Most Recent Links
Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.
By Steven Petrow I have slogged through a number of difficult situations in recent months, among them the ongoing crises of my elderly parents’ illnesses and the suicide of a friend. I never lost my appetite nor burst into tears, and I didn’t suffer from any of the other typical symptoms of depression. Maybe I was more irritable than usual, a bit more prone to snap. And yes, I buried myself in my work. But I didn’t think I’d tripped down into the rabbit hole of depression. You would think I would have been more self-aware, both personally and professionally. As a health journalist, I have often used my own stories to write about difficult-to-discuss medical conditions, including learning I had testicular cancer at age 26 and my misdiagnosis with H.I.V./AIDS — back when it was a death sentence. But I had never written about suffering from depression, even though it’s plagued me since I first put pen to paper, at age 11, when I started keeping a diary. Still, I’m far from alone. At least six million men in the United States suffer from depression, according to the National Institute of Mental Health. The true number is likely to be even higher, said Dr. Matthew Rudorfer, the institute’s associate director for treatment research, since men are less likely than women to report classic symptoms like low mood, sadness or crying, so they often go undiagnosed. Men, he told me, more often demonstrate “externalizing” symptoms like irritability, anger and aggressiveness, substance and alcohol abuse, risk-taking behaviors and “workaholism.” Oh, that macho thing: Men don’t get depressed; they just work, drink and compete harder. Andrew Solomon, author of the pathbreaking memoir about depression, “Noonday Demon,” told me that ridiculous attitude is part of the mind-set that guys should “cover up our moods with militarism or athleticism.” © 2016 The New York Times Company
Link ID: 21874 - Posted: 02.09.2016
By NATALIE ANGIER Whether to enliven a commute, relax in the evening or drown out the buzz of a neighbor’s recreational drone, Americans listen to music nearly four hours a day. In international surveys, people consistently rank music as one of life’s supreme sources of pleasure and emotional power. We marry to music, graduate to music, mourn to music. Every culture ever studied has been found to make music, and among the oldest artistic objects known are slender flutes carved from mammoth bone some 43,000 years ago — 24,000 years before the cave paintings of Lascaux. Given the antiquity, universality and deep popularity of music, many researchers had long assumed that the human brain must be equipped with some sort of music room, a distinctive piece of cortical architecture dedicated to detecting and interpreting the dulcet signals of song. Yet for years, scientists failed to find any clear evidence of a music-specific domain through conventional brain-scanning technology, and the quest to understand the neural basis of a quintessential human passion foundered. Now researchers at the Massachusetts Institute of Technology have devised a radical new approach to brain imaging that reveals what past studies had missed. By mathematically analyzing scans of the auditory cortex and grouping clusters of brain cells with similar activation patterns, the scientists have identified neural pathways that react almost exclusively to the sound of music — any music. It may be Bach, bluegrass, hip-hop, big band, sitar or Julie Andrews. A listener may relish the sampled genre or revile it. No matter. When a musical passage is played, a distinct set of neurons tucked inside a furrow of a listener’s auditory cortex will fire in response. Other sounds, by contrast — a dog barking, a car skidding, a toilet flushing — leave the musical circuits unmoved. Nancy Kanwisher and Josh H. McDermott, professors of neuroscience at M.I.T., and their postdoctoral colleague Sam Norman-Haignere reported their results in the journal Neuron. The findings offer researchers a new tool for exploring the contours of human musicality. © 2016 The New York Times Company
It’s well known that some people report that their mood is influenced by the seasons. But can the time of year affect other cognitive functions? To find out, Gilles Vandewalle and colleagues at the University of Liege in Belgium scanned the brains of 28 volunteers while they performed attention and working memory tests at different times of the year. To ensure the results were influenced by the seasons rather than the environmental conditions on the test day, the participants were confined to a lab for 4.5 days prior to the test, exposed to a constant light level and temperature. Although their test scores didn’t change with the seasons, activity in some brain areas showed a consistent seasonal pattern among the volunteers: brain activity peaked in the summer on the attention task and in the autumn on the memory task. Many seasonally changing factors could regulate such a pattern, including day length (known as photoperiod), temperature, humidity, social interaction and physical activity. Since these weren’t all controlled for in the study, it’s impossible to say what is responsible for the seasonal changes seen. “In our data it seems that photoperiod, or the rate of change of photoperiod, was more likely to explain what we were seeing. But we can’t exclude all the others,” says Vandewalle. The results suggest that over the course of a year, the brain might work in different ways to compensate for seasonal factors that could affect its function, enabling it to maintain a stable performance. Vandewalle speculates that these mechanisms might not work as well in some people, for example, those vulnerable to the winter blues. © Copyright Reed Business Information Ltd.
Laura Sanders A preliminary report from scientists at the biotech company Amgen Inc. questions a cancer drug’s ability to fight Alzheimer’s disease. In experiments described February 4 in F1000Research, bexarotene, a drug approved by the FDA to treat lymphoma, didn’t reduce levels of the Alzheimer’s-related amyloid-beta protein. In the original work, described in Science in 2012 (SN: 3/10/12, p. 5), neuroscientist Gary Landreth of Case Western Reserve University in Cleveland and colleagues showed that bexarotene swiftly clears A-beta from the brains of mice, reducing both the sticky plaques and smaller forms of the protein that circulate in the brain. The mice also showed signs of improved learning and memory. A year after that work appeared, four reports, also in Science, disputed some of those findings. In tests on rats, the Amgen scientists found that bexarotene didn’t drop levels of plaques or smaller forms of A-beta. The new study didn’t describe behavioral tests. Landreth points out that this study, and previous experiments that failed to find a benefit, used a formulation of the drug that wouldn’t persist at high enough levels in the brain to be useful. “The controversy with the preclinical data is going to go away in the face of solid clinical trials,” Landreth says. A small clinical trial published online January 29 in Alzheimer’s Research & Therapy found that bexarotene reduced A-beta in the brains of people, but only people without a particular version of the ApoE gene, a known risk factor for Alzheimer’s. © Society for Science & the Public 2000 - 2016
Link ID: 21871 - Posted: 02.09.2016
By Jesse Singal On paper, Dr. Kenneth Zucker isn’t the sort of person who gets suddenly and unceremoniously fired. For decades, the 65-year-old psychologist had led the Child Youth and Family Gender Identity Clinic (GIC), in Toronto, one of the most well-known clinics in the world for children and adolescents with gender dysphoria — that is, the feeling that the body they were born with doesn’t fit their true gender identity. Zucker had built up quite a CV during his time leading the clinic: In addition to being one of the most frequently cited names in the research literature on gender dysphoria and gender-identity development, and the editor of the prestigious journal Archives of Sexual Behavior, he took a leading role helping devise diagnostic and treatment guidelines for gender dysphoric and transgender individuals. He headed the group which developed the DSM-5’s criteria for its “gender dysphoria” entry, for example, and also helped write the most recent “standards of care” guidelines for the World Professional Association for Transgender Health — one of the bibles for clinicians who treat transgender and gender-dysphoric patients. An impressive career, yes, but it’s doubtful any of this gave him much comfort on December 15. That was when he was called in from vacation for an 8:30 a.m. meeting with his employer, the Centre for Addiction and Mental Health (CAMH), one of the largest mental health and addiction research hospitals in Canada. Given the long-brewing investigation of his clinic by the hospital, it’s unlikely Zucker was feeling optimistic about what awaited him in downtown Toronto. The GIC, which operates out of CAMH, pronounced “Cam-H,” had been standing firm against a changing tide in the world of psychological treatment for children with gender dysphoria. The “gender-affirmative” approach, which focuses on identifying young transgender children and helping them socially transition — that is, express their gender to others through their everyday clothes, name changes, or other means — has been on the rise in recent years, and has become the favored protocol of many activists and clinicians. GIC clinicians, who saw clients between ages 3 and 18, had a much more cautious stance on social transitioning for their younger clients — they believed that in many cases, it was preferable to first “help children feel comfortable in their own bodies,” as they often put it, since in the GIC’s view gender is quite malleable at a young age and gender dysphoria will likely resolve itself with time. © 2016, New York Media LLC
By RACHEL NUWER For all the havoc that zebra mussels, Asian carp, round gobies and dozens of other alien species have wrought on the Great Lakes, those waters have never known a foe like the sea lamprey. The vampirelike parasites cost many millions each year in depleted fisheries and eradication efforts. Wildlife managers have long used lampricide — the lamprey version of pesticide — with mixed results. Now, an innovative control program seeks to improve on that method by using pheromones to trick the bloodsuckers into voluntarily corralling themselves in designated areas, to then be trapped or poisoned. But achieving this depends on cracking the fish’s olfactory language. “The broad goal is to understand how this animal makes decisions,” said Michael Wagner, a fish ecologist at Michigan State University. “Then, we want to use that understanding to guide lampreys’ movements by manipulating the landscape of fear and opportunity.” Lampreys look like the stuff of horror films: a slithering, tubular body topped with a suction-cup mouth ringed with row upon row of hooked yellow teeth. With this mouth, a sea lamprey anchors to its fish prey and uses its rasping tongue to drill into the victim’s flesh. It remains there for up to a month, feeding on blood and body fluids. Even if a fish survives the attack, the gaping wound left behind often results in death. In their natural ranges, lampreys are important components of food webs. The problems begin only when they shift from native to invader. Sea lampreys slipped into Lake Ontario through the Erie Canal in the mid-19th century, and then made it past Niagara Falls around 1919 with the renovation of the Welland Canal. In the lakes, lampreys found a utopia: no predators, and bountiful prey that had no natural defenses against their voracious appetites. Biological disaster ensued. © 2016 The New York Times Company
Keyword: Chemical Senses (Smell & Taste)
Link ID: 21869 - Posted: 02.08.2016
Floaters, those small dots or cobweb-shaped patches that move or “float” through the field of vision, can be alarming. Though many are harmless, if you develop a new floater, “you need to be seen pretty quickly” by an eye doctor in order to rule out a retinal tear or detachment, said Dr. Rebecca Taylor, a spokeswoman for the American Academy of Ophthalmology. Floaters are caused by clumping of the vitreous humor, the gel-like fluid that fills the inside of the eye. Normally, the vitreous gel is anchored to the back of the eye. But as you age, it tends to thin out and may shrink and pull away from the inside surface of the eye, causing clumps or strands of connective tissue to become lodged in the jelly, much as “strands of thread fray when a button comes off on your coat,” Dr. Taylor said. The strands or clumps cast shadows on the retina, appearing as specks, dots, clouds or spider webs in your field of vision. Such changes may occur at younger ages, too, particularly if you are nearsighted or have had a head injury or eye surgery. There is no treatment for floaters, though they usually fade with time. But it’s still important to see a doctor if new floaters arise because the detaching vitreous gel can pull on the retina, causing it to tear, which can lead to retinal detachment, a serious condition. The pulling or tugging on the retina may be perceived as lightning-like flashes, “like a strobe light off to the side of your vision,” Dr. Taylor said. See an eye doctor within 24 to 48 hours if you have a new floater, experience a sudden “storm” of floaters, see a gray curtain or shadow move across your field of vision, or have a sudden decrease in vision. © 2016 The New York Times Company
Link ID: 21868 - Posted: 02.08.2016
Laura Sanders The brain can bounce back after a single head hit, but multiple hits in quick succession don’t give the brain time to recover, a new study suggests. Although the finding comes from mice, it may help scientists better understand the damage caused by repetitive impacts such as those sustained in football, soccer and other contact sports. The results, published in the March issue of the American Journal of Pathology, hint that a single, mild head hit isn’t necessarily cause for alarm. “There are things to be afraid of after a concussion,” says study coauthor Mark Burns of Georgetown University Medical Center in Washington, D.C. “But not every concussion is going to cause long-term damage.” Burns and his colleagues subjected some mice to a single, mild head hit. The relatively weak hit consistently slowed anesthetized mice’s return to consciousness, but didn’t cause major trauma. The impact was designed to mimic a mild traumatic brain injury, or concussion, in a person. Tests a day after the impact showed that about 13 percent of dendritic spines, docking sites that help connect brain cells, had vanished in a particular part of the brain. Three days after the injury, these missing connections reappeared, even surpassing the original number of connections. This fluctuating number of dendritic spines may actually help the brain recover, Burns says. “The cells weren’t dying,” he says. “They were responding to the injury.” © Society for Science & the Public 2000 - 2016.
Keyword: Brain Injury/Concussion
Link ID: 21867 - Posted: 02.06.2016
By Jeneen Interlandi The human brain’s memory-storage capacity is an order of magnitude greater than previously thought, researchers at the Salk Institute for Biological Studies reported last week. The findings, recently detailed in eLife, are significant not only for what they say about storage space but more importantly because they nudge us toward a better understanding of how, exactly, information is encoded in our brains. The question of just how much information our brains can hold is a longstanding one. We know that the human brain is made up of about 100 billion neurons, and that each one makes 1,000 or more connections to other neurons, adding up to some 100 trillion in total. We also know that the strengths of these connections, or synapses, are regulated by experience. When two neurons on either side of a synapse are active simultaneously, that synapse becomes more robust; the dendritic spine (the antenna on the receiving neuron) also becomes larger to support the increased signal strength. These changes in strength and size are believed to be the molecular correlates of memory. The different antenna sizes are often compared with bits of computer code, only instead of 1s and 0s they can assume a range of values. Until last week scientists had no idea how many values, exactly. Based on crude measurements, they had identified just three: small, medium and large. But a curious observation led the Salk team to refine those measurements. In the course of reconstructing a rat hippocampus, an area of the mammalian brain involved in memory storage, they noticed some neurons would form two connections with each other: the axon (or sending cable) of one neuron would connect with two dendritic spines (or receiving antennas) on the same neighboring neuron, suggesting that duplicate messages were being passed from sender to receiver. © 2016 Scientific American
Keyword: Learning & Memory
Link ID: 21866 - Posted: 02.06.2016
Colombia says three people have died after contracting the Zika virus and developing a rare nerve disorder. Health Minister Alejandro Gaviria said there was a "causal connection" between Zika, the Guillain-Barre disorder and the three deaths. Earlier, Brazilian scientists said they had detected for the first time active samples of Zika in urine and saliva. However, it is not clear whether the virus can be transmitted through bodily fluids. Zika, a mosquito-borne disease, has been linked to cases of babies born in Brazil with microcephaly - underdeveloped brains. "We have confirmed and attributed three deaths to Zika," said the head of Colombia's National Health Institute, Martha Lucia Ospina. "In this case, the three deaths were preceded by Guillain-Barre syndrome." Guillain-Barre is a rare disorder in which the body's immune system attacks part of the nervous system. It isn't normally fatal. Ms Ospina said another six deaths were being investigated for possible links to Zika. "Other cases (of deaths linked to Zika) are going to emerge," she said. "The world is realising that Zika can be deadly. The mortality rate is not very high, but it can be deadly." Mr Gaviria said one of the fatalities took place in San Andres and the other two in Turbo, in Antioquia department. UK virologist Prof Jonathan Ball, of the University of Nottingham, told the BBC: "We have been saying Zika has been associated with Guillain-Barre. One of the complications of that could be respiratory failure. But it is still probably a very rare event." Although Zika usually causes mild, flu-like symptoms, it has been linked to thousands of suspected birth defects. However, it has not yet been proved that Zika causes either microcephaly or Guillain-Barre. © 2016 BBC
Could a painkiller turn people away from suicide? A preliminary trial of an opioid called buprenorphine shows that the drug can reduce suicidal thoughts after just one week. If validated in larger studies, it could become the first fast-acting anti-suicide drug. Such a drug is sorely needed. The US Centers for Disease Control and Prevention (CDC) estimates that more than 9 million adults in the country reported having suicidal thoughts in 2013. Over a million went on to attempt suicide. “Around 400,000 suicidal people are coming to emergency rooms every year,” says Elizabeth Ballard at the National Institute of Mental Health. “Pharmacologically, nothing has been approved for acute treatment of suicidal ideation so anything that can help them is greatly needed.” When people seek help, they may be offered behavioural therapy or drugs such as antidepressants. But neither of these is guaranteed to alleviate feelings, and both can take six weeks or more to kick in. Ketamine, a drug being considered as an immediate treatment, can cause hallucinations and its effects wear off quickly. “Having something you could use on your own outside of a hospital would be beneficial,” says Ballard. Jaak Panksepp at Washington State University and his colleagues decided to see whether an opioid can counter suicidal feelings. Opioids are one of the brain’s natural feel-good chemicals. They are released to relieve pain when we hurt ourselves, and are involved when we deal with mental pain, such as that caused by social rejection, a common trigger for suicidal thoughts. © Copyright Reed Business Information Ltd.
By Jonathan Leo Last week, according to many media accounts, scientists from Harvard Medical School, Boston Children’s Hospital, and the Broad Institute discovered the genetic basis of schizophrenia. The researchers reported in Nature that people with schizophrenia were more likely to have the overactive forms of a gene called complement component 4, or C4, which is involved in pruning synapses during adolescence. However, suggesting a biologic mechanism for a small subset of those diagnosed with schizophrenia is not the same as confirming the genetic theory of schizophrenia. Benedict Carey, science reporter for the New York Times, delved into the details and reported the all-important fact that having the C4 variant would increase a person’s risk by about 25 percent over the 1-percent base rate of schizophrenia—that is, to 1.25 percent. Genes for schizophrenia and depression have been discovered before, and in those cases, the subsequent enthusiastic headlines were shortly followed by retractions and more sober thinking. There are so many open questions (for instance, why do many people with the problematic variant not develop schizophrenia, and why do many people who don’t have the variant develop schizophrenia?) that the same may occur with the C4 discovery. The idea that mental illness is the result of a genetic predisposition is the foundation for modern-day psychiatry and has been the driving force for how research money is allocated, how patients are treated, and how society views people diagnosed with conditions identified in the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition. Schizophrenia holds a unique spot in the annals of mental health research because of its perceived anatomical underpinnings and is often cited as evidence in favor of a genetic predisposition to other conditions.
Rare ‘allergy’ to vibrations tied to faulty gene By Kelly Servick If you have the rare condition known as vibratory urticaria, you may be wary of handling lawnmowers and electric mixers. Rubbing or vibration against your skin—even from drying off with a towel—can cause you to break out in hives, make your face flush, give you headaches, or produce the sensation of a metallic taste. The condition, which runs in families, is so rare that the researchers who work on it have only tracked down a few cases over years of searching. But a genetic study on three such unique families has revealed a potential mechanism for the strange symptoms. Research published online today in the New England Journal of Medicine describes a mutation in a gene called ADGRE2, found in 22 people with vibratory urticaria, but not in 14 of their unaffected relatives. The gene codes for a receptor protein that was found on the surface of mast cells—immune cells in the skin that dump out inflammatory molecules such as histamines that increase blood flow to an area and can cause hives. The researchers observed that shaking mast cells in a dish breaks apart two subunits of this receptor protein, which prompts histamine release. In people with the newly discovered mutation, the receptor is more prone to breakage, which causes this protective immune response at the site of physical trauma to run amok. © 2016 American Association for the Advancement of Science.
By JOHN BRANCH Shortly before he died in July, the former N.F.L. quarterback Ken Stabler was rushed away by doctors, desperate to save him, in a Mississippi hospital. His longtime partner followed the scrum to the elevator, holding his hand. She told him that she loved him. Stabler said that he loved her, too. “I turned my head to wipe the tears away,” his partner, Kim Bush, said recently. “And when I looked back, he looked me dead in the eye and said, ‘I’m tired.’ ” They were the last words anyone in Stabler’s family heard him speak. “I knew that was it,” Bush said. “I knew that he had gone the distance. Because Kenny Stabler was never tired.” The day after Stabler died on July 8, a victim of colon cancer at 69, his brain was removed during an autopsy and ferried to scientists in Massachusetts. It weighed 1,318 grams, or just under three pounds. Over several months, it was dissected for clues, as Stabler had wished, to help those left behind understand why his mind seemed to slip so precipitously in his final years. On the neuropathologist’s scale of 1 to 4, Stabler had high Stage 3 chronic traumatic encephalopathy, or C.T.E., the degenerative brain disease believed to be caused by repeated blows to the head, according to researchers at Boston University. The relationship between blows to the head and brain degeneration is still poorly understood, and some experts caution that other factors, like unrelated mood problems or dementia, might contribute to symptoms experienced by those later found to have had C.T.E. Stabler, well known by his nickname, the Snake (“He’d run 200 yards to score from 20 yards out,” Stabler’s junior high school coach told Sports Illustrated in 1977), is one of the highest-profile football players to have had C.T.E. The list, now well over 100 names long, includes at least seven members of the Pro Football Hall of Fame, including Junior Seau, Mike Webster and Frank Gifford. © 2016 The New York Times Company
Keyword: Brain Injury/Concussion
Link ID: 21861 - Posted: 02.04.2016
By Diana Kwon Antidepressants are some of the most commonly prescribed medications out there. More than one out of 10 Americans over age 12—roughly 11 percent—take these drugs, according to a 2011 report by the National Center for Health Statistics. And yet, recent reports have revealed that important data about the safety of these drugs—especially their risks for children and adolescents—has been withheld from the medical community and the public. In the latest and most comprehensive analysis, published last week in BMJ (the British Medical Journal),a group of researchers at the Nordic Cochrane Center in Copenhagen showed that pharmaceutical companies were not presenting the full extent of serious harm in clinical study reports, which are detailed documents sent to regulatory authorities such as the U.S. Food and Drug Administration and the European Medicines Agency (EMA) when applying for approval of a new drug. The researchers examined documents from 70 double-blind, placebo-controlled trials of two common types of antidepressants—selective serotonin reuptake inhibitors (SSRI) and serotonin and norepinephrine reuptake inhibitors (SNRI)—and found that the occurrence of suicidal thoughts and aggressive behavior doubled in children and adolescents who used these medications. This paper comes on the heels of disturbing charges about conflicts of interest in reports on antidepressant trials. Last September a study published in the Journal of Clinical Epidemiology revealed that a third of meta-analyses of antidepressant studies were written by pharma employees and that these were 22 times less likely than other meta-studies to include negative statements about the drug. © 2016 Scientific American
Link ID: 21860 - Posted: 02.04.2016
By Christian Jarrett Back in the 1980s, the American scientist Benjamin Libet made a surprising discovery that appeared to rock the foundations of what it means to be human. He recorded people’s brain waves as they made spontaneous finger movements while looking at a clock, with the participants telling researchers the time at which they decided to waggle their fingers. Libet’s revolutionary finding was that the timing of these conscious decisions was consistently preceded by several hundred milliseconds of background preparatory brain activity (known technically as “the readiness potential”). The implication was that the decision to move was made nonconsciously, and that the subjective feeling of having made this decision is tagged on afterward. In other words, the results implied that free will as we know it is an illusion — after all, how can our conscious decisions be truly free if they come after the brain has already started preparing for them? For years, various research teams have tried to pick holes in Libet’s original research. It’s been pointed out, for example, that it’s pretty tricky for people to accurately report the time that they made their conscious decision. But, until recently, the broad implications of the finding have weathered these criticisms, at least in the eyes of many hard-nosed neuroscientists, and over the last decade or so his basic result has been replicated and built upon with ever more advanced methods such as fMRI and the direct recording of neuronal activity using implanted electrodes. © 2016, New York Media LLC
Link ID: 21859 - Posted: 02.04.2016
By Susana Martinez-Conde Take a look at the red chips on the two Rubik cubes below. They are actually orange on the left and purple on the right, if you look at them in isolation. They only appear more or less equally red across the images because your brain is interpreting them as red chips lit by either yellow or blue light. This kind of misperception is an example of perceptual constancy, the mechanism that allows you to recognize an object as being the same in different environments, and under very diverse lighting conditions. Constancy illusions are adaptive: consider what would have happened if your ancestors thought a friend became a foe whenever a cloud hid the sun, or if they lost track of their belongings–and even their own children—every time they stepped out of the cave and into the sunlight. Why, they might have even eaten their own kids! You are here because the perceptual systems of your predecessors were resistant to annoying changes in the physical reality–as is your own (adult) perception. There are many indications that constancy effects must have helped us survive (and continue to do so). One such clue is that we are not born with perceptual constancy, but develop it many months after birth. So at first we see all differences, and then we learn to ignore certain types of differences so that we can recognize the same object as unchanging in many varied scenarios. When perceptual constancy arises, we lose the ability to detect multiple contradictions that are nevertheless highly noticeable to young babies. © 2016 Scientific American
Mo Costandi The human brain is immediately recognizable by its cortex (meaning bark in Latin), the prominent outer layer of tissue, with its characteristic pattern of ridges and furrows, which sits atop the deep structures. The cortex is just several millimetres thick, but has a surface area of about two-and-a-half square feet, and is therefore heavily convoluted so it can be packed into the skull. This fleshy landscape begins to form during the second trimester of pregnancy, and continues into the first year of life. It is often assumed to be the result of genetics, like most other aspects of brain development. Forty years ago, however, Harvard researchers put forward the controversial idea that the brain folds up because of physical forces, and a new study now provides the first evidence this. According to this old model, the brain’s folds form as a result of differential growth which causes the cortex to grow in size far more quickly than other brain structures, leading it to buckle and fold as its surface area increases, due to the constraints of the skull. To test this, Tuomos Tallinen of the University of Jyväskylä in Finland and his colleagues used magnetic resonance images to create a 3D-printed cast of an unfolded 22-week-old human brain. This was made with a technique called layer-by-layer drop casting, and consisted of a soft polymer core coated with a thin sheet of an absorbent elastomer gel representing the cortex. © 2016 Guardian News and Media Limited
Keyword: Development of the Brain
Link ID: 21857 - Posted: 02.04.2016
By Nicholas Bakalar Women with sleeping difficulties are at increased risk for Type 2 diabetes, researchers report. Scientists used data from 133,353 women who were generally healthy at the start of the study. During 10 years of follow-up, they found 6,407 cases of Type 2 diabetes. The researchers looked at four sleep problems: self-reported difficulty falling or staying asleep, frequent snoring, sleep duration of less than six hours, and either sleep apnea or rotating shift work. The study is in Diabetologia. Self-reported difficulty sleeping was associated with higher B.M.I., less physical activity, and more hypertension and depression. But even after adjusting for these and other health and behavioral characteristics, sleeping difficulty was still associated with a 22 percent increased risk for Type 2 diabetes. Compared to women with no sleep problems, those with two of the sleep conditions studied had double the risk, and those with all four had almost four times the risk of developing the illness. The senior author, Dr. Frank B. Hu, a professor of nutrition and epidemiology at Harvard, said that sleep problems are associated with excess secretion of two hormones: ghrelin, which increases appetite, and cortisol, which increases stress and insulin resistance. Both are linked to metabolic problems that increase the risk for diabetes. “And,” he added, “it’s not just quantity of sleep, but quality as well” that is associated with these health risks. © 2016 The New York Times Company
Heidi Ledford Difficulty with concentration, memory and other cognitive tasks is often associated with depression. In the past quarter of a century, a wave of drugs has transformed the treatment of depression. But the advances have struggled to come to grips with symptoms that often linger long after people start to feel better: cognitive problems such as memory loss and trouble concentrating. On 3 February, the US Food and Drug Administration (FDA) will convene a meeting of its scientific advisers to discuss whether such cognitive impairments are components of the disorder that drugs might be able to target — or just a result of depressed mood. The discussion will help the agency to decide whether two companies that sell the antidepressant vortioxetine should be allowed to label it as a treatment for the cognitive effects. A ‘yes’ could spur drug developers to invest in ways to test cognitive function during their antidepressant trials. Psychiatrists have long noted that some people with depression also struggle to concentrate and to make decisions. The question has been whether such difficulties are merely an offshoot of altered mood and would thus clear up without specific treatment, says Diego Pizzagalli, a neuroscientist at McLean Hospital, an affiliate of Harvard Medical School in Belmont, Massachusetts. But some patients who report improved mood after treatment still struggle with cognitive deficits — so psychiatrists sometimes prescribe concentration-enhancing drugs that are approved to treat attention deficit hyperactivity disorder to people with depression. © 2016 Nature Publishing Group