Chapter 16. None
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THERE’S more to semen than sperm. In many animals, seminal fluid alters both the bodies and sometimes even the behaviour of females. Human semen, too, triggers changes in the uterus, and might have wider effects on women, aimed at just one goal. “It’s all about maximising the chances of the male reproducing,” says Sarah Robertson of the University of Adelaide in Australia. The effects are most striking in fruit flies: seminal fluid can make the females eat more, lay more eggs and be less receptive to other males. Now a team led by Tracey Chapman at the University of East Anglia in Norwich, UK, has found that male fruit flies selectively alter the chemical make-up of their seminal fluid. In the presence of rivals, the males produce more seminal proteins. “It came as a real surprise,” says Chapman. “It’s a sophisticated response to the social and sexual situation.” Some of their findings were presented at the Society for Molecular Biology and Evolution conference in Vienna, Austria, last week, including their discovery that one of these proteins is a “master regulator” of genes. Females exposed to it show a wide range of changes in gene expression. Chapman thinks this kind of seminal signalling is widespread in the animal world. The semen of people, pigs and mice affects the female reproductive tract, and the question is whether it can also produce behavioural responses in female mammals similar to those seen in fruit flies. © Copyright Reed Business Information Ltd.
Jessie Rack If you've ever had hiccups in a quiet room, you know how embarrassing and completely uncontrollable they can feel. What if, instead of the hiccups, your body jerked involuntarily or you blurted out words without meaning to? That's a rough idea of what living with Tourette syndrome can be like. Designers of a new computer program called TicHelper hope that they will be able to help children recognize and control these impulses themselves. People with Tourette's perform repetitive movements or vocalizations called tics. A simple tic might be something like head jerking, eye blinking, or throat clearing, and a complex tic might involve patterns of movement or saying multiple words or phrases. We don't know exactly what causes Tourette's, says Douglas Woods, a psychologist at Texas A&M University. Woods, who is also co-chair of the Tourette Association of America Medical Advisory Board, is one of the minds behind TicHelper. "Sometimes kids will grow out of [Tourette's]," Woods says. But if the wait-and-see approach isn't working, and the tics are interfering with daily life, there are a few treatment options. One option is medication. Woods says there are a few different antipsychotic drugs that are used to manage Tourette syndrome, but they have side effects and don't always work. An alternative to pharmaceutical treatment is behavioral therapy. A form of behavioral therapy called comprehensive behavioral intervention for tics, or CBIT for short, is commonly used. CBIT training teaches people with Tourette's to recognize the onset of a tic and to perform a different behavior when they feel one coming on. © 2015 NPR
Link ID: 21208 - Posted: 07.23.2015
By Warren Cornwall The number of U.S. school children placed in special education programs due to autism more than tripled from 2000 to 2010, to nearly 420,000. But a new study argues much of that increase likely came as educators swapped one diagnosis for another. The overall percentage of kids diagnosed with a collection of brain development problems that includes autism remained unchanged, suggesting that children who used to be labeled with conditions such as “intellectual disability” were in fact autistic. “If you asked me, ‘Is there a real increase in the prevalence of autism?’ maybe there is, but probably much lower than the reported magnitude,” says Santhosh Girirajan, a geneticist at Pennsylvania State University (Penn State), University Park. In the new study, Girirajan and colleagues combed through data collected in each state for approximately 6.2 million U.S. school children with disabilities who are enrolled in special education programs. The information is collected each year under the federal Individuals with Disabilities Education Act. Based on his or her diagnosis, each child was assigned to one of 13 broader categories, ranging from autism to physical challenges such as blindness. Between 2000 and 2010, the number of children in the autism category more than tripled from 93,624 in 2000 to 419,647 a decade later. Yet nearly two-thirds of that increase was matched by a decline in the rate at which children were labeled as having an “intellectual disability.” The number of kids in that category fell from 637,270 to 457,478. © 2015 American Association for the Advancement of Science.
Link ID: 21207 - Posted: 07.23.2015
By Sandhya Somashekhar NEW WESTMINSTER, B.C. — Alanna Whitney was a weird kid. She had a strange knack for pronouncing long words. Anchovies on pizza could send her cowering under a table. Her ability to geek out on subjects such as Greek mythology and world religions could be unsettling. She drank liquids obsessively, and in her teens, her extreme water intake landed her in the hospital. Years later, she found a word that explained it all: Autistic. Instead of grieving, she felt a rush of relief. “It was the answer to every question I’d ever had,” she recalled. “It was kind of like a go-ahead to shed all of those things I could or couldn’t do and embrace myself for who I am.” So it came to be that Whitney, 24, was arranging strawberries and store-bought cookies on platters at the Queensborough Community Center for a celebration of “Autistic Pride Day,” her shoulder-length hair dyed mermaid green to match her purse and sandals. A bowl of orange earplugs sat nearby in case any of the guests found the ambient sounds overwhelming. Whitney is part of a growing movement of autistic adults who are finding a sense of community, identity and purpose in a diagnosis that most people greet with dread. These “neurodiversity” activists contend that autism — and other brain afflictions such as dyslexia and attention deficit hyperactivity disorder — ought to be treated not as a scourge to be eradicated but rather as a difference to be understood and accepted.
Link ID: 21206 - Posted: 07.23.2015
By Hanae Armitage Cataracts cloud the eyes of tens of millions of people around the world and nearly 17.2% of Americans over the age of 40. Currently, the only treatment is surgery—lasers or scalpels cut away the molecular grout that builds in the eye as cataracts develop, and surgeons sometimes replace the lens. But now, a team of scientists and ophthalmologists has tested a solution in dogs that may be able to dissolve the cataract right out of the eye’s lens. And the solution is itself a solution: a steroid-based eye drop. Though scientists don’t fully understand how cataracts form, they do know that the “fog” often seen by patients is a glob of broken proteins, stuck together in a malfunctioning clump. When healthy, these proteins, called crystallins, help the eye’s lens keep its structure and transparency. But as humans and animals alike get older, these crystallin proteins start to come unglued and lose their ability to function. Then they clump together and form a sheathlike obstruction in the lens, causing the signature “steamy glass” vision that accompanies cataracts. Coming up with a solution other than surgery has been tough. Scientists have been hunting for years for mutations in crystallin proteins that might offer new insights and pave the way to an alternate therapy. Now, it looks like a team led by University of California (UC), San Diego, molecular biologist Ling Zhao may have done just that. Her team came up with the eye drop idea after finding that children with a genetically inherited form of cataracts shared a mutation that stopped the production of lanosterol, an important steroid in the body. When their parents did not have the same mutation, the adults produced lanosterol and had no cataracts. © 2015 American Association for the Advancement of Science.
Link ID: 21205 - Posted: 07.23.2015
By James Gallagher Health editor, BBC News website The first hints a drug can slow the progression of Alzheimer's disease have emerged at a conference. Data from pharmaceutical company Eli Lilly suggests its solanezumab drug can cut the rate of the dementia's progression by about a third. The results are being met with cautious optimism, with a separate trial due to report next year. The death of brain cells in Alzheimer's is currently inexorable. Solanezumab may be able to keep them alive. Current medication, such as Aricept, can only manage the symptoms of dementia by helping the dying brain cells function. But solanezumab attacks the deformed proteins, called amyloid, that build up in the brain during Alzheimer's. It is thought the formation of sticky plaques of amyloid between nerve cells leads to damage and eventually brain cell death. Solanezumab has long been the great hope of dementia research, yet an 18-month trial of the drug seemingly ended in failure in 2012. But when Eli Lilly looked more closely at the data, there were hints it could be working for patients in the earliest stages of the disease. So the company asked just over 1,000 of the patients in the original trial with mild Alzheimer's to take the drug for another two years. And the results from this extension of the original trial have now been presented, at the Alzheimer's Association International Conference. Dr Eric Siemers, from the Lilly Research Laboratories, in Indiana, told the BBC: "It's another piece of evidence that solanezumab does have an effect on the underlying disease pathology. "We think there is a chance that solanezumab will be the first disease-modifying medication to be available." The company also started a completely separate trial in mild patients in 2012, and these results could prove to be the definitive moment for the drug. © 2015 BBC.
Link ID: 21203 - Posted: 07.22.2015
Ewen Callaway A mysterious group of humans crossed the Bering land bridge from Siberia into the Americas thousands of years ago, genetic analyses reveal. Modern-day signatures of this ‘ghost population’ survive in people who live deep in the Brazilian Amazon, but the two research teams who have made the discovery have different ideas about when and how these migrants reached the Americas1, 2. "This is an unexpected finding," says Jennifer Raff, an anthropological geneticist at the University of Texas at Austin who was not involved in either study. "It’s honestly one of the most exciting results we’ve seen in a while." North and South America were the last continents that humans settled. Previous studies of DNA from modern and ancient Native Americans suggest that the trek was made at least 15,000 years ago (although the timing is not clear-cut) by a single group dubbed the ‘First Americans’, who crossed the Bering land bridge linking Asia and North America. “The simplest hypothesis would be that a single population penetrated the ice sheets and gave rise to most of the Americans,” says David Reich, a population geneticist at Harvard Medical School in Boston, Massachusetts. In 2012, his team found evidence for a single founding migration in the genomes from members of 52 Native American groups3. So Reich was flabbergasted when a colleague called Pontus Skoglund mentioned during a conference last year that he had found signs of a second ancient migration to the Americas lurking in the DNA of contemporary Native Amazonians. Reich wasted no time in verifying the discovery. “During the session afterward, he passed his laptop over the crowd, and he had corroborated the results,” says Skoglund, who is now a researcher in Reich’s lab. © 2015 Nature Publishing Group
Keyword: Genes & Behavior
Link ID: 21201 - Posted: 07.22.2015
By Smitha Mundasad Health reporter A type of diabetes drug may offer a glimmer of hope in the fight against Parkinson's disease, research in the journal Plos Medicine suggests. Scientists found people taking glitazone pills were less likely to develop Parkinson's than patients on other diabetes drugs. But they caution the drugs can have serious side-effects and should not be given to healthy people. Instead, they suggest the findings should prompt further research. 'Unintended benefits' There are an estimated 127,000 people in the UK with Parkinson's disease, which can lead to tremor, slow movement and stiff muscles. And charities say with no drugs yet proven to treat the condition, much more work is needed in this area. The latest study focuses solely on people with diabetes who did not have Parkinson's disease at the beginning of the project. Researchers scoured UK electronic health records to compare 44,597 people prescribed glitazone pills with 120,373 people using other anti-diabetic treatment. They matched participants to ensure their age and stage of diabetes treatment were similar. Scientists found fewer people developed Parkinson's in the glitazone group - but the drug did not have a long-lasting benefit. Any potential protection disappeared once patients switched to another type of pill. Dr Ian Douglas, lead researcher at the London School of Hygiene and Tropical Medicine, said: "We often hear about negative side-effects associated with medications, but sometimes there can also be unintended beneficial effects. "Our findings provide unique evidence that we hope will drive further investigation into potential drug treatments for Parkinson's disease." © 2015 BBC
Link ID: 21199 - Posted: 07.22.2015
By BENEDICT CAREY Bill Cosby stands accused of committing date rape long before drugs like GHB or Rohypnol were widely used for that purpose. Many of Mr. Cosby’s accusers believed they had been drugged — but with what? And how? In a recently obtained legal deposition, Mr. Cosby acknowledged giving quaaludes to some women with whom he had sex, but said consumption of the drug was consensual, “the same as a person would say, ‘Have a drink.’ ” In a transcript of the deposition, reported on Sunday in The New York Times, the comedian told lawyers had had obtained seven prescriptions for quaaludes. Originally approved and marketed as a “safer” sleeping pill, less addictive than barbiturates, the drug (known generically as methaqualone) was both sedating and hypnotic. Recreational use was common, but the federal government withdrew them from the market in 1982. “It was inevitable that it would be tried by people looking for a ‘better high,’ ” Dr. David Smith, medical director of the Haight-Ashbury Free Clinic, and Dr. Donald Wesson noted in The Journal of Psychedelic Drugs. Intoxication with quaaludes “soon developed a reputation for being especially pleasant.” Young people in the 1970s used quaaludes as they would a strong drink: to loosen up, to relax, to socialize. The pills also won a reputation for inducing periods of euphoria, as well as sexual arousal — “heroin for lovers,” some called it. By the middle of the decade, quaaludes were a staple of the club scene, often taken with alcohol. So embedded were quaaludes in the cultural scene that even years later the Dead Kennedys and Billy Idol were singing about the drug’s captivating effects. But reckless users risked overdose, especially when combining the pills with alcohol, which could lead to coma, convulsions and sometimes death. In a 1973 review of 252 hospital admissions for drug overdose, doctors in Edinburgh found that the third most common cause of “self-poisoning,” after barbiturates and LSD, was Mandrax — the British version of quaaludes, widely abused in South Africa as well. © 2015 The New York Times Company
Keyword: Drug Abuse
Link ID: 21198 - Posted: 07.22.2015
Carl Zimmer An ant colony is an insect fortress: When enemies invade, soldier ants quickly detect the incursion and rip their foes apart with their oversize mandibles. But some invaders manage to slip in with ease, none more mystifyingly than the ant nest beetle. Adult beetles stride into an ant colony in search of a mate, without being harassed. They lay eggs, from which larva hatch. As far as scientists can tell, workers feed the young beetles as if they were ants. When the beetles grow into adults, the ants swarm around them, grooming their bodies. In exchange for this hospitality, the beetles sink their jaws into ant larvae and freshly moulted adults in order to drink their body fluids. “They’re like vampire beetles wandering in the ant nests,” said Andrea Di Giulio, an entomologist at Roma Tre University in Rome. Dr. Di Giulio and his colleagues have now uncovered a remarkable trick that the beetles use to fool their hosts. It turns out they can perform uncanny impressions, mimicking a range of ant calls. Dr. Di Giulio and his colleagues study a species of ant nest beetle called Paussus favieri, which lives in the Atlas Mountains of Morocco, where it infiltrates the nests of Moroccan ants, known as Pheidole pallidula. Like many ant species, Pheidole pallidula makes noises by rubbing its legs against ridges on its body. The meanings of these signals vary from species to species; leaf-cutting ants summon bodyguards for the march back to the nest; in other species, a queen trills to her workers to attend to her. Scientists have found that Pheidole pallidula ants make three distinct sounds, each produced by a different caste: soldiers, workers and the queen. © 2015 The New York Times Company
by Stephen Buchmann Flowers, bugs and bees: Stephen Buchmann wanted to study them all when he was a kid. "I never grew out of my bug-and-dinosaur phase," he tells NPR's Arun Rath. "You know, since about the third grade, I decided I wanted to chase insects, especially bees." These days, he's living that dream. As a pollination ecologist, he's now taking a particular interest in how flowers attract insects. In his new book, The Reason for Flowers, he looks at more than just the biology of flowers — he dives into the ways they've laid down roots in human history and culture, too. On the real 'reason for flowers' The reason for flowers is actually one word: sex. So, flowers are literally living scented billboards that are advertising for sexual favors, whether those are from bees, flies, beetles, butterflies or us, because quite frankly most of the flowers in the world have gotten us to do their bidding. But that's only the first stage because flowers, if they're lucky, turn into fruits, and those fruits and seeds feed the world. On the raucous secret lives of beetles One of my favorite memories is roaming the Napa foothills as a UC Davis grad student. And I would go to the wineries, of course, and in between I would find western spice bush, which is this marvelous flower that kind of smells like a blend between a cabernet and rotten fruit. And when you find those flowers and open them up, you discover literally dozens of beetles in there, mating, defecating, pollinating — having a grand time. © 2015 NPR
By NANCY L. SEGAL, AARON T. GOETZ and ALBERTO C. MALDONADO SEVERAL years ago, while browsing the campus bookstore, one of us, Professor Segal, encountered a display table filled with Squirtles. A Squirtle is a plush-toy turtle manufactured by the company Russ Berrie. They were adorable and she couldn’t wait to take one home. Afterward, Professor Segal began wondering why this toy was so attractive and suspected that its large, round eyes played a major role. It’s well known that a preference for large eyes emerges in humans by 5 months of age. But the Squirtle was even more appealing than many of its big-eyed competitors. Was there something else about its eyes? Professor Segal consulted one of us, Professor Goetz, a colleague in evolutionary psychology, who suggested that because the Squirtle’s eyes were bordered in white, the cooperative eye hypothesis might have answers. This hypothesis, developed by the Japanese researchers Hiromi Kobayashi and Shiro Kohshima, holds that the opaque white outer coating of the human eye, or sclera, evolved to assist communication between people by signaling the direction of their gaze. The clear visibility of the sclera is a uniquely human characteristic. Other primates, such as the African great apes, also track the gaze direction of others, yet their sclera are pigmented or, if white, not visible. The great apes appear to use head direction more than other cues when following another’s gaze. Do humans have an instinctive preference for the whites of eyes, thus explaining the allure of the Squirtle? We conducted a study, to be published this year in the journal Evolution and Human Behavior, that suggested that the answer was yes. First we had to make some stuffed animals. We used six specially designed sets of three or four animals each (three cats, three dogs, three octopuses, four elephants, four snails and four turtles). The animals within each set were identical except for the eyes, which varied with respect to the size, color and presence of sclera. © 2015 The New York Times Company
Link ID: 21191 - Posted: 07.20.2015
By THE EDITORIAL BOARD Scientific research has a gender gap, and not just among humans. In many disciplines, the animals used to study diseases and drugs are overwhelmingly male, which may significantly reduce the reliability of research and lead to drugs that won’t work in half the population. A new study published in the journal Nature Neuroscience suggests that research done on male animals may not hold up for women. Its authors reported that hypersensitivity to pain works differently in male and female mice. For males, immune cells called microglia appear to be required for pain hypersensitivity, and inhibiting their function also relieves the pain. But in female mice, different cells are involved, and targeting the microglia has no effect. If these differences occur in mice, they may occur in humans too. This means a pain drug targeting microglia might appear to work in male mice, but wouldn’t work on women. Failure to consider gender in research is very much the norm. According to one analysis of scientific studies that were published in 2009, male animals outnumbered females 5.5 to 1 in neuroscience, 5 to 1 in pharmacology, and 3.7 to 1 in physiology. Only 45 percent of animal studies involving depression or anxiety and only 38 percent involving strokes used females, even though these conditions are more common in women. In 1994, the National Institutes of Health confronted gender imbalance in clinical drug trials and began requiring that women and minorities be included in clinical studies; women now make up around half of clinical trial participants. In June, the N.I.H. announced that it would begin requiring researchers to take gender into account in preclinical research on animals as well. © 2015 The New York Times Company
Keyword: Sexual Behavior
Link ID: 21188 - Posted: 07.20.2015
By C. CLAIBORNE RAY Q. Can you hear without an intact eardrum? A. “When the eardrum is not intact, there is usually some degree of hearing loss until it heals,” said Dr. Ashutosh Kacker, an ear, nose and throat specialist at NewYork-Presbyterian Hospital and a professor at Weill Cornell Medical College, “but depending on the size of the hole, you may still be able to hear almost normally.” Typically, Dr. Kacker said, the larger an eardrum perforation is, the more severe the hearing loss it will cause. The eardrum, or tympanic membrane, is a thin, cone-shaped, pearly gray tissue separating the outer and middle ear canals, he explained. Soundwaves hit the eardrum, which in turn vibrates the bones of the middle ear. The bones pass the vibration to the cochlea, which leads to a signal cascade culminating in the sound being processed by the brain and being heard. There are several ways an eardrum can be ruptured, Dr. Kacker said, including trauma, exposure to sudden or very loud noises, foreign objects inserted deeply into the ear canal, and middle-ear infection. “Usually, the hole will heal by itself and hearing will improve within about two weeks to a few months, especially in cases where the hole is small,” he said. Sometimes, when the hole is larger or does not heal well, surgery will be required to repair the eardrum. Most such operations are done by placing a patch over the hole to allow it to heal, and the surgery is usually very successful in restoring hearing, Dr. Kacker said. © 2015 The New York Times Company
Link ID: 21187 - Posted: 07.20.2015
by Sarah Schwartz Brainlike cell bundles grown in a lab may expose some of the biological differences of autistic brains. Researchers chemically reprogrammed human stem cells into small bundles of functional brain cells that mimic the developing brain. These “organoids” appear to be different when built with cells from autistic patients compared with when they are built with cells from the patients’ non-autistic family members, researchers report July 16 in Cell. The brainlike structures created from cells taken from autistic children showed increased activity in genes that control brain-cell growth and development. Too much activity in one of these genes led to an overproduction of a certain type of brain cell that suppresses the activity of other brain cells. At an early stage of development, the miniature organs grown from autistic patients’ stem cells also showed faster cell division rates than those grown from the cells of non-autistic relatives. Though the study was small, using cells from only four autistic patients and eight family members, the results may indicate common factors underlying autism, the scientists say. © Society for Science & the Public 2000 - 2015.
Link ID: 21186 - Posted: 07.18.2015
It’s a good combination. Gene therapy to reverse blindness repairs damaged cells in the eye and also rearranges the brain to help process the new information. Visual pathways in the brain are made up of millions of interconnected neurons. When sensory signals are sent along them, the connections between neurons become strong. If underused – for example, as people lose their sight – the connections become weak and disorganised. Over the past few years, a type of gene therapy – injecting healthy genes into the eye to repair mutations – has emerged as a promising way to treat congenital and degenerative blindness. One of the first successful trials began in 2007. It involved 10 blind volunteers with a hereditary disease called Leber’s congenital amaurosis. The condition causes the retina to degenerate and leaves people completely blind early in life. Mutations in at least 19 genes can cause the disease, but all of the people in the trial had mutations in a gene called RPE65. The participants got an injection of a harmless virus in one of their eyes. The virus inserted healthy copies of RPE65 into their retina. Some of the volunteers went from straining to see a hand waving half a metre from their face to being able to read six lines on a sight chart. Others were able to navigate around an obstacle course in dim light – something that would have been impossible before the therapy. © Copyright Reed Business Information Ltd.
Austin Frakt It’s a Catch-22 that even those with a common cold experience: Illness disrupts sleep. Poor sleep makes the symptoms of the illness worse. What’s true for a cold also holds for more serious conditions that co-occur with insomnia. Depression, post-traumatic stress disorder, alcohol dependence, fibromyalgia, cancer and chronic pain often give rise to insomnia, just as sleeplessness exacerbates the symptoms of these diseases. Historically, insomnia was considered a symptom of other diseases. Today it is considered an illness in its own right and recognized as an amplifier of other mental and physical ailments. When a person is chronically tired, pain can be more painful, depression deeper, anxiety heightened. What should doctors address first, insomnia or the co-occurring condition? How about both at the same time? A new study suggests that a therapy that improves sleep also reduces symptoms of other illnesses that often disrupt it. The study published in JAMA Internal Medicine examined the effect of cognitive behavioral therapy for insomnia in patients with serious mental and physical conditions. As its name suggests, C.B.T.-I. is a treatment that works through the mind. As I wrote about a few weeks ago, the therapy treats insomnia without medications, combining good sleep hygiene techniques with more consistent wake times, relaxation techniques and positive sleep attitudes and thoughts. Several clinical trials have shown that C.B.T.-I. provides as good or better relief of symptoms of insomnia than prescription drugs, with improvements in sleep that are more durable. C.B.T.-I. can usually be delivered relatively inexpensively through an online course costing about $40. Compared with those who didn’t receive C.B.T.-I., patients who did increased the time asleep in bed by about 12 percentage points, fell asleep about 25 minutes faster and decreased the amount of time awake in the middle of the night by about 45 minutes, according to Jade Wu, lead study author and a Boston University doctoral student in psychology. © 2015 The New York Times Company
Link ID: 21181 - Posted: 07.18.2015
By Emily Underwood Glance at a runner's wrist or smartphone, and you'll likely find a GPS-enabled app or gadget ticking off miles and minutes as she tries to break her personal record. Long before FitBit or MapMyRun, however, the brain evolved its own system for tracking where we go. Now, scientists have discovered a key component of this ancient navigational system in rats: a group of neurons called "speed cells" that alter their firing rates with the pace at which the rodents run. The findings may help explain how the brain maintains a constantly updated map of our surroundings. In the 1970s, neuroscientist John O'Keefe, now at University College London, discovered neurons called place cells, which fire whenever a rat enters a specific location. Thirty-five years later, neuroscientists May-Britt and Edvard Moser, now at the Norwegian University of Science and Technology in Trondheim, Norway, discovered a separate group of neurons, called grid cells, which fire at regular intervals as rats traverse an open area, creating a hexagonal grid with coordinates similar to those in GPS. The Mosers and O'Keefe shared last year's Nobel Prize in Physiology and Medicine for their findings, which hint at how the brain constructs a mental map of an animal's environment. Still mysterious, however, is how grid and place cells obtain the information that every GPS system requires: the angle and speed of an object's movement relative to a known starting point, says Edvard Moser, co-author of the new study along with May-Britt Moser, his spouse and collaborator. If the brain does indeed contain a dynamic, internal map of the world, "there has to be a speed signal" that tells the network how far an animal has moved in a given period of time, he says. © 2015 American Association for the Advancement of Science.
Keyword: Learning & Memory
Link ID: 21178 - Posted: 07.16.2015
By Laura Sanders Everybody knows people who seem to bumble through life with no sense of time — they dither for hours on a “quick” e-mail or expect an hour’s drive to take 20 minutes. These people are always late. But even for them, such minor lapses in timing are actually exceptions. We notice these flaws precisely because they’re out of the ordinary. Humans, like other animals, are quite good at keeping track of passing time. This talent does more than keep office meetings running smoothly. Almost everything our bodies and brains do requires precision clockwork — down to milliseconds. Without a sharp sense of time, people would be reduced to insensate messes, unable to move, talk, remember or learn. “We don’t think about it, but just walking down the street is an exquisitely timed operation,” says neuroscientist Lila Davachi of New York University. Muscles fire and joints steady themselves in a precisely orchestrated time series that masquerades as an unremarkable part of everyday life. A sense of time, Davachi says, is fundamental to how we move, how we act and how we perceive the world. Yet for something that forms the bedrock of nearly everything we do, time perception is incredibly hard to study. “It’s a quagmire,” says cognitive neuroscientist Peter Tse of Dartmouth College. The problem is thorny because there are thousands of possible intricate answers, all depending on what exactly scientists are asking. Their questions have begun to reveal an astonishingly complex conglomerate of neural timekeepers that influence each other. © Society for Science & the Public 2000 - 2015.
Link ID: 21177 - Posted: 07.16.2015
By Fredrick Kunkle A new study suggests that Alzheimer’s disease may affect the brain differently in black people compared with whites. The research, conducted by Lisa L. Barnes at the Rush University Medical Center, suggests that African Americans are less likely than Caucasians to have Alzheimer’s disease alone and more likely to have other pathologies associated with dementia. These include the presence of Lewy bodies, which are abnormal proteins found in the brain, and lesions arising from the hardening of tiny arteries in the brain, which is caused mainly by high blood pressure and other vascular conditions. The findings suggest that researchers should seek different strategies to prevent and treat Alzheimer’s disease in blacks. While many therapeutic strategies focus on removing or modifying beta amyloid – a key ingredient whose accumulation leads to the chain of event triggering the neurodegenerative disease – the study suggests that possible treatments should pursue additional targets, particularly for African Americans. But the study also points up the critical need to enroll more black people in clinical trials. Although Barnes said the research was the largest sample of its kind, she also acknowledged that the sample is still small. And that’s at least partially because blacks, for a variety of cultural and historical reasons, are less likely to participate in scientific research.
Link ID: 21176 - Posted: 07.16.2015