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By BENEDICT CAREY Solving a hairy math problem might send a shudder of exultation along your spinal cord. But scientists have historically struggled to deconstruct the exact mental alchemy that occurs when the brain successfully leaps the gap from “Say what?” to “Aha!” Now, using an innovative combination of brain-imaging analyses, researchers have captured four fleeting stages of creative thinking in math. In a paper published in Psychological Science, a team led by John R. Anderson, a professor of psychology and computer science at Carnegie Mellon University, demonstrated a method for reconstructing how the brain moves from understanding a problem to solving it, including the time the brain spends in each stage. The imaging analysis found four stages in all: encoding (downloading), planning (strategizing), solving (performing the math), and responding (typing out an answer). “I’m very happy with the way the study worked out, and I think this precision is about the limit of what we can do” with the brain imaging tools available, said Dr. Anderson, who wrote the report with Aryn A. Pyke and Jon M. Fincham, both also at Carnegie Mellon. To capture these quicksilver mental operations, the team first taught 80 men and women how to interpret a set of math symbols and equations they had not seen before. The underlying math itself wasn’t difficult, mostly addition and subtraction, but manipulating the newly learned symbols required some thinking. The research team could vary the problems to burden specific stages of the thinking process — some were hard to encode, for instance, while others extended the length of the planning stage. The scientists used two techniques of M.R.I. data analysis to sort through what the participants’ brains were doing. One technique tracked the neural firing patterns during the solving of each problem; the other identified significant shifts from one kind of mental state to another. The subjects solved 88 problems each, and the research team analyzed the imaging data from those solved successfully. © 2016 The New York Times Company
By NICHOLAS ST. FLEUR Orangutan hear, orangutan do. Researchers at the Indianapolis Zoo observed an orangutan mimic the pitch and tone of human sounds, for the first time. The finding, which was published Wednesday, provides insight into the evolutionary origin of human speech, the team said. “It really redefines for us what we know about the capabilities of orangutans,” said Rob Shumaker, director of the zoo and an author on the paper. “What we have to consider now is the possibility that the origins of spoken language are not exclusively human, and that they may have come from great apes.” Rocky, an 11-year-old orangutan at the zoo, has a special ability. He can make sounds using his vocal folds, or voice box, that resemble the vowel “A,” and sound like “Ah.” The noises, or “wookies” as the researchers called them, are variations of the same vocalization. Sometimes the great ape would say high-pitched “wookies” and sometimes he would say his “Ahs” in a lower pitch. The researchers note that the sounds are specific to Rocky and ones that he used everyday. No other orangutan, captive or wild, made these noises. Rocky, who had never lived in the rain forest, apparently learned the skill during his time as an entertainment orangutan before coming to the zoo. He was at one point the most seen orangutan in movies and commercials, according to the zoo. The researchers said that Rocky’s grunts show that great apes have the capacity to learn to control their muscles to deliberately alter their sounds in a “conversational” manner. The findings, which were published in the journal Scientific Reports, challenge the notion that orangutans — an endangered species that shares about 97 percent of it DNA with humans — make noises simply in response to something, sort of like how you might scream when you place your hand on a hot stove. © 2016 The New York Times Company
By Richard Kemeny Sleep is essential for memory. Mounting evidence continues to support the notion that the nocturnal brain replays, stabilizes, reorganizes, and strengthens memories while the body is at rest. Recently, one particular facet of this process has piqued the interest of a growing group of neuroscientists: sleep spindles. For years these brief bursts of brain activity have been largely ignored. Now it seems that examining these neuronal pulses could help researchers better understand—perhaps even treat—cognitive impairments. Sleep spindles are a defining characteristic of stage 2 non-rapid eye movement (NREM) sleep. These electrical bursts between 10-16 Hz last only around a second, and are known to occur in the human brain thousands of times per night. Generated by a thin net of neurons enveloping the thalamus, spindles appear across several regions of the brain, and are thought to perform various functions, including maintaining sleep in the face of disturbances in the environment. It appears they are also a fundamental part of the process by which the human brain consolidates memories during sleep. A memory formed during the day is stored temporarily in the hippocampus, before being spontaneously replayed during the night. Information about the memory is distributed out and integrated into the neocortex through an orchestra of slow-waves, spindles, and rapid hippocampal ripples. Spindles, it seems, could be a guiding force—providing the plasticity and coordination needed for this delicate, interregional transfer of information. © 1986-2016 The Scientist
By ERICA GOODE You are getting sleepy. Very sleepy. You will forget everything you read in this article. Hypnosis has become a common medical tool, used to reduce pain, help people stop smoking and cure them of phobias. But scientists have long argued about whether the hypnotic “trance” is a separate neurophysiological state or simply a product of a hypnotized person’s expectations. A study published on Thursday by Stanford researchers offers some evidence for the first explanation, finding that some parts of the brain function differently under hypnosis than during normal consciousness. The study was conducted with functional magnetic resonance imaging, a scanning method that measures blood flow in the brain. It found changes in activity in brain areas that are thought to be involved in focused attention, the monitoring and control of the body’s functioning, and the awareness and evaluation of a person’s internal and external environments. “I think we have pretty definitive evidence here that the brain is working differently when a person is in hypnosis,” said Dr. David Spiegel, a professor of psychiatry and behavioral sciences at Stanford who has studied the effectiveness of hypnosis. Functional imaging is a blunt instrument and the findings can be difficult to interpret, especially when a study is looking at activity levels in many brain areas. Still, Dr. Spiegel said, the findings might help explain the intense absorption, lack of self-consciousness and suggestibility that characterize the hypnotic state. © 2016 The New York Times Company
By Tanya Lewis The tangled buildup of tau protein in brain cells is a hallmark of the cognitive decline linked with Alzheimer’s disease. Antibodies have been shown to block tau’s spread, but some scientists worry it could also fuel inflammation. Now, researchers from Genentech in San Francisco and colleagues have found that an antibody’s ability to recruit immune cells—known as its effector function—is not necessary for stopping tau’s spread, the team reported today (July 28) in Cell Reports. “Our results suggest that, given that effector function is not required for efficacy [in treating tau accumulation], going without it could offer a safer approach for immunotherapy,” study coauthor Gai Ayalon of Genentech told The Scientist. Alzheimer’s disease causes a characteristic constellation of pathologies: accumulation of amyloid-β plaques outside neurons, neurofibrillary tangles of tau inside brain cells, and chronic inflammation. Clinical research has mostly focused on targeting amyloid-β with antibody therapies, and several treatments based on this approach are currently in clinical trials. But recent efforts have zeroed in on tau as a new potential target. Antibodies are known to spur the brain’s defense system, microglia, to absorb and degrade tau, but their recruitment of immune cells may also worsen inflammation. Ayalon and colleagues wondered whether effector function was necessary for stopping tau’s spread. © 1986-2016 The Scientist
Laura Sanders Under duress, nerve cells get a little help from their friends. Brain cells called astrocytes send their own energy-producing mitochondria to struggling nerve cells. Those gifts may help the neurons rebound after injuries such as strokes, scientists propose in the July 28 Nature. It was known that astrocytes — star-shaped glial cells that, among other jobs, support neurons — take in and dispose of neurons’ discarded mitochondria. Now it turns out that mitochondria can move the other way, too. This astrocyte-to-neuron transfer is surprising, says neuroscientist Jarek Aronowski of the University of Texas Health Science Center at Houston. “Bottom line: It’s sort of shocking.” Study coauthor Eng Lo of Massachusetts General Hospital and Harvard Medical School cautions that the work is at a very early stage. But he hopes that a deeper understanding of this process might ultimately point out new ways to protect the brain from damage. Mitochondria produce the energy that powers cells in the body. Scientists have spotted the organelles moving into damaged cells in other parts of the body, including the lungs, heart and liver. The new study turns up signs of this mitochondrial generosity in the brain. Astrocytes produce mitochondria and shunt them out into the soup that surrounds cells, Lo and colleagues found. The researchers then put neurons into this mitochondria-rich broth. When starved of glucose and oxygen — a situation that approximates a stroke — the neurons took in the astrocyte-made organelles. |© Society for Science & the Public 2000 - 2016
Janet Raloff Over the last three years, growing evidence has shown that electronic cigarettes are not the harmless alternative to smoking that many proponents have argued. Now, a new study traces a large share of e-cigs’ toxic gases to a heat-triggered breakdown of the liquids used to create the vapors. And the hotter an e-cig gets — and the more it’s used — the more toxic compounds it emits, the study shows. “There is this image that e-cigarettes are a lot better than regular cigarettes, if not harmless,” says Hugo Destaillats, a chemist at Lawrence Berkeley National Laboratory in California. But after his team’s new analyses, published July 27 in Environmental Science & Technology, “we are now definitely convinced that they are far from harmless.” Electronic cigarettes draw liquids over one or more hot metal coils to transform them into vapors. Those liquids — polyethylene glycol, glycerin or a mix of the two — are food-grade solvents laced with flavorings and usually nicotine. The Berkeley team used two current models of e-cigs and three different commercially available e-liquids. The experimental setup mechanically drew air through the devices to create the vapors that a user would normally inhale. Heating up The higher an e-cigarette’s voltage, the more toxic aldehydes it produces in each puff of vapor. Once a certain threshold is hit, each voltage increase produces a disproportionate increase (see last bar) in acrolein, acetaldehyde and formaldehyde, three of the most harmful compounds in the vapor. |© Society for Science & the Public 2000 - 2016
Keyword: Drug Abuse
Link ID: 22490 - Posted: 07.28.2016
By Emily Underwood If your car’s battery dies, you might call on roadside assistance—or a benevolent bystander—for a jump. When damaged neurons lose their “batteries,” energy-generating mitochondria, they call on a different class of brain cells, astrocytes, for a boost, a new study suggests. These cells respond by donating extra mitochondria to the floundering neurons. The finding, still preliminary, might lead to novel ways to help people recover from stroke or other brain injuries, scientists say. “This is a very interesting and important study because it describes a new mechanism whereby astrocytes may protect neurons,” says Reuven Stein, a neurobiologist at The Rabin Institute of Neurobiology in Tel Aviv, Israel, who was not involved in the study. To keep up with the energy-intensive work of transmitting information throughout the brain, neurons need a lot of mitochondria, the power plants that produce the molecular fuel—ATP—that keeps cells alive and working. Mitochondria must be replaced often in neurons, in a process of self-replication called fission—the organelles were originally microbes captured inside a cell as part of a symbiosis. But if mitochondria are damaged or if they can’t keep up with a cell’s needs, energy supplies can run out, killing the cell. In 2014, researchers published the first evidence that cells can transfer mitochondria in the brain—but it seemed more a matter of throwing out the trash. When neurons expel damaged mitochondria, astrocytes swallow them and break them down. Eng Lo and Kazuhide Hayakawa, both neuroscientsists at Massachusetts General Hospital in Charlestown, wondered whether the transfer could go the other way as well—perhaps astrocytes donated working mitochondria to neurons in distress. Research by other groups supported that idea: A 2012 study, for example, found that stem cells from bone marrow can donate mitochondria to lung cells after severe injury. © 2016 American Association for the Advancement of Science
By ANDREW POLLACK A new type of drug for Alzheimer’s disease failed to slow the rate of decline in mental ability and daily functioning in its first large clinical trial. There was a hint, though, that it might be effective for certain patients. The drug, called LMTX, is the first one with its mode of action — trying to undo so-called tau tangles in the brain — to reach the final stage of clinical trials. So the results of the study were eagerly awaited. The initial reaction to the outcome was disappointment, with perhaps a glimmer of hopefulness. Over all, the patients who received LMTX, which was developed by TauRx Therapeutics, did not have a slower rate of decline in mental ability or daily functioning than those in the control group. However, the drug did seem to work for the subset of patients — about 15 percent of those in the study — who took LMTX as their only therapy. The other 85 percent of patients took an existing Alzheimer’s drug in addition to either LMTX or a placebo. “There were highly significant, clinically meaningful, large effects in patients taking the drug as monotherapy, and no effect in patients taking it as an add-on,” Claude Wischik, a founder and the chief executive of TauRx, said in an interview. He spoke from Toronto, where the results were being presented at the Alzheimer’s Association International Conference. Dr. Wischik said a second clinical trial sponsored by the company, whose results will be announced later, found the same phenomenon. He said the company planned to apply for approval of LMTX to be used by itself. But some experts not involved in the study were skeptical about drawing conclusions from a small subset of patients, especially since there was no obvious explanation why LMTX would be expected to work only in patients not getting other drugs. on © 2016 The New York Times Company
Link ID: 22488 - Posted: 07.28.2016
Ian Sample and Nicky Woolf When Bill Gates pulled on a red and white-striped cord to upturn a bucket of iced water positioned delicately over his head, the most immediate thought for many was not, perhaps, of motor neurone disease. But the ice bucket challenge, the charity campaign that went viral in the summer of 2014 and left scores of notable persons from Gates and Mark Zuckerberg to George W. Bush and Anna Wintour shivering and drenched, has paid off in the most spectacular way. Dismissed by some at the time as “slacktivism” - an exercise that appears to do good while achieving very little - the ice bucket challenge raised more than $115m (£88m) for motor neurone disease in a single month. Now, scientists funded with the proceeds have discovered a gene variant associated with the condition. In the near term the NEK1 gene variant, described in the journal Nature Genetics this week, will help scientists understand how the incurable disorder, known also as Amyotrophic Lateral Sclerosis (ALS) or Lou Gehrig’s disease, takes hold. Once the mechanisms are more clearly elucidated, it may steer researchers on a path towards much-needed treatments. The work may never have happened were it not for the curious appeal of the frozen water drenchings. The research grants that scientists are awarded do not get close to the €4m the study required. Instead, Project MinE, which aims to unravel the genetic basis of the disease and ultimately find a cure, was funded by the ALS Association through ice bucket challenge donations. © 2016 Guardian News and Media Limited
By Gretchen Reynolds Learning requires more than the acquisition of unfamiliar knowledge; that new information or know-how, if it’s to be more than ephemeral, must be consolidated and securely stored in long-term memory. Mental repetition is one way to do that, of course. But mounting scientific evidence suggests that what we do physically also plays an important role in this process. Sleep, for instance, reinforces memory. And recent experiments show that when mice and rats jog on running wheels after acquiring a new skill, they learn much better than sedentary rodents do. Exercise seems to increase the production of biochemicals in the body and brain related to mental function. Researchers at the Donders Institute for Brain, Cognition and Behavior at Radboud University in the Netherlands and the University of Edinburgh have begun to explore this connection. For a study published this month in Current Biology, 72 healthy adult men and women spent about 40 minutes undergoing a standard test of visual and spatial learning. They observed pictures on a computer screen and then were asked to remember their locations. Afterward, the subjects all watched nature documentaries. Two-thirds of them also exercised: Half were first put through interval training on exercise bicycles for 35 minutes immediately after completing the test; the others did the same workout four hours after the test. Two days later, everyone returned to the lab and repeated the original computerized test while an M.R.I. machine scanned their brain activity. Those who exercised four hours after the test recognized and recreated the picture locations most accurately. Their brain activity was subtly different, too, showing a more consistent pattern of neural activity. The study’s authors suggest that their brains might have been functioning more efficiently because they had learned the patterns so fully. But why delaying exercise for four hours was more effective than an immediate workout remains mysterious. By contrast, rodents do better in many experiments if they work out right after learning. © 2016 The New York Times Company
Keyword: Learning & Memory
Link ID: 22486 - Posted: 07.28.2016
Jon Hamilton Two studies released at an international Alzheimer's meeting Tuesday suggest doctors may eventually be able to screen people for this form of dementia by testing the ability to identify familiar odors, like smoke, coffee and raspberry. In both studies, people who were in their 60s and older took a standard odor detection test. And in both cases, those who did poorly on the test were more likely to already have — or go on to develop — problems with memory and thinking. "The whole idea is to create tests that a general clinician can use in an office setting," says Dr. William Kreisl, a neurologist at Columbia University, where both studies were done. The research was presented at the Alzheimer's Association International Conference in Toronto. Currently, any tests that are able to spot people in the earliest stages of Alzheimer's are costly and difficult. They include PET scans, which can detect sticky plaques in the brain, and spinal taps that measure the levels of certain proteins in spinal fluid. The idea of an odor detection test arose, in part, from something doctors have observed for many years in patients with Alzheimer's, Kreisl says. "Patients will tell us that food does not taste as good," he says. The reason is often that these patients have lost the ability to smell what they eat. That's not surprising, Kreisl says, given that odor signals from the nose have to be processed in areas of the brain that are among the first to be affected by Alzheimer's disease. But it's been tricky to develop a reliable screening test using odor detection. © 2016 npr
By PAM BELLUCK The World Health Organization is moving toward declassifying transgender identity as a mental disorder in its global list of medical conditions, with a new study lending additional support to a proposal that would delete the decades-old designation. The change, which has so far been approved by each committee that has considered it, is under review for the next edition of the W.H.O. codebook, which classifies diseases and influences the treatment of patients worldwide. “The intention is to reduce barriers to care,” said Geoffrey Reed, a psychologist who is coordinating the mental health and behavior disorders section in the upcoming edition of the codebook, called the International Classification of Diseases, or I.C.D. Dr. Reed, a professor at the National Autonomous University of Mexico and an author of the new study, said the proposal to remove transgender from the mental disorder category was “not getting opposition from W.H.O.,” suggesting that it appears likely to be included in the new edition. The revised volume would be the first in more than 25 years, and is scheduled to be approved in May 2018. Removing the mental health label from transgender identity would be a powerful signifier of acceptance, advocates and mental health professionals say. “It’s sending a very strong message that the rest of the world is no longer considering it a mental disorder,” said Dr. Michael First, a professor of clinical psychiatry at Columbia University and the chief technical consultant to the new edition of the codebook, which is known by its initials and the edition number I.C.D.-11. “One of the benefits of moving it out of the mental disorder section is trying to reduce stigma.” © 2016 The New York Times Company
Keyword: Sexual Behavior
Link ID: 22484 - Posted: 07.27.2016
By Jesse Singal As anyone who has read much about the subject can attest, the discussion about kids with gender dysphoria — that is, discomfort with their body and the feeling that they should have been born the other sex, or that they are the other sex — can get extremely heated and tricky. Much of the controversy stems from questions of age: How young is too young to help a child socially transition — that is, to change their name and pronoun, and possibly the way they present themselves? To prescribe them cross-sex hormones to begin the process of physically transitioning? For children with persistent gender dysphoria who are approaching adolescence, current best practice is to prescribe them so-called puberty blockers. Delaying the onset of puberty both forestalls the sometimes very uncomfortable experience of a child going through puberty in a body they aren’t comfortable in, and buys them and their families time to figure out what to do. Sometimes, this eventually leads to the prescription of cross-sex hormones, and sometimes it leads to surgery after that. Some people, though, are arguing that kids — particularly those who have socially transitioned at a young age — shouldn’t have to wait that long. Recently in the Guardian, for example, Kate Lyons reported on the current state of this debate in Britain: specifically, whether children who identify as transgender should be given access to cross-sex hormones, or possibly even surgery, at younger ages than what is current practice. © 2016, New York Media LLC.
Keyword: Sexual Behavior
Link ID: 22483 - Posted: 07.27.2016
An orangutan copying sounds made by researchers offers new clues to how human speech evolved, scientists say. Rocky mimicked more than 500 vowel-like noises, suggesting an ability to control his voice and make new sounds. It had been thought these great apes were unable to do this and, since human speech is a learned behaviour, it could not have originated from them. Study lead Dr Adriano Lameira said this "notion" could now be thrown "into the trash can". Dr Lameira, who conducted the research at Amsterdam University prior to joining Durham University, said Rocky's responses had been "extremely accurate". The team wanted to make sure the ape produced a new call, rather than adapting a "normal orangutan call with a personal twist" or matching sounds randomly or by coincidence, he said. The new evidence sets the "start line for scientific inquiry at a higher level", he said. "Ultimately, we should be now in a better position to think of how the different pieces of the puzzle of speech evolution fit together." The calls Rocky made were different from those collected in a large database of recordings, showing he was able to learn and produce new sounds rather than just match those already in his "vocabulary". In a previous study Dr Lameira found a female orangutan at Cologne Zoo in Germany was able to make sounds with a similar pace and rhythm to human speech. Researchers were "astounded" by Tilda's vocal skills but could not prove they had been learned, he said. However, the fact that "other orangutans seem to be exhibiting equivalent vocal skills shows that Rocky is not a bizarre or abnormal individual", Dr Lameira said. © 2016 BBC.
By KATHARINE Q. SEELYE PORTLAND, Me. — A woman in her 30s was sitting in a car in a parking lot here last month, shooting up heroin, when she overdosed. Even after the men she was with injected her with naloxone, the drug that reverses opioid overdoses, she remained unconscious. They called 911. Firefighters arrived and administered oxygen to improve her breathing, but her skin had grown gray and her lips had turned blue. As she lay on the asphalt, the paramedics slipped a needle into her arm and injected another dose of naloxone. In a moment, her eyes popped open. Her pupils were pinpricks. She was woozy and disoriented, but eventually got her bearings as paramedics put her on a stretcher and whisked her to a hospital. Every day across the country, hundreds, if not thousands, of people who overdose on opioids are being brought back to life with naloxone. Hailed as a miracle drug by many, it carries no health risk; it cannot be abused and, if given mistakenly to someone who has not overdosed on opioids, does no harm. More likely, it saves a life. As a virulent opioid epidemic continues to ravage the country, with 78 people in the United States dying of overdoses every day, naloxone’s use has increasingly moved out of medical settings, where it has been available since the 1970s, and into the homes and hands of the general public. But naloxone, also known by the brand name Narcan, has also had unintended consequences. Critics say that it gives drug users a safety net, allowing them to take more risks as they seek higher highs. Indeed, many users overdose more than once, some multiple times, and each time, naloxone brings them back. © 2016 The New York Times Company
By PAM BELLUCK “Has the person become agitated, aggressive, irritable, or temperamental?” the questionnaire asks. “Does she/he have unrealistic beliefs about her/his power, wealth or skills?” Or maybe another kind of personality change has happened: “Does she/he no longer care about anything?” If the answer is yes to one of these questions — or others on a new checklist — and the personality or behavior change has lasted for months, it could indicate a very early stage of dementia, according to a group of neuropsychiatrists and Alzheimer’s experts. They are proposing the creation of a new diagnosis: mild behavioral impairment. The idea is to recognize and measure something that some experts say is often overlooked: Sharp changes in mood and behavior may precede the memory and thinking problems of dementia. The group made the proposal on Sunday at the Alzheimer’s Association International Conference in Toronto, and presented a 38-question checklist that may one day be used to identify people at greater risk for Alzheimer’s. “I think we do need something like this,” said Nina Silverberg, the director of the Alzheimer’s Disease Centers program at the National Institute on Aging, who was not involved in creating the checklist or the proposed new diagnosis. “Most people think of Alzheimer’s as primarily a memory disorder, but we do know from years of research that it also can start as a behavioral issue.” Under the proposal, mild behavioral impairment (M.B.I.) would be a clinical designation preceding mild cognitive impairment (M.C.I.), a diagnosis created more than a decade ago to describe people experiencing some cognitive problems but who can still perform most daily functions. © 2016 The New York Times Company
Link ID: 22480 - Posted: 07.26.2016
By Sharon Begley, STAT For the first time ever, researchers have managed to reduce people’s risk for dementia — not through a medicine, special diet, or exercise, but by having healthy older adults play a computer-based brain-training game. The training nearly halved the incidence of Alzheimer’s disease and other devastating forms of cognitive and memory loss in older adults a decade after they completed it, scientists reported on Sunday. If the surprising finding holds up, the intervention would be the first of any kind — including drugs, diet, and exercise — to do that. “I think these results are highly, highly promising,” said George Rebok of the Johns Hopkins Bloomberg School of Public Health, an expert on cognitive aging who was not involved in the study. “It’s exciting that this intervention pays dividends so far down the line.” The results, presented at the Alzheimer’s Association International Conference in Toronto, come from the government-funded ACTIVE (Advanced Cognitive Training for Independent and Vital Elderly) study. Starting in 1998, ACTIVE’s 2,832 healthy older adults (average age at the start: 74) received one of three forms of cognitive training, or none, and were evaluated periodically in the years after. In actual numbers, 14 percent of ACTIVE participants who received no training had dementia 10 years later, said psychologist Jerri Edwards of the University of South Florida, who led the study. Among those who completed up to 10 60-to-75-minute sessions of computer-based training in speed-of-processing — basically, how quickly and accurately they can pay attention to, process, and remember brief images on a computer screen — 12.1 percent developed dementia. Of those who completed all 10 initial training sessions plus four booster sessions a few years later, 8.2 percent developed dementia. © 2016 Scientific American
By Tim Page When I returned to California, I brought my diaries into the back yard every afternoon and read them through sequentially, with the hope of learning more about the years before my brain injury. I remembered much of what I’d done professionally, and whatever additional information I needed could usually be found on my constantly vandalized Wikipedia page. Here was the story of an awkward, imperious child prodigy who made his own films and became famous much too early; a music explainer who won a Pulitzer Prize; a driven and obsessive loner whose fascinations led to collaborations with Glenn Gould, Philip Glass and Thomas Pynchon. In 2000, at age 45, I was diagnosed with Asperger’s syndrome. In retrospect, the only surprise is that it took so long. But the diaries offered a more intimate view. Reading them was slow going, and I felt as though my nose was pressed up against the windowpane of my own life. The shaggy-dog accretion of material — phone numbers, long-ago concert dates, coded references to secret loves — all seemed to belong to somebody else. My last clear memory was of a muggy, quiet Sunday morning in July, three months earlier, as I waited for a train in New London, Conn. It was 11:13 a.m., and the train was due to arrive two minutes later. I was contented, proud of my punctuality and expecting an easy ride to New York in the designated “quiet car,” with just enough time to finish whatever book I was carrying. There would be dinner in Midtown with a magical friend, followed by overnight family visits in Baltimore and Washington, and then a flight back to Los Angeles and the University of Southern California, at which point a sabbatical semester would be at an end.
Dean Burnett On July 31st 2016, this blog will have been in existence for four years exactly. A huge thanks to everyone who’s made the effort to read it in that time (an alarming number of you). Normally there’d be a post on the day to mark the occasion, but this year the 31st is a) a Sunday, and b) my birthday, so even if I could be bothered to work that day, it’s unlikely anyone would want to read it. However, today also marks the ridiculously-unlikely-but-here-we-are American release of my book. How did it get to this point? I’ve been a “professional” science writer now for four years, and I’ve been involved in neuroscience, in one guise or another, since 2000, the year I started my undergraduate degree. In that time, I’ve heard/encountered some seriously bizarre claims about how the brain works. Oftentimes it was me not understanding what was being said, or misinterpreting a paper, or just my own lack of competence. Sometimes, it was just a media exaggeration. However, there have been occasions when a claim made about the brain thwarts all my efforts to find published evidence or even a rational basis for it, leaving me scratching my head and wondering “where the hell did THAT come from?” Here are some of my favourites. In the past, one terabyte of storage capacity would have seemed incredibly impressive. But Moore’s law has put paid to that. My home desktop PC presently has 1.5 TB of storage space, and that’s over seven years old. Could my own clunky desktop be, in terms of information capacity, smarter than me? Apparently. Some estimates put the capacity of the human brain as low as 1TB. A lifetimes worth of memories wouldn’t fill a modern-day hard drive? That seems far-fetched, at least at an intuitive level.
Keyword: Development of the Brain
Link ID: 22477 - Posted: 07.26.2016