Chapter 7. Life-Span Development of the Brain and Behavior
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By Megan Allison Diagnoses of Attention Hyperactivity Disorder are on the rise. The Centers for Disease Control and Prevention calculated that by 2011, 11 percent of children had been diagnosed with ADHD, and 6.1 percent of all US children were taking an ADHD medication. But could a solution be as simple as exercise? A study published this month in the Journal of Abnormal Child Psychology found that aerobic activity sessions before school helped children with ADHD with their moods and attention spans. The study involved a group of just over 200 students in kindergarten through second grade at schools in Indiana and Vermont. For 12 weeks, the students did 31 minutes of physical activity. The control group participated in classroom activities during this time. Although the results showed that all students showed improvement, authors noted that the exercise especially helped kids with ADHD. “It benefits all the kids, but I definitely see where it helps the kids with ADHD a lot,” said Jill Fritz, a fourth-grade teacher in Jacksonville, Fla. in an interview with The Wall Street Journal. “It really helps them get back on track and get focused.” In the Boston area, Dr. Sarah Sparrow Benes, Program Director of Physical and Health Education Programs at Boston University, teaches elementary and special educators how to use movement as a strategy in their classroom for learning. She finds that all students can benefit from exercise.
By Linda Searing THE QUESTION Benzodiazepines such as Valium, Xanax and Ativan, widely prescribed to relieve anxiety and alleviate insomnia, are known to affect memory and cognition in the short term. Might they also have a more serious, longer-term effect on the brain? THIS STUDY analyzed data on 8,990 adults older than 66, including 1,796 with Alzheimer’s disease. In a five-to-10-year span before the start of the study, 3,767 of the participants (52 percent) had taken benzodiazepines. Overall, those who had taken the drugs were 51 percent more likely to have Alzheimer’s than were those who had never taken benzodiazepines. The longer people took the drugs, the greater their risk for Alzheimer’s. Those who took the drugs for less than 90 days had essentially the same risk as those who never took them. But risk nearly doubled for people who took them for longer than six months. Risk also was greater for longer-acting vs. shorter-acting benzodiazepines. WHO MAY BE AFFECTED? Adults, especially older people, who take benzodiazepines. The drugs have a calming effect on the body and work quickly, unlike antidepressants, which can take weeks to have an effect. The American Geriatrics Society lists benzodiazepines as inappropriate for treating older people for insomnia or agitation because of their negative effect on cognition seen in that age group and an increased likelihood of falls and accidents. However, some recent estimates note that roughly half of older adults take benzodiazepines. CAVEATS Some study participants may have been prescribed benzodiazepines to treat early symptoms of unrecognized dementia, which can include depression, anxiety and sleep disorders; the study authors noted that use of the drugs “might be an early marker of a condition associated with an increased risk of dementia and not the cause.”
By ANDREW POLLACK New York State’s attorney general filed an antitrust lawsuit on Monday seeking to stop a pharmaceutical company from forcing patients with Alzheimer’s disease to switch to a new version of a widely used drug. The lawsuit contends that the switch is designed to blunt competition from low-priced generic versions of the medication. Forest Laboratories, now owned by Actavis, announced in February that it would stop selling the existing tablet form of the drug, Namenda, in favor of new extended-release capsules called Namenda XR that can be taken once a day instead of twice. While the company said that patients preferred the newer drug, it has made little secret of its desire to switch all patients to the newer form, which has a longer patent life, before the old tablets face generic competition in July. The strategy would make it much harder for the generics to gain traction. The lawsuit, filed in Federal District Court in Manhattan, says the step is an illegal attempt by Forest to maintain its monopoly even after its patent expires. “A drug company manipulating vulnerable patients and forcing physicians to alter treatment plans unnecessarily, simply to protect corporate profits, is unethical and illegal,” the attorney general, Eric T. Schneiderman, said in a statement. A spokesman for Actavis said the company did not comment on pending litigation as a matter of policy. The company said that the once-a-day drug had “significant advantages” for patients and their caregivers. The lawsuit argues that the benefit of switching is not very great. It says the company decided to force the switch because it feared that not enough patients would switch voluntarily. © 2014 The New York Times Company
Link ID: 20078 - Posted: 09.16.2014
by Michael Slezak It's one of the biggest mysteries of Alzheimer's. The disease is associated with the formation of protein plaques in the brain, but why is it that some people with plaques seem not to have the disease? Research suggests that some people's brains are able to reorganise during the early stages of Alzheimer's, delaying the appearance of initial symptoms. The plaques in question are small mounds of a protein called beta-amyloid, and are found in the brains of people with Alzheimer's disease. Whether these plaques are a cause of the disease has been hotly debated. One reason for doubt is the appearance of plaques in many older people who have no symptoms Movie Cameraof dementia at all. Using fMRI to measure changes in blood flow around the brain, William Jagust from the University of California in Berkley and colleagues compared brain function in three groups of people without symptoms of dementia: 22 young people, 16 older people with beta-amyloid plaques and 33 older people without the plaques. He asked each of them to memorise a photographed scene while inside the machine. Jagust found that older people with plaques had increased blood flow – which means stronger activation of that brain area – in the regions of the brain that are usually activated during memory formation, compared with the older people who did not have plaques. The team then analysed whether this extra brain activation might be helping to compensate for the plaques. © Copyright Reed Business Information Ltd.
David Cyranoski A Japanese patient with a debilitating eye disease is about to become the first person to be treated with induced pluripotent stem cells, which have generated enthusiastic expectations and earned their inventor a Nobel Prize. A health-ministry committee has vetted researchers' safety tests and cleared the team to begin the experimental procedure. Masayo Takahashi, an ophthalmologist at the RIKEN Center for Developmental Biology (CDB) in Kobe, has been using induced pluripotent stem (iPS) cells to prepare a treatment for age-related macular degeneration. Unlike embryonic stem cells, iPS cells are produced from adult cells, so they can be genetically tailored to each recipient. They are capable of becoming any cell type in the body, and have the potential to treat a wide range of diseases. The CDB trial will be the first opportunity for the technology to prove its clinical value. In age-related macular degeneration, extra blood vessels form in the eye, destabilizing a supportive base layer of the retina known as the retinal pigment epithelium. This results in the loss of the light-sensitive photoreceptors that are anchored in the epithelium, and often leads to blindness. Takahashi took skin cells from people with the disease and converted them to iPS cells. She then coaxed these cells to become retinal pigment epithelium cells, and then to grow into thin sheets that can be transplanted to the damaged retina. Takahashi and her collaborators have shown in monkey studies1 that iPS cells generated from the recipients' own cells do not provoke an immune reaction that causes them to be rejected. There have been concerns that iPS cells could cause tumours, but Takahashi's team has found that to be unlikely in mice2 and monkeys1. © 2014 Nature Publishing Group
By Helen Briggs Health editor, BBC News website There may be a link between a rare blood type and memory loss in later life, American research suggests. People with AB blood, found in 4% of the population, appear more likely to develop thinking and memory problems than those with other blood groups. The study, published in Neurology, builds on previous research showing blood type may influence heart risk. A charity said the best way to keep the brain healthy was a balanced diet, regular exercise and not smoking. A US team led by Dr Mary Cushman, of the University of Vermont College of Medicine, Burlington, analysed data from about 30,000 US citizens aged 45 and above. It identified 495 participants who had developed thinking and memory problems, or cognitive impairment, during the three-year study. They were compared to 587 people with no cognitive problems. People with AB blood type made up 6% of the group who developed cognitive impairment, which is higher than the 4% found in the general population. They were 82% more likely to have difficulties with day-to-day memory, language and attention, which can signal the onset of dementia. However, the study did not look at the risk of dementia. The study supported the idea that having a certain blood group, such as O, may give a lower risk for cardiovascular disease, which in turn protected the brain, the researchers said. "Our study looks at blood type and risk of cognitive impairment, but several studies have shown that factors such as high blood pressure, high cholesterol and diabetes increase the risk of cognitive impairment and dementia," said Dr Cushman. BBC © 2014
Ian Sample, science editor Heartbreak can impair the immune system of older people and make them more prone to infections, researchers have found. Scientists said older people who had suffered a recent bereavement had poorer defences against bacteria, which could leave them more vulnerable to killer infections, such as pneumonia. Blood tests showed that the same group had imbalances in their stress hormones, which are known to have a direct impact on the body's ability to fight off bugs. Anna Phillips, a reader in behavioural medicine at Birmingham University, said the damaging effects of bereavement on the immune system were not seen in younger people, whose defences seemed more resilient. The finding suggests that in the weeks and months after the loss of a loved one, older people should keep in touch with their friends and family, and exercise and eat well, to reduce stress levels and boost their immune systems. "Bereavement is a really key stressor that happens to all of us at some point so it's worth being aware of the negative impact it can have on your health," Phillips said. "It's a key time to look after yourself in terms of your psychological and physical wellbeing. Don't try and cope by staying in, drinking more and exercising less. Try to cope by having social interactions, looking after yourself by keeping a certain level of fitness and eating well," she added. For her study, Phillips recruited people who had lost a loved one, either a spouse or family member, in the past two months. She then looked at how well bacteria-killing immune cells called neutrophils performed. © 2014 Guardian News and Media Limited
By Helen Briggs Health editor, BBC News website Long-term use of pills for anxiety and sleep problems may be linked to Alzheimer's, research suggests. A study of older Canadian adults found that past benzodiazepine use for three months or more was linked to an increased risk (up to 51%) of dementia. NHS guidelines say the drugs should be used for eight to 12 weeks at most. The French-Canadian team says while the link is not definitive, it is another warning that treatments should not exceed three months. "Benzodiazepine use is associated with an increased risk of Alzheimer's disease," lead researcher, Sophie Billioti de Gage of the University of Bordeaux, France, and colleagues wrote in the BMJ. "Unwarranted long-term use of these drugs should be considered as a public health concern." The study involved about 2,000 cases of Alzheimer's disease in adults aged over 66 living in Quebec. All had been prescribed benzodiazepines. They were compared with about 7,000 healthy people of the same age living in the same community. While an increased risk was found in those on benzodiazepines, the nature of the link was unclear. Dr Eric Karran, director of research at Alzheimer's Research UK, said: "This study shows an apparent link between the use of benzodiazepines and Alzheimer's disease although it's hard to know the underlying reason behind the link. BBC © 2014
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