Chapter 7. Life-Span Development of the Brain and Behavior
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By Elizabeth Norton A single dose of a century-old drug has eliminated autism symptoms in adult mice with an experimental form of the disorder. Originally developed to treat African sleeping sickness, the compound, called suramin, quells a heightened stress response in neurons that researchers believe may underlie some traits of autism. The finding raises the hope that some hallmarks of the disorder may not be permanent, but could be correctable even in adulthood. That hope is bolstered by reports from parents who describe their autistic children as being caught behind a veil. "Sometimes the veil parts, and the children are able to speak and play more normally and use words that didn't seem to be there before, if only for a short time during a fever or other stress" says Robert Naviaux, a geneticist at the University of California, San Diego, who specializes in metabolic disorders. Research also shows that the veil can be parted. In 2007, scientists found that 83% of children with autism disorders showed temporary improvement during a high fever. The timing of a fever is crucial, however: A fever in the mother can confer a higher risk for the disorder in the unborn child. As a specialist in the cell's life-sustaining metabolic processes, Naviaux was intrigued. Autism is generally thought to result from scrambled signals at synapses, the points of contact between nerve cells. But given the specific effects of something as general as a fever, Naviaux wondered if the problem lay "higher up" in the cell's metabolism. © 2014 American Association for the Advancement of Science.
Link ID: 19749 - Posted: 06.19.2014
As the popularity of soccer grows among children, doctors and researchers say the dangers of concussions need to be taken more seriously in the sport. When researchers at St. Michael's Hospital in Toronto reviewed the evidence on concussions and heading in soccer this winter, they found a higher incidence of concussions among females than males playing the world's most popular sport. Doctors warn that heading — purposely using the head to control and hit the ball — is a unique aspect of the beautiful game that needs more attention. Heading the ball isn’t necessarily going to cause an overt concussion with symptoms, but the accumulation of those impacts over time could cause difficulties with thinking, concentration and memory, said study author Monica Maher, a graduate student at the University of Toronto, and a former soccer goalkeeper. Maher doesn't want people to stop playing soccer or stop heading the ball. She does suggest limits on head exposure in younger children and padding on goal posts to prevent injury to the youngest players. Dr. David Robinson, a sports medicine physician at McMaster University in Hamilton, sees 10 to 15 concussions a week, including many related to soccer. "It's not a stretch to think that these chronic subconcussive blows may be softening the brain, injuring the brain over time," Robinson said. He calls it a step forward that balls are becoming lighter for young people. He reminds parents and coaches that if a concussion is suspected, it's best to remove an athlete from play. As for the differences in injury rates between males and females, Maher pointed to a few potential explanations: © CBC 2014
Associated Press In one of the most ambitious attempts yet to thwart Alzheimer's disease, a major study got under way Monday to see if an experimental drug can protect healthy seniors whose brains harbor silent signs that they're at risk. Scientists plan to eventually scan the brains of thousands of older volunteers in the U.S., Canada and Australia to find those with a sticky build-up believed to play a key role in development of Alzheimer's - the first time so many people without memory problems get the chance to learn the potentially troubling news. Having lots of that gunky protein called beta-amyloid doesn't guarantee someone will get sick. But the big question: Could intervening so early make a difference for those who do? "We have to get them at the stage when we can save their brains," said Dr. Reisa Sperling of Boston's Brigham and Women's Hospital and Harvard Medical School, who is leading the huge effort to find out. Researchers are just beginning to recruit volunteers, and on Monday, a Rhode Island man was hooked up for an IV infusion at Butler Hospital in Providence, the first treated. Peter Bristol, 70, of Wakefield, R.I., figured he was at risk because his mother died of Alzheimer's and his brother has it. "I felt I needed to be proactive in seeking whatever therapies might be available for myself in the coming years," said Bristol, who said he was prepared when a PET scan of his brain showed he harbored enough amyloid to qualify for the research. "Just because I have it doesn't mean I'm going to get Alzheimer's," he stressed. But Bristol and his wife are "going into the situation with our eyes wide open." He won't know until the end of what is called the A4 Study - it stands for Anti-Amyloid Treatment in Asymptomatic Alzheimer's - whether he received monthly infusions of the experimental medicine, Eli Lilly & Co.'s solanezumab, or a dummy drug. © 2014 Hearst Communications, Inc.
Link ID: 19717 - Posted: 06.10.2014
by Ashley Yeager Being put under anesthesia as an infant may make it harder for a person to recall details or events when they grow older. Previous studies on animals had shown that anesthesia impairs parts of the brain that help with recollection. But it was not clear how this type of temporary loss of consciousness affected humans. Comparing the memory of 28 children ages 6 to 11 who had undergone anesthesia as infants to 28 children similar in age who had not been put under suggests that the early treatment impairs recollection later in life, researchers report June 9 in Neuropsychopharmacology. The team reported similar results for a small study on rats and notes that early anesthesia did not appear to affect the children's familiarity with objects and events or their IQ. © Society for Science & the Public 2000 - 2013.
by Laura Sanders Transplanted cells can flourish for over a decade in the brain of a person with Parkinson’s disease, scientists write in the June 26 Cell Reports. Finding that these cells have staying power may encourage clinicians to pursue stem cell transplants, a still-experimental way to counter the brain deterioration that comes with Parkinson’s. Penelope Hallett of Harvard University and McLean Hospital in Belmont, Mass., and colleagues studied postmortem brain tissue from five people with advanced Parkinson’s. The five had received stem cell transplants between four and 14 years earlier. In all five people’s samples, neurons that originated from the transplanted cells showed signs of good health and appeared capable of sending messages with the brain chemical dopamine, a neurotransmitter that Parkinson’s depletes. Results are mixed about whether these transplanted cells are a good way to ease Parkinson’s symptoms. Some patients have shown improvements after the new cells stitched themselves into the brain, while others didn’t benefit from them. The cells can also cause unwanted side effects such as involuntary movements. P. J. Hallett et al. Long-term health of dopaminergic neuron transplants in Parkinson’s disease patients. Cell Reports. Vol. 7, June 26, 2014. doi: 10.1016/j.celrep.2014.05.027. © Society for Science & the Public 2000 - 2013
By Jenny Graves The claim that homosexual men share a “gay gene” created a furor in the 1990s. But new research two decades on supports this claim – and adds another candidate gene. To an evolutionary geneticist, the idea that a person’s genetic makeup affects their mating preference is unsurprising. We see it in the animal world all the time. There are probably many genes that affect human sexual orientation. But rather than thinking of them as “gay genes,” perhaps we should consider them “male-loving genes.” They may be common because these variant genes, in a female, predispose her to mate earlier and more often and to have more children. Likewise, it would be surprising if there were not “female-loving genes” in lesbian women that, in a male, predispose him to mate earlier and have more children. We can detect genetic variants that produce differences between people by tracking traits in families that display differences. Patterns of inheritance reveal variants of genes (called “alleles”) that affect normal differences, such as hair color, or disease states, such as sickle cell anemia. Quantitative traits, such as height, are affected by many different genes, as well as environmental factors. It’s hard to use these techniques to detect genetic variants associated with male homosexuality partly because many gay men prefer not to be open about their sexuality. It is even harder because, as twin studies have shown, shared genes are only part of the story. Hormones, birth order and environment play roles, too.
Laura Spinney One day in 1991, neurologist Warren Strittmatter asked his boss to look at some bewildering data. Strittmatter was studying amyloid-β, the main component of the molecular clumps found in the brains of people with Alzheimer's disease. He was hunting for amyloid-binding proteins in the fluid that buffers the brain and spinal cord, and had fished out one called apolipoprotein E (ApoE), which had no obvious connection with the disease. Strittmatter's boss, geneticist Allen Roses of Duke University in Durham, North Carolina, immediately realized that his colleague had stumbled across something exciting. Two years earlier, the group had identified a genetic association between Alzheimer's and a region of chromosome 19. Roses knew that the gene encoding ApoE was also on chromosome 19. “It was like a lightning bolt,” he says. “It changed my life.” In humans, there are three common variants, or alleles, of the APOE gene, numbered 2, 3 and 4. The obvious step, Roses realized, was to find out whether individual APOE alleles influence the risk of developing Alzheimer's disease. The variants can be distinguished from one another using a technique called the polymerase chain reaction (PCR). But Roses had little experience with PCR, so he asked the postdocs in his team to test samples from people with the disease and healthy controls. The postdocs refused: they were busy hunting for genes underlying Alzheimer's, and APOE seemed an unlikely candidate. The feeling in the lab, recalls Roses, was that “the chief was off on one of his crazy ideas”. Roses then talked to his wife, Ann Saunders, a mouse geneticist who was skilled at PCR. She had just given birth to their daughter and was on maternity leave, so they struck a deal. “She did the experiments while I held the baby,” he says. Within three weeks, they had collected the data that would fuel a series of landmark papers showing that the APOE4 allele is associated with a greatly increased risk of Alzheimer's disease1. © 2014 Nature Publishing Group,
By Charles Q. Choi Scientists have found a kind of brain cell in mice that can instruct stem cells to start making more neurons, according to a new study. In addition, they found that electrical signals could trigger this growth in rodents, raising the intriguing possibility that devices could one day help the human brain repair itself. The study appears in the journal Nature Neuroscience. We knew the brain can generate new neurons, a process known as neurogenesis, via neural stem cells. And neuroscientists knew these stem cells got their instructions from a variety of sources from chemicals in the bloodstream, for instance, and from cells in the structures that hold the cerebrospinal fluid that cushion the brain. Earlier research had suggested brain cells might also be able to command these stem cells to create neurons. Neuroscientist Chay Kuo at the Duke University School of Medicine in Durham, N.C., and his colleagues have now discovered such cells in mice. "It's really cool that the brain can tell stem cells to make more neurons," Kuo says. To begin their experiments, the researchers tested how well a variety of neurotransmitters performed at spurring mouse neural stem cells to produce new neurons; they found that a compound known as acetylcholine performed best. The team then discovered a previously unknown type of neuron that produces an enzyme needed to make acetylcholine. These neurons are found in a part of the adult mouse brain known as the subventricular zone, where neurogenesis occurs. ©2014 Hearst Communication, Inc
Link ID: 19694 - Posted: 06.05.2014
Ian Sample, science correspondent Research on children in Denmark has found that boys with autism were more likely to have been exposed to higher levels of hormones in their mother's wombs than those who developed normally. Boys diagnosed with autism and related disorders had, on average, raised levels of testosterone, cortisol and other hormones in the womb, according to analyses of amniotic fluid that was stored after their mothers had medical tests during pregnancy. The findings add to a growing body of evidence that the biological foundations of autism are laid down well before birth and involve factors that go beyond the child's genetic make-up. The results may help scientists to unravel some of the underlying causes of autism and explain why boys are four to five times more likely to be diagnosed with the condition, which affects around one percent of the population. Amniotic fluid surrounds babies in the womb and contains hormones and other substances that they have passed through their urine. The liquid is collected for testing when some women have an amniocentesis around four months into their pregnancy. Scientists in Cambridge and Copenhagen drew on Danish medical records and biobank material to find amniotic fluid samples from 128 boys who were later diagnosed with autism. Compared to a control group, the boys with autism and related conditions had higher levels of four "sex steroid" hormones that form a biological production line in the body that starts with progesterone and ends with testosterone. "In the womb, boys produce about twice as much testosterone as girls, but compared with typical boys, the autism group has even higher levels. It's a significant difference and may have a large effect on brain development," said Simon Baron-Cohen, director of the Autism Research Centre at Cambridge University. © 2014 Guardian News and Media Limited
Learning a second language can have a positive effect on the brain, even if it is taken up in adulthood, a University of Edinburgh study suggests. Researchers found that reading, verbal fluency and intelligence were improved in a study of 262 people tested either aged 11 or in their seventies. A previous study suggested that being bilingual could delay the onset of dementia by several years. The study is published in Annals of Neurology. The big question in this study was whether learning a new language improved cognitive functions or whether individuals with better cognitive abilities were more likely to become bilingual. Dr Thomas Bak, from the Centre for Cognitive Ageing and Cognitive Epidemiology at the University of Edinburgh, said he believed he had found the answer. Using data from intelligence tests on 262 Edinburgh-born individuals at the age of 11, the study looked at how their cognitive abilities had changed when they were tested again in their seventies. The research was conducted between 2008 and 2010. All participants said they were able to communicate in at least one language other than English. Of that group, 195 learned the second language before the age of 18, and 65 learned it after that time. The findings indicate that those who spoke two or more languages had significantly better cognitive abilities compared to what would have been expected from their baseline test. The strongest effects were seen in general intelligence and reading. The effects were present in those who learned their second language early, as well as later in life. BBC © 2014
Elizabeth Norton It's a sad fact that children born in poverty start out at a disadvantage and continue to fall further behind kids who are more privileged as they grow up. In developing countries, chiefly in Africa and Asia, some 200 million children under age 5 won't reach the same milestones—for physical growth, school performance, and earnings later on—as children who are less deprived. But a new analysis of a long-term study in Jamaica shows that surprisingly simple ways of stimulating children’s mental development can have dramatic benefits later in life. The children were participants in the Jamaican Study, a project geared toward improving cognitive development begun in the mid-1980s by child health specialists Sally Grantham-McGregor of University College London and Susan Walker of the University of the West Indies, Mona, in Jamaica. They focused on children between the ages of 9 and 24 months whose growth was stunted, placing them in the bottom 5% of height for their age and sex (an easy-to-quantify gauge of extreme poverty). Children of normal height in the same neighborhoods were also studied for comparison. For 2 years, community health workers visited the families weekly. One group was given nutritional assistance only (a formula containing 66% of daily recommended calories, along with vitamins and minerals). One group received a mental and social stimulation program only, and one group got stimulation and nutritional assistance. A final group had no intervention and served as a control. The mental stimulation program involved giving parents simple picture books and handmade toys, and encouraging them to read and sing to their children and point out names of objects, shapes, and colors. They were also taught better ways to converse and respond to their toddlers. These everyday interactions aren't always part of the culture in low-income countries, explains Paul Gertler, an economist at the University of California, Berkeley. "Parents might have five or six kids and few toys. They might be working really hard and have a lot of competing demands. They might not have been taught how to talk to their children, or how important and effective it is," he says. Past research attests to the importance of everyday conversation for children’s mental development: A recent study suggests that children of affluent parents do better in life in large part because their parents talk to them more. © 2014 American Association for the Advancement of Science
Pain is a symptom of many disorders; chronic pain can present as a disease in of itself. The economic cost of pain is estimated to be hundreds of billions of dollars annually in lost wages and productivity. “This database will provide the public and the research community with an important tool to learn more about the breadth and details of pain research supported across the federal government. They can search for individual research projects or sets of projects grouped by themes uniquely relevant to pain,” said Linda Porter, Ph.D., Policy Advisor for Pain at the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health (NIH). “It also can be helpful in identifying potential collaborators by searching for topic areas of interest or for investigators.” Users of the database easily can search over 1,200 research projects in a multi-tiered system. In Tier 1, grants are organized as basic, translational (research that can be applied to diseases), or clinical research projects. In Tier 2, grants are sorted among 29 scientific topic areas related to pain, such as biobehavioral and psychosocial mechanisms, chronic overlapping conditions, and neurobiological mechanisms. The Tier 2 categories are also organized into nine research themes: pain mechanisms, basic to clinical, disparities, training and education, tools and instruments, risk factors and causes, surveillance and human trials, overlapping conditions, and use of services, treatments, and interventions.
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