Chapter 16. None
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The structure of the living cell is defined by the difference between what’s inside and what’s not. Biologists have taken great pains over the years to document the minute workings of the openings in cell membranes that allow hydrogen, sodium, calcium and other ions to make their way inside across the barrier that envelops the cell and its contents. Five scholars of the brain have built upon these observations to suggest that these activities may provide a foundation for a badly needed theory to understand consciousness and some of the cognitive processes that underlie it. They contend that when animal cells open and close themselves to the outside world, these actions can be construed as more than just responses to external stimuli. In fact, they constitute the basis for perception, cognition and movement in the animal kingdom—and may underlie consciousness itself. Read about what the five have to say and then continue to Koch’s reply. The five authors and NYU neurology professor Oliver Sacks; Antonio Damasio and Gil B. Carvalho from the University of Southern California, Norman D. Cook from the faculty of Kansai University in Osaka, Japan and Harry T. Hunt from Brock University in Ontario. They have framed their ideas in the form of an open letter to Christof Koch, president of the Allen Institute for Brain Science, and a Scientific American MIND columnist (Consciousness Redux) and member of Scientific American’s board of advisers.
Link ID: 21065 - Posted: 06.17.2015
By James Gallagher Health editor, BBC News website Scientists have discovered a chemical in blood that indicates whether people will have declining brain function. Looking for the earliest signs of Alzheimer's disease, they analysed levels of 1,129 proteins circulating in the blood of more than 200 twins. These were compared with data from cognitive-function tests over the next decade, in Translational Psychiatry. And levels of one protein, MAPKAPK5, tended to be lower in those people whose brains declined. MAPKAPK5 is involved in relaying chemical messages within the body, although its connection with cognitive decline is unclear. Dementia cases are expected to treble globally by 2050, but there is no cure or treatment. It can take more than a decade from the first changes in the brain to culminate in symptoms such as memory loss, confusion and personality change. And drug companies believe they need to treat patients years before symptoms appear in order to protect the brain. Dr Steven Kiddle, a Medical Research Council scientist at King's College London, told the BBC News website: "People think it may be hard to reverse 20 years of potential damage to your brain. "But if you could start much earlier in that process, then you might be able to find something that works." He said a blood test could help identify people for clinical trials. But he added: "A test you could go in to your doctor to say, 'Do I have Alzheimer's disease or not?' I think that's a long way off." © 2015 BBC
Link ID: 21064 - Posted: 06.17.2015
By Tori Rodriguez Joint flexibility is an oft-coveted trait that provides a special advantage to dancers and athletes, but there can be too much of this good thing. A growing body of research suggests a surprising link between high levels of flexibility and anxiety. A study published last year in the journal Frontiers in Psychology is among the most recent to confirm the association, finding that people with hypermobile joints have heightened brain activity in anxiety regions. Joint hypermobility, which affects approximately 20 percent of the population, confers an unusually large range of motion. Hypermobile people can often, for instance, touch their thumb to their inner forearm or place their hands flat on the floor without bending their knees. The trait appears to be genetic and is a result of variation in collagen, the main structural protein of connective tissue. Being double-jointed has long been linked with an increased risk for asthma and irritable bowel syndrome, among other physical disorders. “Joint hypermobility has an impact on the whole body and not just joints,” says Jessica Eccles, a psychiatrist and researcher at the University of Sussex in England. It was only a matter of time before scientists also looked at whether joint hypermobility was linked to mental disorders. The investigation began in 1993 and heated up in 1998 when researcher Rocío Martín-Santos, now at the Hospital Clinic of the University of Barcelona, and her colleagues discovered that patients with anxiety were 16 times more likely to have lax joints. Their findings have since been replicated numerous times in large populations. © 2015 Scientific American
By Rachel Feltman Here's why you hate the sound of your own voice(1:07) If you've ever listened to your voice recorded, chances are you probably didn't like what you heard. So, why do most people hate the sound of their own voice? The answer: It's all in how sound travel to your ears. (Pamela Kirkland/The Washington Post) Whether you've heard yourself talking on the radio or just gabbing in a friend's Instagram video, you probably know the sound of your own voice -- and chances are pretty good that you hate it. As the video above explains, your voice as you hear it when you speak out loud is very different from the voice the rest of the world perceives. That's because it comes to you via a different channel than everyone else. When sound waves from the outside world -- someone else's voice, for example -- hit the outer ear, they're siphoned straight through the ear canal to hit the ear drum, creating vibrations that the brain will translate into sound. When we talk, our ear drums and inner ears vibrate from the sound waves we're putting out into the air. But they also have a another source of vibration -- the movements caused by the production of the sound. Our vocal cords and airways are trembling, too, and those vibrations make their way over to auditory processing as well. Your body is better at carrying low, rich tones than the air is. So when those two sources of sound get combined into one perception of your own voice, it sounds lower and richer. That's why hearing the way your voice sounds without all the body vibes can be off-putting -- it's unfamiliar -- or even unpleasant, because of the relative tinniness.
Link ID: 21062 - Posted: 06.17.2015
You remember your first kiss. You remember your childhood phone number, where you parked your car, and the last time you got really drunk. You probably remember the digits of pi, or at least the first three of them (slacker). Each day you accumulate fresh memories—kissing new people, acquiring different phone numbers and (possibly) competing in pi-memorizing championships (we would root for you). With all those new adventures stacking up, you might start worrying that your brain is growing full. But, wait—is that how it works? Can your brain run out of space, like a hard drive? It depends on what kind of memory you’re talking about. “It’s not like each memory takes a cell and then that cell is used up,” says Nelson Cowan, cognitive psychologist at the University of Missouri. Over the long term, memories are encoded in neural patterns—circuits of connected neurons. And your brain’s ability to knit together new patterns is limitless, so theoretically the number of memories stored in those patterns is limitless as well. Memories don’t always keep to themselves, though. They can crossbreed, like similar but distinct species, creating the recollection equivalent of a mule. If you can’t remember it, a memory is pretty much worthless—and similar memories can interfere with each other, getting in the way of surfacing the right one. Though memory interference is well documented, researchers like Cowan are still guessing at the phenomenon’s neural mechanics.
Keyword: Learning & Memory
Link ID: 21061 - Posted: 06.17.2015
By David Shultz Not usually lauded for their cuddly appearance, opossums were long thought to have a social inclination to match their looks; the marsupials have mostly been observed lurking alone and hissing at others who encroach on their personal space. However, a new study published online today in Biology Letters suggests that opossums sometimes live in groups and may form pair bonds with mates before the mating season starts. Based on 17,127 observations of 312 artificial nests over 8 years, scientists at the Federal University of Pernambuco in Recife, Brazil, discovered 10 instances of multiple opossums sharing the same den with no signs of hostility or ongoing reproductive activity. An additional observation made on the university campus revealed a group of 13 opossums from three separate age groups all sharing a single den. The researchers speculate that this type of “gregarious denning” may be relatively common in the wild and that males and females may work cooperatively to build a nest—a ritual that could trigger the onset of an estrous cycle in females. Furthermore, the group of 13 animals was discovered in a large concrete box housing electrical equipment, much bigger than the typical artificial dens used by scientists studying opossums. The team suspects that building larger artificial dens may promote more social interactions like the ones they observed. © 2015 American Association for the Advancement of Science
Link ID: 21059 - Posted: 06.17.2015
by Michael Le Page It is perhaps the most extraordinary eye in the living world – so extraordinary that no one believed the biologist who first described it more than a century ago. Now it appears that the tiny owner of this eye uses it to catch invisible prey by detecting polarised light. This suggestion is also likely to be greeted with disbelief, for the eye belongs to a single-celled organism called Erythropsidinium. It has no nerves, let alone a brain. So how could it "see" its prey? Fernando Gómez of the University of São Paulo, Brazil, thinks it can. "Erythropsidinium is a sniper," he told New Scientist. "It is waiting to see the prey, and it shoots in that direction." Erythropsidinium belongs to a group of single-celled planktonic organisms known as dinoflagellates. They can swim using a tail, or flagellum, and many possess chloroplasts, allowing them to get their food by photosynthesis just as plants do. Others hunt by shooting out stinging darts similar to the nematocysts of jellyfishMovie Camera. They sense vibrations when prey comes near, but they often have to fire off several darts before they manage to hit it, Gómez says. Erythropsidinium and its close relatives can do better, Gómez thinks, because they spot prey with their unique and sophisticated eye, called the ocelloid, which juts out from the cell. "It knows where the prey is," he says. At the front of the ocelloid is a clear sphere rather like an eyeball. At the back is a dark, hemispherical structure where light is detected. The ocelloid is strikingly reminiscent of the camera-like eyes of vertebrates, but it is actually a modified chloroplast. © Copyright Reed Business Information Ltd.
Almost half of 346,000 deaths from 12 cancers among U.S. adults in one year are attributed to cigarette smoking, despite 50 years of progress on butting out, new research suggests. Cancer researchers updated the estimate on deaths due to cigarette smoking to reflect changes in smoking patterns and how some data now suggest that the risk of cancer death among smokers can increase over time. Of 345,962 cancer deaths in the U.S. in 2011, 167,805 or 48.5 per cent were attributed to smoking cigarettes, Rebecca Siegel and her co-authors said in a research letter published in Monday's issue of JAMA Internal Medicine. The largest proportions of cancer deaths linked to smoking among those 35 and older were for cancers of the lung, bronchus and trachea (125,799 of 156, 855 deaths or 80 per cent) and larynx (2,856 of 3,728 deaths or nearly 77 per cent). About half of the deaths from cancers of the oral cavity, esophagus and urinary bladder were also attributable to smoking. Smoking was also cited as the cause of many deaths from cancer of the colon, kidney, liver, pancreas, stomach, cervix, and from myeloid leukemia. "Cigarette smoking continues to cause numerous deaths from multiple cancers despite half a century of decreasing prevalence," Rebecca Siegel from the American Cancer Society in Atlanta and her co-authors said. Dr. Norman Edelman, a senior scientific advisor to the American Lung Association, said when people hear about smoking and cancer, their thoughts often turn to lung cancer alone. ©2015 CBC/Radio-Canada.
Keyword: Drug Abuse
Link ID: 21057 - Posted: 06.16.2015
By BENEDICT CAREY Marijuana use did not increase among teenagers in the states in which medical marijuana has become legal, researchers reported Monday. The new analysis is the most comprehensive effort to date to answer a much-debated question: Does decriminalization of marijuana lead more adolescents to begin using it? The study found that states that had legalized medical use had higher prevailing rates of teenage marijuana use before enacting the laws, compared with states where the drug remains illegal. Those higher levels were unaffected by the changes in the law, the study found. The report, published in The Lancet Psychiatry, covered a 24-year period and was based on surveys of more than one million adolescents in 48 states. The research says nothing about the effect of legalizing recreational use, however. A primary concern on both sides of the debate over medical marijuana has been that loosening marijuana restrictions might send the wrong message to young people, and make the drug both more available and more appealing. Teenagers who develop and sustain a heavy, daily habit increase their risk of having cognitive difficulties later on, several studies now suggest. Previous research on usage trends in the wake of the laws has been mixed, some reporting evidence of an increase among adolescents and others — including two recent, multistate studies — finding no difference. The new analysis should carry far more weight, experts said, not only because of its size and scope but also because the funders included the National Institute of Drug Abuse, whose director has been outspoken about the risks of increased use. © 2015 The New York Times Company
Keyword: Drug Abuse
Link ID: 21056 - Posted: 06.16.2015
by Colin Barras Bacteria aren't renowned for their punctuality – but perhaps one day they will be. A working circadian clock has been inserted in E. coli that allows the microbes to keep to a 24-hour schedule. The tiny timekeepers could eventually be used in biological computers or for combating the effects of jet lag. Many plants and animals use circadian clocks to regulate their daily activities – but bacterial circadian rhythms are much less well understood. The best studied belongs to photosynthetic cyanobacteria: other common microbes, like E. coli, don't carry clocks at all, says Pamela Silver of Harvard Medical School. The cyanobacterial clock is based around the kaiABC gene cluster and ATP – the molecular fuel that nearly all living cells rely on. During the day, while the cyanobacteria are active, the KaiA protein encourages the KaiC protein to bind to phosphate groups from ATP. At night, the KaiB protein kicks into action, disrupting the activity of KaiA and encouraging KaiC to hand back the phosphate. Silver, her former student Anna Chen and other colleagues have transplanted this kaiABC clock wholesale into E. coli – the first time such a sophisticated clock has been slotted into a new microbe. But would the bacteria use their new clocks to keep time? "That's the cleverest part – and it's down to Anna's genius," says Silver. Chen suggested hooking up the kaiABC clock to a green fluorescent protein so that the phosphorylated KaiC protein would make the E. coli glow. Sure enough, the E. coli became gradually more fluorescent and then returned to a non-fluorescent state over a 24-hour period, proving that the kaiABC clock kept ticking even after it was transplanted. © Copyright Reed Business Information Ltd.
Keyword: Biological Rhythms
Link ID: 21055 - Posted: 06.16.2015
Aaron E. Carroll One of my family’s favorite shows is “The Biggest Loser.” Although some viewers don’t appreciate how it pushes people so hard to lose weight, the show probably inspires some overweight people to regain control of their lives. But one of the most frustrating parts of the show, at least for me, is its overwhelming emphasis on exercise. Because when it comes to reaching a healthy weight, what you don’t eat is much, much more important. Think about it this way: If an overweight man is consuming 1,000 more calories than he is burning and wants to be in energy balance, he can do it by exercising. But exercise consumes far fewer calories than many people think. Thirty minutes of jogging or swimming laps might burn off 350 calories. Many people, fat or fit, can’t keep up a strenuous 30-minute exercise regimen, day in and day out. They might exercise a few times a week, if that. Or they could achieve the same calorie reduction by eliminating two 16-ounce sodas each day. Proclamations that people need to be more active are ubiquitous in the media. The importance of exercise for proper weight management is reinforced when people bemoan the loss of gym class in schools as a cause of the obesity epidemic. Michelle Obama’s Let’s Move program places the focus on exercise as a critical component in combating excess weight and obesity. Exercise has many benefits, but there are problems with relying on it to control weight. First, it’s just not true that Americans, in general, aren’t listening to calls for more activity. From 2001 to 2009, the percentage of people who were sufficiently physically active increased. But so did the percentage of Americans who were obese. The former did not prevent the latter. © 2015 The New York Times Company
Link ID: 21054 - Posted: 06.15.2015
By Stephen L. Macknik, Susana Martinez-Conde and Bevil Conway This past February a photograph of a dress nearly broke the Internet. It all started when a proud mother-in-law-to-be snapped a picture of the dress she planned to wear to her daughter's wedding. When she shared her picture with her daughter and almost-son-in-law, the couple could not agree on the color: she saw white and gold, but he saw blue and black. A friend of the bride posted the confusing photo on Tumblr. Followers then reposted it to Twitter, and the image went viral. “The Dress” pitted the opinions of superstar celebrities against one another (Kanye and Kim disagreed, for instance) and attracted millions of views on social media. The public at large was split into white-and-gold and blue-and-black camps. So much attention was drawn, you would have thought the garment was conjured by a fairy godmother and accessorized with glass slippers. To sort out the conundrum, the media tapped dozens of neuroscientists and psychologists for comment. Pride in our heightened relevance to society gave way to embarrassment as we realized that our scientific explanations for the color wars were not only diverse but also incomplete. Especially perplexing was the fact that people saw it differently on the same device under the same viewing conditions. This curious inconsistency suggests that The Dress is a new type of perceptual phenomenon, previously unknown to scientists. Although some early explanations for the illusion focused on individual differences in the ocular structure of the eye, such as the patterning and function of rod and cone photoreceptor cells or the light-filtering properties internal to the eye, the most important culprit may be the brain's color-processing mechanisms. These might vary from one person to the next and can depend on prior experiences and beliefs. © 2015 Scientific American
Link ID: 21053 - Posted: 06.15.2015
Hannah Devlin Science correspondent When Lucy Tonge started drifting off in front of the television as a 13-year-old, her parents put it down to typical teenage lethargy. And when she developed a strange habit of slumping forward when she laughed, her mum told her: “Stop doing that stupid thing when you laugh. It makes you look silly.” But she couldn’t. It was only when she started collapsing with no warning that her family sought medical advice that led to a diagnosis of narcolepsy. Soon afterwards, Tonge discovered that her sleeping disorder was very likely to have been triggered by the swine flu vaccine, which she had received in 2009 a couple of months before her symptoms first emerged. Swine flu vaccine can trigger narcolepsy, UK government concedes The government has acknowledged the rare side-effect of the Pandemrix jab, which was given to 6 million people in Britain during the 2009 and 2010 swine flu pandemic, but the Department for Work and Pensions (DWP)has rejected the compensation claims of about 80 people including Tonge on the grounds that their disabilities were not “severe”. This week, the group was given fresh hope that the challenges they face will be acknowledged after a tribunal ordered the government to pay £120,000 in damages to a 12-year-old boy whose narcolepsy was also linked to Pandemrix. © 2015 Guardian News and Media Limited
Link ID: 21052 - Posted: 06.15.2015
By Michael Hedrick I’ve had a little success dating in the nearly 10 years I’ve lived with schizophrenia. But there are a lot of obstacles. Schizophrenia is a terrifying word for many people. It conjures up ideas of murderous intent, lack of control and a host of other scary things. I live with this word, though; I am the word. But it is not a word you can just drop into a conversation and follow with “It’s not a big deal, though.” I seem to fall in love easily, but it’s always with girls who don’t feel the same way about me. I have seen more rejection than I care to admit, putting myself on the line like that, and it’s been a chore for me not to let my emotions get the best of me. If it’s not outright rejection, it seems to be something else that always seems to happen. I can remember one date I went on some months back. She was a big girl with blonde hair and eyes that had that squinty “I’m up to no good” look. We met over Match.com, and I was struck by how much time she spent going to Phish shows. Her profile was scattered with a number of bands that I had loved at different points in my life. She was a teacher, and she mentioned in her profile something along the lines that because of her love of sparkles, arts-and- crafts, and rainbows, she was a 6-year-old in a woman’s body. Before I knew it, I was asking if she wanted to go get a beer. She said yes, a little too eagerly I thought. I got to the restaurant about 15 minutes early and ordered a beer, apprehensive knowing that eventually I would have to tell her about my illness. Soon enough she walked in, and I was struck by the fact that she seemed a little disappointed to be there. There was no smile as she sat down to join me. © 2015 The New York Times Company
Link ID: 21051 - Posted: 06.15.2015
by Michael Sean Pepper and Beverley Kramer People who are attracted to others of the same sex develop their orientation before they are born. This is not a choice. And scientific evidence shows their parents cannot be blamed. Research proving that there is biological evidence for sexual orientation has been available since the 1980s. The links have been emphasised by new scientific research. In 2014, researchers confirmed the association between same-sex orientation in men and a specific chromosomal region. This is similar to findings originally published in the 1990s, which, at that time, gave rise to the idea that a “gay gene” must exist. But this argument has never been substantiated, despite the fact that studies have shown that homosexuality is a heritable trait. Evidence points towards the existence of a complex interaction between genes and environment, which are responsible for the heritable nature of sexual orientation. These findings are part of a report released by the Academy of Science South Africa. The report is the outcome of work conducted by a panel put together in 2014 to evaluate all research on the subject of sexual orientation done over the last 50 years. It did this against the backdrop of a growing number of new laws in Africa which discriminate against people attracted to others of the same sex. The work was conducted in conjunction with the Ugandan Academy of Science.
Keyword: Sexual Behavior
Link ID: 21049 - Posted: 06.15.2015
By ANDREW HIGGINS WIJK BIJ DUURSTEDE, Netherlands — The hiss of gas, released by a red lever turned by Arie den Hertog in the back of his white van, signaled the start of the massacre. The victims, crammed into a sealed, coffin-like wooden case, squawked as they struggled to breathe. Then, after barely two minutes, they fell silent. Glancing at the timer on his cellphone, Mr. Den Hertog declared the deed done. “Now it is all over,” he said proudly of his gruesomely efficient handiwork, on a gloriously sunny day beneath a row of poplar trees on the banks of the Lower Rhine. Reviled as a Nazi by animal rights activists but hailed as a hero by Dutch farmers, Mr. Den Hertog, 40, is the Netherlands’ peerless expert in the theory and practice of killing large numbers of wild geese. On his recent outing to Wijk bij Duurstede, a village in the Utrecht region southeast of Amsterdam, he killed 570 graylag geese in his portable gas chamber, fitted with two big canisters of carbon dioxide. That brought his death toll to more than 7,000 for the week. “It is not fun, but it has to be done,” he said of his work. The Dutch authorities insist it must be done, too. They pay Mr. Den Hertog to keep a ballooning geese population from devouring the grass of cow pastures and flying into planes taking off from Amsterdam’s Schiphol Airport, a major hub in Europe. He is the unpleasant answer to what has become a problem on a grand scale for the Netherlands. Geese populations here have skyrocketed, buoyed by a 1999 ban on hunting them; farmers’ increasing use of nitrogen-rich fertilizer, which geese apparently love; and the expansion of protected nature areas. That combination, plus an abundance of rivers and canals, has made the country a “goose El Dorado,” said Julia Stahl, head of research at Sovon, a group that monitors wild bird populations in the Netherlands. © 2015 The New York Times Company
Keyword: Animal Rights
Link ID: 21048 - Posted: 06.15.2015
By Nicholas Bakalar Statins, the widely used cholesterol-lowering drugs, have been blamed for memory loss, but a new study suggests that the association is an illusion. The report, in JAMA Internal Medicine, found that the apparent association was likely a result of detection bias — visiting the doctor and starting a new medicine makes people more acutely aware of health issues they might otherwise not notice. Researchers compared 482,543 statin users with the same number of people using no lipid-lowering drugs and with 26,484 people using non-statin lipid lowering drugs. Use of statin drugs was associated with an increase in memory loss during the first 30 days of starting the drugs compared with people who did not take cholesterol-lowering drugs. But so was use of non-statin lipid-lowering drugs. After accounting for many health and behavioral variables, the scientists concluded that either all lipid lowering drugs, statins or not, cause memory loss or, more likely, that previous findings were based on the expectations of the patients rather than any physiological effect of the medicine. “As you think about whether you should be taking statins, there are questions about uncommon side effects worth raising,” said the lead author, Dr. Brian L. Strom, chancellor of Rutgers Biomedical and Health Sciences. “But the question of impairing memory is a nonissue.” © 2015 The New York Times Company
Keyword: Learning & Memory
Link ID: 21047 - Posted: 06.15.2015
by Penny Sarchet Children with ADHD are more likely to succeed in cognitive tasks when they are fidgeting. Rather than telling them to stop, is it time to let them squirm in class? The results, from a small study of teens and pre-teens, add to growing evidence that movement may help children with attention-deficit hyperactivity disorder to think. One of the theories about ADHD is that the brain is somehow under-aroused. Physical movements could help wake it up or maintain alertness, perhaps by stimulating the release of brain-signalling chemicals like dopamine or norepinephrine. This hypothesis would help explain why countries like the US are experiencing an epidemic of ADHD – it might be that a lack of physical activity leads to reduced brain function. Fidget britches In the latest study, Julie Schweitzer of the University of California, Davis, and her colleagues asked 44 children with ADHD and 29 kids without to describe an arrangement of arrows. The children with ADHD were more likely to focus on the task and answer correctly if the test coincided with them fidgeting, as tracked by an ankle monitor. Intriguingly, Schwietzer found that it is the vigour of movements, rather than how often children make them, that seems to be related to improvements in test scores. This might mean, for example, that it helps children to swing their legs in longer arcs, but not to swing them faster. "I think we need to consider that fidgeting is helpful," says Schweitzer. "We need to find ways that children with ADHD can move without being disruptive to others." Dustin Sarver at the University of Mississippi, who recently found a link between fidgeting and improved working memory, agrees. "We should revisit the targets we want for these children, such as improving the work they complete and paying attention, rather than focusing on sitting still." He suggests that movements that are not disruptive to other schoolchildren, such as squirming, bouncing and leg movements, as opposed to getting up in the middle of lessons, could be encouraged in classrooms. © Copyright Reed Business Information Ltd
Boer Deng A genetic variant protected some practitioners of cannibalism from prion disease. Scientists who study a rare brain disease that once devastated entire communities in Papua New Guinea have described a genetic variant that appears to stop misfolded proteins known as prions from propagating in the brain1. Kuru was first observed in the mid-twentieth century among the Fore people of Papua New Guinea. At its peak in the late 1950s, the disease killed up to 2% of the group's population each year. Scientists later traced the illness to ritual cannibalism2, in which tribe members ate the brains and nervous systems of their dead. The outbreak probably began when a Fore person consumed body parts from someone who had sporadic Creutzfeldt-Jakob disease (CJD), a prion disease that spontaneously strikes about one person in a million each year. Scientists have noted previously that some people seem less susceptible to prion diseases if they have an amino-acid substitution in a particular region of the prion protein — codon 1293. And in 2009, a team led by John Collinge — a prion researcher at University College London who is also the lead author of the most recent analysis — found another protective mutation among the Fore, in codon 1274. The group's latest work, reported on 10 June in Nature1, shows that the amino-acid change that occurs at this codon, replacing a glycine with a valine, has a different and more powerful effect than the substitution at codon 129. The codon 129 variant confers some protection against prion disease only when it is present on one of the two copies of the gene that encodes the protein. But transgenic mice with the codon-127 mutation were completely resistant to kuru and CJD regardless of whether they bore one or two copies of it. The researchers say that the mutation in codon 127 appears to confer protection by preventing prion proteins from becoming misshapen. © 2015 Nature Publishing Group,
Link ID: 21043 - Posted: 06.13.2015
Joe Palca Scientists found a molecule crucial to perceiving the sensation of itching. It affects how the brain responds to serotonin, and may explain why anti-depressants that boost serotonin make some itch. JOE PALCA, BYLINE: How do you go about discovering what makes us itch? Well, if you're Diana Bautista at the University of California, Berkeley, you ask what molecules are involved. DIANA BAUTISTA: We say OK, what are the possible molecular players out there that might be contributing to itch or touch? PALCA: Bautista says it turns out itch and touch, and even pain, all seem to be related - at least in the way our brains makes sense of these sensations. But how to tell which molecules are key players? Bautista says basically you try everything you can. BAUTISTA: We test a lot of candidates. And if we're really lucky, one of our candidates - we can prove that it plays a really important role. PALCA: And now she thinks she's found one. Working with colleagues at the Buck Institute for Research on Aging, she's found a molecule that's made by a gene called HTR7. When there's less of this molecule, animals with itchy skin conditions, like eczema, do less scratching. When there's more of it, itching gets worse. The way this molecule works is kind of interesting. It changes how sensitive brain cells are to a chemical called serotonin. Now, serotonin is a chemical that's related to depression. So Bautista's research might explain why certain antidepressant drugs that boost serotonin have a peculiar side effect. For some people, the drugs make them itch. Bautista says the new research is certainly not the end of the story when it comes to understanding itch. © 2015 NPR
Keyword: Pain & Touch
Link ID: 21042 - Posted: 06.13.2015