Chapter 16. None
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By CATHERINE SAINT LOUIS Many cases of so-called crib death, about one in eight, occur among infants who have been placed on sofas, researchers reported on Monday. Dr. Jeffrey Colvin, a pediatrician at Children’s Mercy Hospital in Kansas City, Mo., and his colleagues analyzed data on 7,934 sudden infant deaths in 24 states, comparing those that occurred on sofas with those in cribs, bassinets or beds. Previous research had shown that couches were particularly hazardous for infants. The new analysis, published in the journal Pediatrics, tried to identify factors significant in these deaths. “It’s not only one risk that’s higher relative to other sleep environments,” said Barbara Ostfeld, a professor of pediatrics at Rutgers Robert Wood Johnson Medical School who was not involved in the new study. “It’s multiple risks.” Nearly three-quarters of the deaths occurred among infants age 3 months or younger, the researchers found. Pediatricians have long advised putting infants to sleep only on their backs, alone and on a firm, flat surface without a pillow. The new study found parents were more likely to lay their infants face down on a sofa than, for instance, face down in a crib. There’s a “fallacy that if I’m awake or watching, SIDS won’t happen,” Dr. Colvin said, referring to sudden infant death syndrome. © 2014 The New York Times Company
By MICHAEL S. A. GRAZIANO OF the three most fundamental scientific questions about the human condition, two have been answered. First, what is our relationship to the rest of the universe? Copernicus answered that one. We’re not at the center. We’re a speck in a large place. Second, what is our relationship to the diversity of life? Darwin answered that one. Biologically speaking, we’re not a special act of creation. We’re a twig on the tree of evolution. Third, what is the relationship between our minds and the physical world? Here, we don’t have a settled answer. We know something about the body and brain, but what about the subjective life inside? Consider that a computer, if hooked up to a camera, can process information about the wavelength of light and determine that grass is green. But we humans also experience the greenness. We have an awareness of information we process. What is this mysterious aspect of ourselves? Many theories have been proposed, but none has passed scientific muster. I believe a major change in our perspective on consciousness may be necessary, a shift from a credulous and egocentric viewpoint to a skeptical and slightly disconcerting one: namely, that we don’t actually have inner feelings in the way most of us think we do. Imagine a group of scholars in the early 17th century, debating the process that purifies white light and rids it of all colors. They’ll never arrive at a scientific answer. Why? Because despite appearances, white is not pure. It’s a mixture of colors of the visible spectrum, as Newton later discovered. The scholars are working with a faulty assumption that comes courtesy of the brain’s visual system. The scientific truth about white (i.e., that it is not pure) differs from how the brain reconstructs it. © 2014 The New York Times Company
Link ID: 20196 - Posted: 10.11.2014
by Mallory Locklear Do you have an annoying friend who loves bungee jumping or hang-gliding, and is always blathering on about how it never scares them? Rather than being a macho front, their bravado may have a biological basis. Research from Stony Brook University in New York shows that not all risk-takers are cut from the same cloth. Some actually seem to feel no fear – or at least their bodies and brains don't respond to danger in the usual way. The study is the first to attempt to tease apart the differences in the risk-taking population. In order to ensure every participant was a card-carrying risk-taker, the team led by Lilianne Mujica-Parodi, recruited 30 first-time skydivers. "Most studies on sensation-seeking compare people who take risks and people who don't. We were interested in something more subtle – those who take risks adaptively and those who do so maladaptively." In other words, do all risk-takers process potential danger in the same way or do some ignore the risks more than others? To find out, the researchers got their participants to complete several personality questionnaires, including one that asked them to rank how well statements such as, "The greater the risk the more fun the activity," described them. Next, the team used fMRI imaging to observe whether the participants' corticolimbic brain circuit – which is involved in risk assessment - was well-regulated. A well-regulated circuit is one that reacts to a threat and then returns to a normal state afterwards. © Copyright Reed Business Information Ltd
By Carl T. Hall Even Clayton Kershaw, the Los Angeles Dodgers’ pitching ace, makes mistakes now and then. And although very few of his mistakes seemed to do Giants hitters much good this season, a team of San Francisco scientists found a way to take full advantage. A new study by UCSF researchers revealed a tendency of the brain’s motion-control system to run off track in a predictable way when we try to perform the same practiced movement over and over. The scientists found the phenomenon first in macaque monkeys, then documented exactly the same thing in Kershaw’s game video. Although he struggled in a playoff appearance last week, the left-hander’s pitching performance during the regular season was among the best on record. It included a minuscule 1.77 earned run average, a nearly flawless no-hitter in June, 239 strikeouts and only 31 walks. He led the major leagues with 10.85 strikeouts per nine innings pitched. In what turned out to be an early warm-up to the playoffs, UCSF scientists Kris Chaisanguanthum, Helen Shen and Philip Sabes delved into the motor-control system of the primate brain. Their study, published in the Journal of Neuroscience, could help design better prosthetic limbs — or make robots that move less like robots and more like Kershaw. Unlike most machines, our brains seem to never stop trying to adapt to new information, making subtle adjustments each time we repeat a particular movement no matter how practiced. This trial-by-trial form of learning has obvious advantages in a fast-changing world, but also seems prone to drift away from spot-on accuracy as those small adjustments go too far.
Keyword: Learning & Memory
Link ID: 20193 - Posted: 10.11.2014
By David Shultz The next time you see a fruit fly hovering around your pint of beer, don’t swat it—appreciate it. You’re witnessing a unique relationship between yeast and insect. A new study reveals that the single-celled organisms have evolved to secrete a fruity scent that attracts fruit flies, which they hitch a ride on for greener pastures. The findings may also explain the sweet aroma of some craft beers. Like many scientific discoveries, the new work was the product of a happy accident. Kevin Verstrepen, a geneticist at KU Leuven in Belgium, was working with two types of yeast: a normal strain and another with a mutation in a gene called ATF1 that causes the cells to produce fewer odors during fermentation. “Nobody really knew what was happening until I was lazy enough to leave the lab on a Friday with these yeast left out on the bench,” he says. By coincidence, a group of fruit flies (Drosophila melanogaster) chose that weekend to escape from a neighboring genetics lab. When Verstrepen returned to work on Monday, he discovered that the insects had found their way into the smelly yeast culture but had ignored the mutant colony. To probe further, Verstrepen and colleagues set up an enclosed “arena” and pumped ATF1 aromas, which are either fruity, flowery, or solventlike, into one corner. Another corner received a dose of odors from the ATF1-deficient yeast. The remaining two corners emitted odorless streams of air to serve as controls. As expected, the flies congregated almost exclusively in the corner emitting the fragrant odors of yeast with intact ATF1 genes. Analyses of the insects’ brains revealed that the neurons in flies exposed to smelly yeast responded in an entirely different way from those exposed to odorless air or the scent of ATF1-deficient yeast strain, the researchers report online today in Cell Reports. © 2014 American Association for the Advancement of Science
Keyword: Chemical Senses (Smell & Taste)
Link ID: 20192 - Posted: 10.11.2014
BY Ashley Yeager A protein made by gut bacteria may trigger a chain of interactions in the body that contribute to eating disorders such as anorexia and bulimia. When the protein is produced, the body makes antibodies to bind to it, but the antibodies also attach to a hormone that controls fullness. In tests, mice given bacteria that produce the protein changed how much they ate compared with mice given bacteria that did not make the protein, a new study shows. Researchers also found that the antibodies to the protein were higher in patients with anorexia and bulimia. The results, which appear October 7 in Translational Psychiatry, seem to be some of the earliest to link gut bacteria to eating disorders. © Society for Science & the Public 2000 - 2014.
Keyword: Anorexia & Bulimia
Link ID: 20188 - Posted: 10.11.2014
By Elizabeth Pennisi Four years ago, Igor Spetic lost his right arm in an industrial accident. Doctors outfitted him with a prosthetic arm that restored some function, but they couldn't restore his sense of touch. Without it, simple tasks like picking up a glass or shaking hands became hit-or-miss propositions. The lack of touch also robs Spetic of basic pleasures. “I would love to feel my wife’s hand,” he says. In time, he may regain that pleasure: Two independent research teams have now equipped artificial hands with sensors that send signals to the wearer’s nerves to recreate this missing sense. The sensing technologies work only in the lab, but they have proved durable, and amputees who have tried them, including Spetic, say that they are effective. One technology advances the range of touch sensations available, while the other promises to enable touch through a better way to attach the prosthesis. “All of these results are very positive,” says Mandayam Srinivasan, a neuroengineer at the Massachusetts Institute of Technology in Cambridge, who was not involved in either project. “Each of them fills a piece of the puzzle in terms of [prosthesis] development.” Almost 40 years ago, researchers tried to provide sensory feedback by adding pressure sensors to prostheses that relayed the sensation through electrodes attached to nerves. But for the most part, they just made it seem like the hand was tingling. And durability has been an issue in such efforts, too. In February, Silvestro Micera, a neuroengineer at the Sant'Anna School of Advanced Studies in Pisa, Italy, and the Swiss Federal Institute of Technology in Lausanne and his team showed that it was possible for sensor-equipped prosthetic arms to gently or powerfully grab objects and even to distinguish a round from a square object. But the study lasted just 4 weeks, in part because of the delicate interface with the body. © 2014 American Association for the Advancement of Science.
BY Sarah Zielinski Bird’s nests come in a wide variety of shapes and sizes, and they’re built out of all sorts of things. Hummingbirds, for instance, create tiny cups just a couple centimeters wide; sociable weavers in Africa, in contrast, work together to build huge nests more than two meters across that are so heavy they can collapse trees. There are nests built on rocky ledges, in mounds on the ground, high in trees and on the edges of buildings. Bowerbirds even construct their nests as tiny houses decorated with an artistic eye to attract the ladies. So perhaps it’s not all that surprising the no one had ever investigated whether birds camouflage their nests to protect their eggs against potential predators. It would make sense that they do, but if you were to test it, where would you start? For Ida Bailey of the University of St. Andrews in Fife, Scotland, and colleagues, the answer was zebra finches. Male finches usually build nests in dense shrubs and layer the outside of the nests with dry grass stems and fine twigs. Predators, usually birds, take a heavy toll on the zebra finches, though. Since birds tend to hunt based on sight rather than smell, camouflaging a nest might work to protect the eggs sequestered inside. And even better, because zebra finches have good color vision, building a camouflaged nest might be possible. So Bailey’s team gathered 21 pairs of zebra finches, some of which were already housed at the University of Glasgow in Scotland, while others were bought from a local pet store. The researchers set each pair up in its own cage. Two walls of the cage were lined with colored paper, and a nest cup was placed in that half of the cage. Then the birds were given two cups containing colored paper — one color that matched the walls and a second contrasting color. The results of the study appear October 1 in The Auk. © Society for Science & the Public 2000 - 2014.
By Erin Allday When the United States’ top public health and political leaders declared the 1990s the “decade of the brain,” Dr. Pratik Mukherjee couldn’t help but feel a little dubious. “I was kind of laughing, because I didn’t think we’d make much progress in just a decade,” said Mukherjee, a neuro-radiologist at UCSF. Twenty-four years later, Mukherjee said he and his peers around the country are primed to plunge into what he’d like to call the century of the brain — a deep dive into the basic biology and mechanics of the impossibly complex organ that controls our every thought, action, behavior and mood. The National Institutes of Health last week announced $47 million in grants as part of President Obama’s Brain Initiative, a project announced 18 months ago to, in the simplest language, reverse-engineer the human brain. The grants were among the first in a roughly 11-year plan that could cost more than $3 billion. Most of the projects are in developing new technologies to help map the brain and study its mechanics — how cells communicate, what makes them turn on and off, and how large regions of the brain interact, for example. Ultimately, scientists hope these tools will help the next generation of neuroscientists solve the brain-centric disorders — from autism and Alzheimer’s to depression and schizophrenia — that have confounded doctors for centuries.
Keyword: Brain imaging
Link ID: 20183 - Posted: 10.09.2014
Patients with schizophrenia are already known to have higher rates of premature death than the general population. The study found that elevated risks of heart disease and metabolic issues such as high blood sugar in people with first episode psychosis are due to an interaction of mental illness, unhealthy lifestyle behaviors and antipsychotic medications that may accelerate these risks. Patients entered treatment with significant health concerns – including excess weight, smoking, and metabolic issues – despite an average age of only 24 years. The study identifies key opportunities for health care systems to improve the treatment of such patients with first episode psychosis. The research was funded by the National Institute of Mental Health (NIMH), part of the National Institutes of Health. Christoph Correll, M.D., of The Zucker Hillside Hospital, Hofstra North Shore-Long Island Jewish School of Medicine, New York, and colleagues, report their findings on Oct. 8, 2014 in JAMA Psychiatry. The study is among the first of several to report results from the Recovery After an Initial Schizophrenia Episode (RAISE) project, which was developed by NIMH to examine first episode psychosis before and after specialized treatment was offered in community settings. The researchers studied nearly 400 individuals between the ages of 15 and 40 with first episode psychosis, who presented for treatment at 34 community-based clinics across 21 states. The frequency of obesity was similar to the same age group in the general population. However, smoking and metabolic syndrome (a combination of conditions including obesity, high blood pressure, high blood sugar, and abnormal blood fats, such as cholesterol and triglycerides) were much more common.
Link ID: 20182 - Posted: 10.09.2014
|By Tara Haelle The first step to treating or preventing a disease is often finding out what drives it. In the case of neurodegenerative disorders, the discovery two decades ago of what drives them changed the field: all of them—including Alzheimer's, Parkinson's, Huntington's and amyotrophic lateral sclerosis (ALS or Lou Gehrig's disease)—involve the accumulation of misfolded proteins in brain cells. Typically when a protein misfolds, the cell destroys it, but as a person ages, this quality-control mechanism starts to fail and the rogue proteins build up. In Huntington's, for example, huntingtin protein—used for many cell functions—misfolds and accumulates. Symptoms such as muscular difficulties, irritability, declining memory, poor impulse control and cognitive deterioration accompany the buildup. Mounting evidence suggests that not only does the accumulation of misfolded proteins mark neurodegenerative disease but that the spread of the proteins from one cell to another causes the disease to progress. Researchers have seen misfolded proteins travel between cells in Alzheimer's and Parkinson's. A series of experiments reported in Nature Neuroscience in August suggests the same is true in Huntington's. In their tests, researchers in Switzerland showed that mutated huntingtin protein in diseased brain tissue could invade healthy brain tissue when the two were placed together. And when the team injected the mutated protein into a live mouse's brain, it spread through the neurons within a month—similar to the way prions spread, says Francesco Paolo Di Giorgio of the Novartis Institutes for BioMedical Research in Basel, who led the research. Prions are misfolded proteins that travel through the body and confer their disease-causing characteristics onto other proteins, as seen in mad cow disease. But it is not known if misfolded proteins involved in Huntington's convert other proteins as true prions do, according to Di Giorgio. © 2014 Scientific American
Link ID: 20181 - Posted: 10.08.2014
David Cyranoski Unlike its Western counterparts, Japan’s effort will be based on a rare resource — a large population of marmosets that its scientists have developed over the past decade — and on new genetic techniques that might be used to modify these highly social animals. The goal of the ten-year Brain/MINDS (Brain Mapping by Integrated Neurotechnologies for Disease Studies) project is to map the primate brain to accelerate understanding of human disorders such as Alzheimer’s disease and schizophrenia. On 11 September, the Japanese science ministry announced the names of the group leaders — and how the project would be organized. Funded at ¥3 billion (US$27 million) for the first year, probably rising to about ¥4 billion for the second, Brain/MINDS is a fraction of the size of the European Union’s Human Brain Project and the United States’ BRAIN (Brain Research through Advancing Innovative Neurotechnologies) Initiative, both of which are projected to receive at least US$1 billion over the next decade. But researchers involved in those efforts say that Brain/MINDS fills a crucial gap between disease models in smaller animals that too often fail to mimic human brain disorders, and models of the human brain that need validating data. “It is essential that we have a genetic primate model to study cognition and cognitive brain disorders such as schizophrenia and depression, for which we do not have good mouse models,” says neuroscientist Terry Sejnowski at the Salk Institute in La Jolla, California, who is a member of the National Institutes of Health BRAIN Initiative Working Group. “Other groups in the United States and China have started transgenic-primate projects, but none is as large or as well organized as the Japanese effort.” © 2014 Nature Publishing Group,
By Virginia Morell Two years ago, scientists showed that dolphins imitate the sounds of whales. Now, it seems, whales have returned the favor. Researchers analyzed the vocal repertoires of 10 captive orcas (Orcinus orca), three of which lived with bottlenose dolphins (Tursiops truncatus) and the rest with their own kind. Of the 1551 vocalizations these seven latter orcas made, more than 95% were the typical pulsed calls of killer whales. In contrast, the three orcas that had only dolphins as pals busily whistled and emitted dolphinlike click trains and terminal buzzes, the scientists report in the October issue of The Journal of the Acoustical Society of America. (Watch a video as bioacoustician and co-author Ann Bowles describes the difference between killer whale and orca whistles.) The findings make orcas one of the few species of animals that, like humans, is capable of vocal learning—a talent considered a key underpinning of language. © 2014 American Association for the Advancement of Science.
By CLAIRE MALDARELLI Whether it’s lying wide awake in the middle of the night or falling asleep at an international business meeting, many of us have experienced the funk of jet lag. New research has uncovered some of the mysteries behind how our cells work together to maintain one constant daily rhythm, offering the promise of defense against this disorienting travel companion. Many organisms, including humans and fruit flies, have pacemaker neurons — specialized cells in the brain that have their own molecular clocks and oscillate in 24-hour cycles. But in order for an organism to regulate itself, all of these internal clocks must tick together to create one master clock. While scientists understood how individual neurons set their own clock, they didn’t know how that master clock was set. Working with young fruit flies, whose neuronal system is simpler than adults with fewer cells and easier to study, the researchers found that two types of neurons, which they called dawn cells and dusk cells, maintain a continuous cycle. As the sun rises, special “timeless” proteins, as they’re called, help the dawn cells to first signal to each other and then signal to the dusk cells. Then as the sun sets, proteins help the dusk cells signal to each other and then signal back to the dawn cells. Each signal tells the cells to synchronize with each other. Together, these two distinct signals drive the daily sleep and wake cycle. “This really shifts our view of these cells as super strong, independent oscillators to much more of a collective group working together to keep time,” said Justin Blau, a neurobiologist at New York University and co-author of the study. © 2014 The New York Times Company
|By Brian Bienkowski and Environmental Health News On his farm in Iowa, Matt Peters worked from dawn to dusk planting his 1,500 acres of fields with pesticide-treated seeds. “Every spring I worried about him,” said his wife, Ginnie. “Every spring I was glad when we were done.” In the spring of 2011, Ginnie Peters' “calm, rational, loving” husband suddenly became depressed and agitated. “He told me ‘I feel paralyzed’,” she said. “He couldn’t sleep or think. Out of nowhere he was depressed.” A clinical psychologist spoke to him on the phone and urged him to get medical help. “He said he had work to do, and I told him if it’s too wet in the morning to plant beans come see me,” Mike Rossman said. “And the next day I got the call.” Peters took his own life. He was 55 years old. No one knows what triggered Peters’ sudden shift in mood and behavior. But since her husband’s death, Ginnie Peters has been on a mission to not only raise suicide awareness in farm families but also draw attention to the growing evidence that pesticides may alter farmers’ mental health. “These chemicals that farmers use, look what they do to an insect. It ruins their nervous system,” Peters said. “What is it doing to the farmer?” Farming is a stressful job – uncontrollable weather, physical demands and economic woes intertwine with a personal responsibility for land that often is passed down through generations. But experts say that some of the chemicals used to control pests may make matters worse by changing farmers’ brain chemistry. © 2014 Scientific American
By LAWRENCE K. ALTMAN A British-American scientist and a pair of Norwegian researchers were awarded this year’s Nobel Prize in Physiology or Medicine on Monday for discovering “an inner GPS in the brain” that enables virtually all creatures to navigate their surroundings. John O’Keefe, 75, a British-American scientist, will share the prize of $1.1 million with May-Britt Moser, 51, and Edvard I. Moser, 52, only the second married couple to win a Nobel in medicine, who will receive the other half. The three scientists’ discoveries “have solved a problem that has occupied philosophers and scientists for centuries — how does the brain create a map of the space surrounding us and how can we navigate our way through a complex environment?” said the Karolinska Institute in Sweden, which chooses the laureates. The positioning system they discovered helps us know where we are, find our way from place to place and store the information for the next time, said Goran K. Hansson, secretary of the Karolinska’s Nobel Committee. The researchers documented that certain cells are responsible for the higher cognitive function that steers the navigational system. Dr. O’Keefe began using neurophysiological methods in the late 1960s to study how the brain controls behavior and sense of direction. In 1971, he discovered the first component of the inner navigational system in rats. He identified nerve cells in the hippocampus region of the brain that were always activated when a rat was at a certain location. © 2014 The New York Times Company
Keyword: Learning & Memory
Link ID: 20169 - Posted: 10.07.2014
By Clare Wilson If you’re facing surgery, this may well be your worst nightmare: waking up while under the knife without medical staff realizing. The biggest-ever study of this phenomenon is shedding light on what such an experience feels like and is causing debate about how best to prevent it. For a one-year period starting in 2012, an anesthetist at every hospital in the United Kingdom and Ireland recorded every case where a patient told a staff member that he had been awake during surgery. Prompted by these reports, the researchers investigated 300 cases, interviewing the patient and doctors involved. One of the most striking findings, says the study’s lead author, Jaideep Pandit of Oxford University Hospitals, was that pain was not generally the worst part of the experience: It was paralysis. For some operations, paralyzing drugs are given to relax muscles and stop reflex movements. “Pain was something they understood, but very few of us have experienced what it’s like to be paralyzed,” Pandit says. “They thought they had been buried alive.” “I thought I was about to die,” says Sandra, who regained consciousness but was unable to move during a dental operation when she was 12 years old. “It felt as though nothing would ever work again — as though the anesthetist had removed everything apart from my soul.”
Link ID: 20168 - Posted: 10.07.2014
Aaron E. Carroll For a drug to be approved by the Food and Drug Administration, it must prove itself better than a placebo, or fake drug. This is because of the “placebo effect,” in which patients often improve just because they think they are being treated with something. If we can’t compare a new drug with a placebo, we can’t be sure that the benefit seen from it is anything more than wishful thinking. But when it comes to medical devices and surgery, the requirements aren’t the same. Placebos aren’t required. That is probably a mistake. At the turn of this century, arthroscopic surgery for osteoarthritis of the knee was common. Basically, surgeons would clean out the knee using arthroscopic devices. Another common procedure was lavage, in which a needle would inject saline into the knee to irrigate it. The thought was that these procedures would remove fragments of cartilage and calcium phosphate crystals that were causing inflammation. A number of studies had shown that people who had these procedures improved more than people who did not. However, a growing number of people were concerned that this was really no more than a placebo effect. And in 2002, a study was published that proved it. A total of 180 patients who had osteoarthritis of the knee were randomly assigned (with their consent) to one of three groups. The first had a standard arthroscopic procedure, and the second had lavage. The third, however, had sham surgery. They had an incision, and a procedure was faked so that they didn’t know that they actually had nothing done. Then the incision was closed. The results were stunning. Those who had the actual procedures did no better than those who had the sham surgery. They all improved the same amount. The results were all in people’s heads. © 2014 The New York Times Company
Keyword: Pain & Touch
Link ID: 20167 - Posted: 10.07.2014
Fiona Fox Last week the UK Home Office published the findings of its investigations into allegations of animal suffering, made after undercover infiltrations at two animal research facilities. You will not find coverage of any of the conclusions in the national news media. Instead any search for media coverage will unearth the original infiltration stories under headlines such as: “Horrific video shows distress of puppies and kittens waiting to be dissected at animal testing lab”; “Graphic content: horrifying video shows puppies and kittens tested at UK laboratory”; and “Rats beheaded with scissors and kept in ‘pitiful state’.” These “shocking exposés”, brought to the newspapers by the animal rights group BUAV, include distressing images, links to videos that are difficult to watch, and quote allegedly secretly recorded researchers saying terrible things about the animals in their care. The newspapers seem in no doubt that the allegations they are carrying add up to “appalling suffering on a very large scale”, and appear to be proud of their role in bringing the abuses to light: “The Sunday Express today publishes details of an undercover investigation … that shines a light on the secret world of vivisection laboratories.” You may well see these articles as reassuring evidence that we still have public interest journalism in the UK. These animal rights supporters have done exactly what investigative journalists used to do in a time when newspapers had enough money to shine a light on the darker corners of our institutions and uncover hidden abuses. And you would be right, but for one thing: we now know that the stories were largely untrue. © 2014 Guardian News and Media Limited
Keyword: Animal Rights
Link ID: 20165 - Posted: 10.07.2014
by Michael Marshall When we search for the seat of humanity, are we looking at the wrong part of the brain? Most neuroscientists assume that the neocortex, the brain's distinctive folded outer layer, is the thing that makes us uniquely human. But a new study suggests that another part of the brain, the cerebellum, grew much faster in our ape ancestors. "Contrary to traditional wisdom, in the human lineage the cerebellum was the part of the brain that accelerated its expansion most rapidly, rather than the neocortex," says Rob Barton of Durham University in the UK. With Chris Venditti of the University of Reading in the UK, Barton examined how the relative sizes of different parts of the brain changed as primates evolved. During the evolution of monkeys, the neocortex and cerebellum grew in tandem, a change in one being swiftly followed by a change in the other. But starting with the first apes around 25 million years ago through to chimpanzees and humans, the cerebellum grew much faster. As a result, the cerebellums of apes and humans contain far more neurons than the cerebellum of a monkey, even if that monkey were scaled up to the size of an ape. "The difference in ape cerebellar volume, relative to a scaled monkey brain, is equal to 16 billion extra neurons," says Barton. "That's the number of neurons in the entire human neocortex." © Copyright Reed Business Information Ltd.