Chapter 7. Life-Span Development of the Brain and Behavior
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By By Tanya Lewis, It's not every day you see a mouse with a mohawk. But that's what researchers saw while studying mice that had a genetic mutation linked to autism. The mohawks that the mice were sporting actually resulted from their "over-grooming" behavior, repeatedly licking each other's hair in the same direction. The behavior resembles the repetitive motions displayed by some people with autism, and the researchers say their experiments reveal a link between the genetic causes of autism and their effects on the brain, suggesting potential avenues for treating the disorder. "Our study tells us that to design better tools for treating a disease like autism, you have to get to the underlying genetic roots of its dysfunctional behaviors, whether it is over-grooming in mice or repetitive motor behaviors in humans," study researcher Gordon Fishell, a neuroscientist at NYU Langone Medical Center, said in a statement. Autism is a spectrum of developmental disorders that involve social impairments and communication deficits. People with autism may also engage in repetitive behaviors, such as rocking or hand flapping. In the study, detailed today (May 25) in the journal Nature, the researchers bred mice that lacked a gene for a protein called Cntnap4, which is found in brain cells called interneurons. Having low levels of this protein leads to the abnormal release of two brain-signaling molecules, known as dopamine and GABA. Dopamine is involved in sensations of pleasure; GABA (which stands for gamma-aminobutyric acid) dampens neural activity and regulates muscle tone. Mice that lacked the gene for this critical brain protein were found to obsessively groom their fellow animals' fur into mohawk-like styles, suggesting a link between genetics, brain function and autistic behaviors.
Claudia M. Gold When Frank was a young boy, and he committed some typical toddler transgression such as having a meltdown when it was time to leave the playground, his father would slap him across the face, hurting and humiliating him in a very public way. When I spoke with Frank over 20 years later, in the context of helping him with his own son Leo's frequent tantrums in my behavioral pediatrics practice, he did not describe this experience as "trauma." Rather, he described it in a very matter-of-fact tone. But when we explored in detail his response to his son's tantrums, we discovered that, flooded by the stress of his own memories, Frank in a sense would shut down. Normally a thoughtful and empathic person, he simply told Leo to "cut it out." As we spoke he recognized how he was emotionally absent during these moments, which were increasing in frequency. It seemed as if Leo was testing Frank, perhaps looking for a more appropriate response that would help him manage this normal behavior. Once this process was brought in to awareness, Frank was able to be present with Leo- to tolerate his tantrums and understand them from his 2-year-old perspective. Soon the frequency and intensity of the tantrums returned to a level typical for Leo's developmental stage. Frank, greatly relieved, once again found himself enjoying his son. The upcoming Boston conference; Psychological Trauma: Neuroscience, Attachment, and Therapeutic Interventions, promises to offer insight in to the developmental neuroscience behind this story. What Frank experienced as a young child might be termed "quotidian" or "everyday" trauma. It was not watching a relative get shot, or having his house washed away in an avalanche. It was a daily mismatch with his father- he was looking for reassurance and containment and instead got a slap across the face. It was what leading researcher Ed Tronick would term "unrepaired mismatch." Frank, in a way that is extremely common- termed "intergenerational transmission of trauma"- was then repeating this cycle with his own child. When this dynamic was brought in to awareness, he was able to "repair the mismatch," setting his relationship with his own son on a healthier path. ©2014 Boston Globe Media Partners, LLC
By Neuroskeptic Nothing that modern neuroscience can detect, anyway. This is the message of a provocative article by Pace University psychologist Terence Hines, just published in Brain and Cognition: Neuromythology of Einstein’s brain As Hines notes, the story of how Einstein’s brain was preserved is well known. When the physicist died in 1955, his wish was to be cremated, but the pathologist who performed the autopsy decided to save his brain for science. Einstein’s son Hans later gave his blessing to this fait accompli. Samples and photos of the brain were then made available to neuroscientists around the world, who hoped to discover the secret of the great man’s genius. Many have claimed to have found it. But Hines isn’t convinced. Some researchers, for instance, have used microscopy to examine Einstein’s brain tissue on a histological (cellular) level. Most famous amongst these studies is Diamond et al, who in 1985 reported that Einstein’s brain had a significantly higher proportion of glial cells than those of matched, normal control brains. However, Hines points out that this ‘finding’ may have been a textbook example of the multiple-comparisons problem: Diamond et al. (1985) reported four different t-tests, each comparing Einstein’s brain to the brains of the controls. Only one of the four tests performed was significant at the .05 level. Although only the results of the neuron to glial cell ratios were reported by Diamond et al. (1985), the paper makes it clear that at least six other dependent measures were examined: (1) number of neurons, (2) total number of glial cells, (3) number of astrocytes, (4) number of oligodendrocytes, (5) neuron to astrocyte ratio and (6) neuron to oligodendrocyte ratio. Thus a total of seven different dependent measures were examined in four different brain areas for a total of 28 comparisons… one p less than 0.05 result out of 28 is not surprising. Other histological studies followed from other researchers, but Hines says that they do not present a coherent picture of clear differences:
By BRUCE WEBER Dr. Gerald M. Edelman at Rockefeller University in 1972, in front of a gamma globulin model. Credit Don Hogan Charles/The New York Times Dr. Gerald M. Edelman, who shared a 1972 Nobel Prize for a breakthrough in immunology and went on to contribute key findings in neuroscience and other fields, becoming a leading if contentious theorist on the workings of the brain, died on Saturday at his home in the La Jolla section of San Diego. He was 84. The precise cause was uncertain, but Dr. Edelman had Parkinson’s disease and prostate cancer, his son David said. Dr. Edelman was known as a problem solver, a man of relentless intellectual energy who asked big questions and attacked big projects. What interested him, he said, were “dark areas” where mystery reigned. “Anybody in science, if there are enough anybodies, can find the answer,” he said in a 1994 interview in The New Yorker. “It’s an Easter egg hunt. That isn’t the idea. The idea is: Can you ask the question in such a way as to facilitate the answer? And I think the great scientists do that.” His Nobel Prize in Physiology or Medicine came in 1972 after more than a decade of work on the process by which antibodies, the foot soldiers of the immune system, mount their defense against infection and disease. He shared the prize with Rodney R. Porter, a British scientist who worked independent of Dr. Edelman. The Nobel committee cited them for their separate approaches in deciphering the chemical structure of antibodies, also known as immunoglobulins. Dr. Edelman discovered that antibodies were not constructed in the shape of one long peptide chain, as thought, but of two different ones — one light, one heavy — that were linked. © 2014 The New York Times Company
By John Horgan Biologist Gerald Edelman–one of the truly great scientific characters I’ve encountered, whose work raised profound questions about the limits of science—has died. I interviewed Edelman in June 1992 at Rockefeller University in New York. Edelman subsequently left Rockefeller to head a center for neuroscience at the Scripps Institute in California. Edelman, 84, died in his home in La Jolla. The following is an edited version of my profile of Edelman in my 1996 book The End of Science. Gerald Edelman, who sought to solve the riddle of consciousness, had "the brain of an empiricist and the heart of a romantic." Gerald Edelman’s career, like that of his rival Francis Crick, has been eclectic, and highly successful. While still a graduate student, Edelman helped to determine the structure of a protein molecule crucial to the body’s immune response. In 1972 he shared a Nobel Prize for that work. Edelman moved on to developmental biology, the study of how a single fertilized cell becomes a full-fledged organism. He found a class of proteins, called cell adhesion molecules, thought to play an important role in embryonic development. All this was merely prelude, however, to Edelman’s grand project of creating a theory of mind. Edelman has set forth his theory in three books: Neural Darwinism, The Remembered Present and Bright Air, Brilliant Fire. The gist of the theory is that just as environmental stresses select the fittest members of a species, so do inputs to the brain select groups of neurons–corresponding to useful memories, for example–by strengthening the connections between them. © 2014 Scientific American
By David Grimm, A shaggy brown terrier approaches a large chocolate Labrador in a city park. When the terrier gets close, he adopts a yogalike pose, crouching on his forepaws and hiking his butt into the air. The Lab gives an excited bark, and soon the two dogs are somersaulting and tugging on each other’s ears. Then the terrier takes off and the Lab gives chase, his tail wagging wildly. When the two meet once more, the whole thing begins again. Watch a couple of dogs play, and you’ll probably see seemingly random gestures, lots of frenetic activity and a whole lot of energy being expended. But decades of research suggest that beneath this apparently frivolous fun lies a hidden language of honesty and deceit, empathy and perhaps even a humanlike morality. Take those two dogs. That yogalike pose is known as a “play bow,” and in the language of play it’s one of the most commonly used words. It’s an instigation and a clarification, a warning and an apology. Dogs often adopt this stance as an invitation to play right before they lunge at another dog; they also bow before they nip (“I’m going to bite you, but I’m just fooling around”) or after some particularly aggressive roughhousing (“Sorry I knocked you over; I didn’t mean it.”). All of this suggests that dogs have a kind of moral code — one long hidden to humans until a cognitive ethologist named Marc Bekoff began to crack it. A wiry 68-year-old with reddish-gray hair tied back in a long ponytail, Bekoff is a professor emeritus at the University of Colorado at Boulder, where he taught for 32 years. He began studying animal behavior in the early 1970s, spending four years videotaping groups of dogs, wolves and coyotes in large enclosures and slowly playing back the tapes, jotting down every nip, yip and lick. “Twenty minutes of film could take a week to analyze,” he says. © 1996-2014 The Washington Post
Sara Reardon The researchers' technique shows neurons throughout the body twinkling with activity. Researchers have for the first time imaged all of the neurons firing in a living organism, the nematode worm Caenorhabditis elegans. The achievement, reported today in Nature Methods1 shows how signals travel through the body in real time. Scientists mapped the connections among all 302 of the nematode's neurons in 19862 — a first that has not been repeated with any other organism. But this wiring diagram, or 'connectome', does not allow researchers to determine the neuronal pathways that lead to a particular action. Nor does it allow researchers to predict what the nematode will do at any point in time, says neuroscientist Alipasha Vaziri of the University of Vienna. By providing a means of displaying signaling activity between neurons in three dimensions and in real-time, the new technique should allow scientists to do both. Vaziri and his colleagues engineered C. elegans so that when a neuron fires and calcium ions pass through its cell membranes, the neuron lights up. To capture those signals, they imaged the whole worm using a technique called light-field deconvolution microscopy, which combines images from a set of tiny lenses and analyses them using an algorithm to give a high-resolution three-dimensional image. The researchers took as many as 50 images per second of the entire worm, enabling them to watch the neurons firing in the brain, ventral cord, and tail (see video). Next, the group applied the technique to the transparent larvae of the zebrafish (Danio rerio), imaging the entire brain as the fish responded to the odours of chemicals pumped into their water. They were able to capture the activity of about 5,000 neurons simultaneously (the zebrafish has about 100,000 total neurons). © 2014 Nature Publishing Group
Keyword: Brain imaging
Link ID: 19631 - Posted: 05.18.2014
By GINIA BELLAFANTE The opening shots of “The Normal Heart,” HBO’s adaptation of Larry Kramer’s 1985 play about the early days of the AIDS crisis in New York, reveal a crew of sinewy and amorous young men disembarking from a ferry on Fire Island on a beautiful July day in 1981. The tableau is meant to suggest the final hour of unburdened desire, the moment before so much youth and beauty would be sacrificed to the cruelest attacks of physiology and cultural indifference. On the way home from the weekend, Ned Weeks, Mr. Kramer’s proxy, a man distanced from the surrounding hedonism, is shown reading a piece in The New York Times headlined, “Rare Cancer Seen in 41 Homosexuals.” The film (which will make its debut on May 25) arrives at a transformative time in the history of AIDS prevention. On May 14, federal health officials, in a move that would have been unimaginable 30 years ago, recommended the use of a prophylactic drug regimen to prevent infection with H.I.V. The drug currently used is known as Truvada, and two years ago, David Duran, a writer and gay-rights campaigner, coined the term “Truvada whore,” controversially, as a judgment against gay men who were abandoning safer sex in favor of taking the antiretroviral. Though he has since characterized this view as “prudish,” there are doctors in the city who continue to harangue patients for what the longtime AIDS activist Peter Staley calls “any break with the condom code.” And yet whatever ideological divisions existed in the period Mr. Kramer’s narrative recalls and whatever have emerged since, the fight against AIDS has been one of the most successful and focused public health movements. In another distinguishing moment, the city health department announced this year that for the first time AIDS had fallen out of the 10 leading causes of death in New York. Replacing it was Alzheimer’s, whose damage is sure to multiply as the number of older New Yorkers increases — by 2030 there will be close to 500,000 more people over age 60 than there were at the beginning of the century. According to a study from Rush University Medical Center in March, the number of deaths attributable to the disease had been vastly undercalculated. The research showed that Alzheimer’s was the underlying cause in 500,000 deaths in the United States in 2010, a figure close to six times the estimate from the Centers for Disease Control. This means that in a single year, Alzheimer’s claimed nearly as many lives as AIDS — responsible for 636,000 deaths in this country — had taken in more than three decades. © 2014 The New York Times Company
Link ID: 19628 - Posted: 05.18.2014
By ALAN SCHWARZ ATLANTA — More than 10,000 American toddlers 2 or 3 years old are being medicated for attention deficit hyperactivity disorder outside established pediatric guidelines, according to data presented on Friday by an official at the Centers for Disease Control and Prevention. The report, which found that toddlers covered by Medicaid are particularly prone to be put on medication such as Ritalin and Adderall, is among the first efforts to gauge the diagnosis of A.D.H.D. in children below age 4. Doctors at the Georgia Mental Health Forum at the Carter Center in Atlanta, where the data was presented, as well as several outside experts strongly criticized the use of medication in so many children that young. The American Academy of Pediatrics standard practice guidelines for A.D.H.D. do not even address the diagnosis in children 3 and younger — let alone the use of such stimulant medications, because their safety and effectiveness have barely been explored in that age group. “It’s absolutely shocking, and it shouldn’t be happening,” said Anita Zervigon-Hakes, a children’s mental health consultant to the Carter Center. “People are just feeling around in the dark. We obviously don’t have our act together for little children.” Dr. Lawrence H. Diller, a behavioral pediatrician in Walnut Creek, Calif., said in a telephone interview: “People prescribing to 2-year-olds are just winging it. It is outside the standard of care, and they should be subject to malpractice if something goes wrong with a kid.” Friday’s report was the latest to raise concerns about A.D.H.D. diagnoses and medications for American children beyond what many experts consider medically justified. Last year, a nationwide C.D.C. survey found that 11 percent of children ages 4 to 17 have received a diagnosis of the disorder, and that about one in five boys will get one during childhood. A vast majority are put on medications such as methylphenidate (commonly known as Ritalin) or amphetamines like Adderall, which often calm a child’s hyperactivity and impulsivity but also carry risks for growth suppression, insomnia and hallucinations. Only Adderall is approved by the Food and Drug Administration for children below age 6. However, because off-label use of methylphenidate in preschool children had produced some encouraging results, the most recent American Academy of Pediatrics guidelines authorized it in 4- and 5-year-olds — but only after formal training for parents and teachers to improve the child’s environment were unsuccessful. © 2014 The New York Times Company
By Pippa Stephens Health reporter, BBC News An anti-depressant drug could be used to slow the onset of Alzheimer's disease, say scientists in the US. Research into 23 people, and transgenic mice, found citalopram hampered a protein which helps to build destructive plaques in the brains of Alzheimer's patients. Scientists said they hoped the study could help prevent the disease. Experts said the study was "interesting" and that using an approved drug could be beneficial. Alzheimer's disease is the most common cause of dementia, affecting around 496,000 people in the UK. It affects the brain through protein plaques and tangles which lead to the death of brain cells, and a shortage of chemicals important for transmitting messages. Symptoms include loss of memory, mood changes, and problems with communication and reasoning. Researchers at the University of Pennsylvania and Washington University School of Medicine carried out the study between 2012 and 2014. They bred mice with Alzheimer's disease and looked at the levels of the peptide - or protein component - amyloid beta (AB), in the brain. AB clusters in plaques which, alongside the tau protein, are thought to trigger Alzheimer's. After giving the mice citalopram, the level of AB fell by 25%, compared to the control group, with no anti-depressant. And after two months of anti-depressants, the growth of new plaques was reduced, and existing plaques did not grow any further, the study said. But it noted the drug could not cause existing plaques to shrink, or decrease in number. BBC © 2014
Bullying casts a long shadow. Children who are bullied are more prone to depression and suicidal tendencies even when they grow up; they're also more likely to get sick and have headaches and stomach troubles, researchers have discovered. A new study may have found the underlying cause: A specific indicator of illness, called C-reactive protein (CRP), is higher than normal in bullying victims, even when they get older. In contrast, the bullies, by the same gauge, seem to be healthier. The researchers focused on CRP because it's a common, easily tested marker of inflammation, the runaway immune system activity that's a feature of many chronic illnesses including cardiovascular disease, diabetes, chronic pain, and depression, explains lead author William Copeland, a psychologist and epidemiologist at Duke University Medical Center in Durham, North Carolina. To link inflammation to bullying, the researchers asked 1420 youngsters between the ages of 9 and 16 whether, and how often, they had been bullied or had bullied others. Interviewers asked participants whether they felt more teased, bullied, or treated meanly by siblings, friends, and peers than other children—and whether they had upset or hurt other people on purpose, tried to get others in trouble, or forced people to do something by threatening or hurting them. The researchers took finger stick blood tests at each assessment. Interviews took place once a year until the participants turned 16, and again when they were 19 and 21. The children interviewed were participants in the larger Great Smoky Mountains Study, in which some 12,000 children in North Carolina were assessed to track the development of psychiatric conditions. In the short term, the effect of bullying on the victims was immediate. CRP levels increased along with the number of reported bullying instances, and more than doubled in those who said they'd been bullied three times or more in the previous year, compared with kids who had never been bullied. No change was seen in bullies, or in kids who hadn't been involved with bullying one way or the other, the researchers report online today in the Proceedings of the National Academy of Sciences. © 2014 American Association for the Advancement of Science.
by Anil Ananthaswamy Children born with split brains – whereby the two hemispheres of their brains are not connected – can develop new brain wiring that helps to connect the two halves, according to brain scans of people with the condition. Such circuitry is not present in normal brains, and explains how some people with split brains can still maintain normal function. It also suggests that the developing brain is even more adaptable than previously thought. Research into people with split brains goes back to the 1960s, when neuroscientists studied people who had undergone brain surgery to treat particularly severe epilepsy. The surgery involved cutting the corpus callosum, the thick bundle of neuronal fibres that connects the brain's two halves. This disconnection prevented epileptic seizures spreading from one brain hemisphere to the other. The recipients of such split-brain surgery showed a form of disconnection syndrome whereby the two halves of their brains could not exchange information. For instance, if a patient touched an object with their left hand without seeing the object, they would be unable to name it. That is because sensory-motor signals from the left hand are processed in the right hemisphere. To put a name to the object, the tactile information from the hand has to reach the brain's left hemisphere, the seat of language. With the central connection between hemispheres severed, the object's naming information cannot be retrieved. Conversely, if that person were to touch an object with their right hand without seeing it, the sensory-motor signals from that hand would go to the left hemisphere, which hosts the brain's language centres, making naming the object easy. However, children born without a corpus callosum – and therefore whose two brain hemispheres are separated – can often pass such tactile naming tests when they are old enough to take them. Their brain hemispheres are obviously communicating, but it wasn't clear how. © Copyright Reed Business Information Ltd
By Suzanne Allard Levingston, Playing with bubble wrap is a silly activity that delights most preschoolers. But for one 21 / 2-year-old from Silver Spring, loud noises such as the pop of plastic bubbles were so upsetting that he would cover his ears and run away. Some days the sound of a vacuum cleaner would make him scream. The child so persistently avoided activities with too much noise and motion that his preschool’s administrators asked to meet with his family — and soon an assessment led to a diagnosis of sensory processing disorder, or SPD. SPD is a clinical label for people who have abnormal behavioral responses to sensory input such as sound and touch. Some children with SPD seem oversensitive to ordinary stimuli such as a shirt label’s scratching their skin. Others can be underresponsive — seemingly unaffected by the prick of a needle. A third group have motor problems that make holding a pencil or riding a bike seem impossible. Whatever the difficulty, such kids are often described as “out-of-sync,” a term popularized by Carol Stock Kranowitz’s 1998 book “The Out-of-Sync Child,” which has sold nearly 700,000 copies. As many as 16 percent of school-age kids in the United States may face sensory processing challenges. And yet there’s debate over whether these challenges constitute a discrete medical disorder. Some experts contend that SPD may be merely a symptom of some other ailment — autism, attention-deficit hyperactivity disorder, anxiety disorder or fragile X syndrome, for example — while others insist it is a separate condition that should be labeled a disorder when it interferes with daily life. The debate over how to classify SPD is not merely matter of semantics. Such discussions can affect research funding and can guide whether insurers will reimburse therapy costs. © 1996-2014 The Washington Post
Erin Allday A gene variant that scientists already knew to be associated with longer life also seems to make people smarter, and may help offset the effects of normal cognitive decline in old age, according to a team of San Francisco researchers. The findings, published Thursday in the journal Cell Reports, are encouraging news for the roughly 1 in 5 people who have the genetic trait, which is a variant of the klotho gene. Beyond that, scientists hope the findings will help them develop tools for retaining, or even boosting, intelligence in people who have suffered cognitive losses, either from disease or through the normal course of aging. 'Cognitive enhancer' "What we've discovered is a cognitive enhancer," said Dr. Dena Dubal, an assistant professor of neurology at UCSF and lead author of the study, which was done with researchers from the Gladstone Institutes. "This may represent a new way to treat problems of cognition in the brain." The name of the gene comes from Greek mythology - Klotho is one of the three sisters of fate, and she spins the thread of life. The gene is responsible for secretions of the hormone klotho, which is thought to have effects on a variety of biological systems and has been shown to disrupt some processes associated with aging. © 2014 Hearst Communications, Inc.
By DAVID L. KIRP Whenever President Obama proposes a major federal investment in early education, as he did in his two most recent State of the Union addresses, critics have a two-word riposte: Head Start. Researchers have long cast doubt on that program’s effectiveness. The most damning evidence comes from a 2012 federal evaluation that used gold-standard methodology and concluded that children who participated in Head Start were not more successful in elementary school than others. That finding was catnip to the detractors. “Head Start’s impact is no better than random,” The Wall Street Journal editorialized. Why throw good money after bad? Though the faultfinders have a point, the claim that Head Start has failed overstates the case. For one thing, it has gotten considerably better in the past few years because of tougher quality standards. For another, researchers have identified a “sleeper effect” — many Head Start youngsters begin to flourish as teenagers, maybe because the program emphasizes character and social skills as well as the three R’s. Still, few would give Head Start high marks, and the bleak conclusion of the 2012 evaluation stands in sharp contrast to the impressive results from well-devised studies of state-financed prekindergartens. Head Start, a survivor of President Lyndon B. Johnson’s war on poverty, enrolls only poor kids. That’s a big part of the problem — as the adage goes, programs for the poor often become poor programs. Whether it’s health care (compare the trajectories of Medicare, for those 65 and older of all incomes, and Medicaid, only for the poor), education or housing, the sorry truth is that “we” don’t like subsidizing “them.” Head Start is no exception. It has been perpetually underfunded, never able to enroll more than half of eligible children or pay its teachers a decent wage. If Head Start is going to realize its potential, it has to break out of the antipoverty mold. One promising but unfortunately rarely used strategy is to encourage all youngsters, not just poor kids, to enroll, with poor families paying nothing and middle-class families contributing on a sliding scale. Another is to merge Head Start with high-quality state prekindergarten. © 2014 The New York Times Company
Helen Shen For anyone fighting to save old memories, a fresh crop of brain cells may be the last thing they need. Research published today in Science suggests that newly formed neurons in the hippocampus — an area of the brain involved in memory formation — could dislodge previously learned information1. The work may provide clues as to why childhood memories are so difficult to recall. “The finding was very surprising to us initially. Most people think new neurons mean better memory,” says Sheena Josselyn, a neuroscientist who led the study together with her husband Paul Frankland at the Hospital for Sick Children in Toronto, Canada. Humans, mice and several other mammals grow new neurons in the hippocampus throughout their lives — rapidly at first, but more and more slowly with age. Researchers have previously shown that boosting neural proliferation before learning can enhance memory formation in adult mice2, 3. But the latest study shows that after information is learned, neuron growth can degrade those memories. Although seemingly counterintuitive, the disruptive role of these neurons makes some sense, says Josselyn. She notes that some theoretical models have predicted such an effect4. “More neurons increase the capacity to learn new memories in the future,” she says. “But memory is based on a circuit, so if you add to this circuit, it makes sense that it would disrupt it.” Newly added neurons could have a useful role in clearing old memories and making way for new ones, says Josselyn. Forgetting curve The researchers tested newborn and adult mice on a conditioning task, training the animals to fear an environment in which they received repeated electric shocks. All the mice learned the task quickly, but whereas infant mice remembered the negative experience for only one day after training, adult mice retained the negative memory for several weeks. © 2014 Nature Publishing Group
Scientists showed that people who have a variant of a longevity gene, called KLOTHO, have improved brain skills such as thinking, learning and memory regardless of their age, sex, or whether they have a genetic risk factor for Alzheimer’s disease. Increasing KLOTHO gene levels in mice made them smarter, possibly by increasing the strength of connections between nerve cells in the brain. The study was partly funded by the National Institutes of Health. “This could be a major step toward helping millions around the world who are suffering from Alzheimer’s disease and other dementias,” said Dena Dubal, M.D., Ph.D., an assistant professor of neurology, the David A. Coulter Endowed Chair in Aging and Neurodegeneration at the University of California San Francisco (UCSF) and the lead author of the study published in Cell Reports. “If we could boost the brain’s ability to function, we may be able to counter dementias.” As people live longer the effects of aging on the brain will become a greater health issue. This is especially true for dementias, a collection of brain disorders that can cause memory problems, impaired language skills and other symptoms. With the number of dementia cases worldwide estimated to double every 20 years from 35.6 million people in 2010 to 65.7 million in 2030 and 115.4 million in 2050, the need for treatments is growing. Klotho is the name of a Greek mythological goddess of fate, “who spins the thread of life.” People who have one copy of a variant, or form, of the KLOTHO gene, called KL-VS, tend to live longer and have lower chances of suffering a stroke whereas people who have two copies may live shorter lives and have a higher risk of stroke. In this study, the investigators found that people who had one copy of the KL-VS variant performed better on a battery of cognitive tests than subjects who did not have it, regardless of age, sex or the presence of the apolipoprotein 4 gene, the main genetic risk factor for Alzheimer’s disease.
By GRETCHEN REYNOLDS The more physically active you are at age 25, the better your thinking tends to be when you reach middle age, according to a large-scale new study. Encouragingly, the findings also suggest that if you negligently neglected to exercise when young, you can start now and still improve the health of your brain. Those of us past age 40 are generally familiar with those first glimmerings of forgetfulness and muddled thinking. We can’t easily recall people’s names, certain words, or where we left the car keys. “It’s what we scientists call having a C.R.S. problem,” said David R. Jacobs, a professor of public health at the University of Minnesota in Minneapolis and a co-author of the new study. “You can’t remember stuff.” But these slight, midlife declines in thinking skills strike some people later or less severely than others, and scientists have not known why. Genetics almost certainly play a role, most researchers agree. Yet the contribution of lifestyle, and in particular of exercise habits, has been unclear. So recently, Dr. Jacobs and colleagues from universities in the United States and overseas turned to a large trove of data collected over several decades for the Cardia study. The study, whose name is short for Coronary Artery Risk Development in Young Adults, began in the mid-1980s with the recruitment of thousands of men and women then ages 18 to 30 who underwent health testing to determine their cholesterol levels, blood pressure and other measures. Many of the volunteers also completed a treadmill run to exhaustion, during which they strode at an increasingly brisk pace until they could go no farther. The average time to exhaustion among these young adults was 10 minutes, meaning that most were moderately but not tremendously fit. © 2014 The New York Times Company
Erin Allday The game seems pretty simple. An alien-looking creature stands on a block of ice that's flowing down a river. The goal is to maneuver the ice around whales and other hurdles and periodically cause the alien to "jump" to grab green fish as they leap out of the water. The game is played on a tablet, and it looks a lot like any of hundreds of apps that can be downloaded for some mindless entertainment during an afternoon commute on BART. Here's what sets the game apart: It was designed by scientists at UCSF looking for a new way to treat serious symptoms of depression. "We're trying to see whether we can get the same effects with the game as with therapy," said Patricia Arean, a clinical psychologist at UCSF who is studying the potential mental health benefits of video game play in older adults. Arean is joining the burgeoning field of research into the use of video games as tools for promoting brain health. Video games undoubtedly have some kind of effect on our brains, but harnessing the technology and forcing a lasting - and positive - change is the challenge. So far, what little evidence does exist that video games can have a measurable impact on brain activity has been gathered almost entirely on healthy subjects. But in small clinical trials - like Arean's study of depression in older adults - the effects of games on both healthy and unhealthy people are being studied to find out whether they're useful in treating mental illness, such as autism, attention deficit and hyperactivity disorder, and post-traumatic stress disorder. Some neuroscientists say video games may also strengthen neural networks, potentially preventing or slowing down the brain deterioration associated with old age or diseases like Alzheimer's or Parkinson's. "We're in the infancy of this idea that entertaining and gaming stuff can be useful for you," said Joaquin Anguera, a UCSF neuroscientist who designs cognitive training games, including the one Arean is testing with patients. © 2014 Hearst Communications, Inc.
By Eric Niiler, Scientists studying head injuries have found something surprising: Genes may make some people more susceptible to concussion and trauma than others. A person’s genetic makeup, in fact, may play a more important role in the extent of injury than the number of blows a person sustains. While this research is still in its infancy, these scientists are working toward developing a blood test that may one day help a person decide — based on his her or her genetic predisposition — whether to try out for the football team, or perhaps take up swimming or chess instead. “Until now, all the attention has been paid to how hard and how often you get hit,” said Thomas McAllister, a professor of clinical psychiatry at the Indiana University School of Medicine. “No doubt that’s important. But it’s also becoming clear that’s it’s probably an interaction between the injury and the genetics of the person being injured.” This research is being spurred by fears that some athletes and many returning soldiers may face a lifetime of problems from head injuries. The National Football League agreed to settle a class-action concussion lawsuit by retired players last August for $765 million, although a judge rejected the agreement. In addition, the Pentagon estimates that 294,000 troops, many of whom served in Iraq and Afghanistan, suffered some kind of brain injury since 2000. “More and more we are noticing our servicemen are coming home with significant problems with brain function,” said Daniel Perl, a neuropathologist at the Center for Neuroscience and Regenerative Medicine at the Pentagon’s Uniformed Services University for Health Sciences in Bethesda. “We don’t know much about the biology of this. We need to get down to cellular level of resolution, how the brain starts to repair itself.” © 1996-2014 The Washington Post