot of time. Research published online on 17 August in Nature Neuroscience1 suggests that changes in the hippocampus — a brain area associated with memory formation — could help to explain how children eventually pick up efficient strategies for mathematics, and why some children learn more quickly than others. Vinod Menon, a developmental cognitive neuroscientist at Stanford University in California, and his colleagues presented single-digit addition problems to 28 children aged 7–9, as well as to 20 adolescents aged 14–17 and 20 young adults. Consistent with previous psychology studies2, the children relied heavily on counting out the sums, whereas adolescents and adults tended to draw on memorized information to calculate the answers. The researchers saw this developmental change begin to unfold when they tested the same children at two time points, about one year apart. As the children aged, they began to move away from counting on fingers towards memory-based strategies, as measured by their own accounts and by decreased lip and finger movements during the task. Using functional magnetic resonance imaging (fMRI) to scan the children's brains, the team observed increased activation of the hippocampus between the first and second time point. Neural activation decreased in parts of the prefrontal and parietal cortices known to be involved in counting, suggesting that the same calculations had begun to engage different neural circuits. © 2014 Nature Publishing Group
by Andy Coghlan Pioneering studies of post-mortem brain tissues have yielded the first evidence of a potential association between Alzheimer's disease and the epigenetic alteration of gene function. The researchers stress, however, that more research is needed to find out if the changes play a causal role in the disease or occur as a result of it. We already have some evidence that the risk of developing Alzheimer's might be elevated by poor diet, lack of exercise, and inflammatory conditions such as diabetes, obesity and clogging of blood vessels with fatty deposits. The new research hints that the lifestyle changes that raise Alzheimer's risk may be taking effect through epigenetic changes. The idea is strengthened by the fact that the brain tissue samples studied in the new work came from hundreds of people, many of whom had Alzheimer's when they died, and that a number of genes identified were found by two teams working independently, one in the UK and one in the US. "The results are compelling and consistent across four cohorts of patients taken across the two studies," says Jonathan Mill at the University of Exeter, who led the UK-based team. "It's illuminated new genetic pathways affecting the disease and, given the lack of success tackling Alzheimer's so far, new leads are going to be vital." "We can now focus our efforts on understanding how these genes are associated with the disease," says Philip De Jager of the Brigham and Women's Hospital in Boston, who headed the US team. © Copyright Reed Business Information Ltd.