Category: neuroscientist

Could Pot Help Veterans With PTSD? Brain Scientists Say Maybe

On By A.P.In Andrew Holmes, anxiety circuitry, Atlanta, brain, cannabinoids, cannabis, Cannabis sativa, Drugs, Emory University, Emory University School of Medicine, extinction therapy, fear circuitry, Georgia, Jon Hamilton, Kerry Ressler, marijuana, Medicine, military, National Institute of Mental Health, National Institute on Alcohol Abuse and Alcoholism, National Institute on Drug Abuse, Neuropsychiatric Disease, Neuroscience, neuroscientist, post-traumatic stress disorder, pot, psychiatrist, Psychiatry, psychology, psychotherapy, PTSD, Science, tetrahydrocannabinol, THC, VeteransLeave a comment

pot

by Jon Hamilton

Veterans who smoke marijuana to cope with post-traumatic stress disorder may be onto something. There’s growing evidence that pot can affect brain circuits involved in PTSD.

Experiments in animals show that tetrahydrocannabinol, the chemical that gives marijuana its feel-good qualities, acts on a system in the brain that is “critical for fear and anxiety modulation,” says Andrew Holmes, a researcher at the National Institute on Alcohol Abuse and Alcoholism. But he and other brain scientists caution that marijuana has serious drawbacks as a potential treatment for PTSD.

The use of marijuana for PTSD has gained national attention in the past few years as thousands of traumatized veterans who fought in Iraq and Afghanistan have asked the federal government to give them access to the drug. Also, Maine and a handful of other states have passed laws giving people with PTSD access to medical marijuana.

But there’s never been a rigorous scientific study to find out whether marijuana actually helps people with PTSD. So lawmakers and veterans groups have relied on anecdotes from people with the disorder and new research on how both pot and PTSD works in the brain.

An Overactive Fear System

When a typical person encounters something scary, the brain’s fear system goes into overdrive, says Dr. Kerry Ressler of Emory University. The heart pounds, muscles tighten. Then, once the danger is past, everything goes back to normal, he says.

But Ressler says that’s not what happens in the brain of someone with PTSD. “One way of thinking about PTSD is an overactivation of the fear system that can’t be inhibited, can’t be normally modulated,” he says.

For decades, researchers have suspected that marijuana might help people with PTSD by quieting an overactive fear system. But they didn’t understand how this might work until 2002, when scientists in Germany published a mouse study showing that the brain uses chemicals called cannabinoids to modulate the fear system, Ressler says.

There are two common sources of cannabinoids. One is the brain itself, which uses the chemicals to regulate a variety of brain cells. The other common source is Cannabis sativa, the marijuana plant.

So in recent years, researchers have done lots of experiments that involved treating traumatized mice with the active ingredient in pot, tetrahydrocannabinol (THC), Ressler says. And in general, he says, the mice who get THC look “less anxious, more calm, you know, many of the things that you might imagine.”

Problems with Pot

Unfortunately, THC’s effect on fear doesn’t seem to last, Ressler says, because prolonged exposure seems to make brain cells less sensitive to the chemical.

Another downside to using marijuana for PTSD is side effects, says Andrew Holmes at the National Institute on Alcohol Abuse and Alcoholism. “You may indeed get a reduction in anxiety,” Holmes says. “But you’re also going to get all of these unwanted effects,” including short-term memory loss, increased appetite and impaired motor skills.

So for several years now, Holmes and other scientists have been testing drugs that appear to work like marijuana, but with fewer drawbacks. Some of the most promising drugs amplify the effect of the brain’s own cannabinoids, which are called endocannabinoids, he says. “What’s encouraging about the effects of these endocannabinoid-acting drugs is that they may allow for long-term reductions in anxiety, in other words weeks if not months.”

The drugs work well in mice, Holmes says. But tests in people are just beginning and will take years to complete. In the meantime, researchers are learning more about how marijuana and THC affect the fear system in people.

At least one team has had success giving a single dose of THC to people during something called extinction therapy. The therapy is designed to teach the brain to stop reacting to something that previously triggered a fearful response.

The team’s study found that people who got THC during the therapy had “long-lasting reductions in anxiety, very similar to what we were seeing in our animal models,” Holmes says. So THC may be most useful when used for a short time in combination with other therapy, he says.

As studies continue to suggest that marijuana can help people with PTSD, it may be unrealistic to expect people with the disorder to wait for something better than marijuana and THC, Ressler says. “I’m a pragmatist,” he says. “I think if there are medications including drugs like marijuana that can be used in the right way, there’s an opportunity there, potentially.”

http://www.npr.org/blogs/health/2013/12/23/256610483/could-pot-help-veterans-with-ptsd-brain-scientists-say-maybe

Electric brain stimulation in a specific area discovered to induce a sense of determination

On By A.P.In aMCC, anterior midcingulate cortex, brain, Depression, determination, epilepsy, Josef Parvizi, Kebmodee, motivation, neural activity, neural prosthetics, neurologist, Neurology, Neuron, neuroplasticity, neuroprosthetic device, Neuropsychiatric Disease, Neuropsychopharmacology, Neuroscience, neuroscientist, neurosurgeon, neurosurgery, neurotransmitter, neurotrophin, Stanford, The FutureLeave a comment

Doctors in the US have induced feelings of intense determination in two men by stimulating a part of their brains with gentle electric currents.

The men were having a routine procedure to locate regions in their brains that caused epileptic seizures when they felt their heart rates rise, a sense of foreboding, and an overwhelming desire to persevere against a looming hardship.

The remarkable findings could help researchers develop treatments for depression and other disorders where people are debilitated by a lack of motivation.

One patient said the feeling was like driving a car into a raging storm. When his brain was stimulated, he sensed a shaking in his chest and a surge in his pulse. In six trials, he felt the same sensations time and again.

Comparing the feelings to a frantic drive towards a storm, the patient said: “You’re only halfway there and you have no other way to turn around and go back, you have to keep going forward.”

When asked by doctors to elaborate on whether the feeling was good or bad, he said: “It was more of a positive thing, like push harder, push harder, push harder to try and get through this.”

A second patient had similar feelings when his brain was stimulated in the same region, called the anterior midcingulate cortex (aMCC). He felt worried that something terrible was about to happen, but knew he had to fight and not give up, according to a case study in the journal Neuron.

Both men were having an exploratory procedure to find the focal point in their brains that caused them to suffer epileptic fits. In the procedure, doctors sink fine electrodes deep into different parts of the brain and stimulate them with tiny electrical currents until the patient senses the “aura” that precedes a seizure. Often, seizures can be treated by removing tissue from this part of the brain.

“In the very first patient this was something very unexpected, and we didn’t report it,” said Josef Parvizi at Stanford University in California. But then I was doing functional mapping on the second patient and he suddenly experienced a very similar thing.”

“Its extraordinary that two individuals with very different past experiences respond in a similar way to one or two seconds of very low intensity electricity delivered to the same area of their brain. These patients are normal individuals, they have their IQ, they have their jobs. We are not reporting these findings in sick brains,” Parvizi said.

The men were stimulated with between two and eight milliamps of electrical current, but in tests the doctors administered sham stimulation too. In the sham tests, they told the patients they were about to stimulate the brain, but had switched off the electical supply. In these cases, the men reported no changes to their feelings. The sensation was only induced in a small area of the brain, and vanished when doctors implanted electrodes just five millimetres away.

Parvizi said a crucial follow-up experiment will be to test whether stimulation of the brain region really makes people more determined, or simply creates the sensation of perseverance. If future studies replicate the findings, stimulation of the brain region – perhaps without the need for brain-penetrating electrodes – could be used to help people with severe depression.

The anterior midcingulate cortex seems to be important in helping us select responses and make decisions in light of the feedback we get. Brent Vogt, a neurobiologist at Boston University, said patients with chronic pain and obsessive-compulsive disorder have already been treated by destroying part of the aMCC. “Why not stimulate it? If this would enhance relieving depression, for example, let’s go,” he said.

http://www.theguardian.com/science/2013/dec/05/determination-electrical-brain-stimulation

Thanks to Kebmodee for bringing this to the attention of the It’s Interesting community.

How Exercise Beefs Up the Brain

On By A.P.In Alzheimer's disease, Barbara Hempstead, BDNF, Boston, brain derived neurotrophic factor, brown fat, Bruce Spiegelman, Cell Metabolism, Christiane Wrann, Dementia, diabetes, Dr. Rajadhyaksha, Exercise, FNDC5, Harvard Medical School, hippocampus, irisin, Karolinska Institute in Sweden, Medicine, Nature, neurologist, Neurology, Neuropsychiatric Disease, Neuroscience, neuroscientist, neurotrophin, Obesity, Parkinson's disease, PGC-1α, Pontus Boström, Science, The Brain, Weill Cornell Medical College, white fatLeave a comment

exercise

New research explains how abstract benefits of exercise—from reversing depression to fighting cognitive decline—might arise from a group of key molecules.

While our muscles pump iron, our cells pump out something else: molecules that help maintain a healthy brain. But scientists have struggled to account for the well-known mental benefits of exercise, from counteracting depression and aging to fighting Alzheimer’s and Parkinson’s disease. Now, a research team may have finally found a molecular link between a workout and a healthy brain.

Much exercise research focuses on the parts of our body that do the heavy lifting. Muscle cells ramp up production of a protein called FNDC5 during a workout. A fragment of this protein, known as irisin, gets lopped off and released into the bloodstream, where it drives the formation of brown fat cells, thought to protect against diseases such as diabetes and obesity. (White fat cells are traditionally the villains.)

While studying the effects of FNDC5 in muscles, cellular biologist Bruce Spiegelman of Harvard Medical School in Boston happened upon some startling results: Mice that did not produce a so-called co-activator of FNDC5 production, known as PGC-1α, were hyperactive and had tiny holes in certain parts of their brains. Other studies showed that FNDC5 and PGC-1α are present in the brain, not just the muscles, and that both might play a role in the development of neurons.

Spiegelman and his colleagues suspected that FNDC5 (and the irisin created from it) was responsible for exercise-induced benefits to the brain—in particular, increased levels of a crucial protein called brain-derived neurotrophic factor (BDNF), which is essential for maintaining healthy neurons and creating new ones. These functions are crucial to staving off neurological diseases, including Alzheimer’s and Parkinson’s. And the link between exercise and BDNF is widely accepted. “The phenomenon has been established over the course of, easily, the last decade,” says neuroscientist Barbara Hempstead of Weill Cornell Medical College in New York City, who was not involved in the new work. “It’s just, we didn’t understand the mechanism.”

To sort out that mechanism, Spiegelman and his colleagues performed a series of experiments in living mice and cultured mouse brain cells. First, they put mice on a 30-day endurance training regimen. They didn’t have to coerce their subjects, because running is part of a mouse’s natural foraging behavior. “It’s harder to get them to lift weights,” Spiegelman notes. The mice with access to a running wheel ran the equivalent of a 5K every night.

Aside from physical differences between wheel-trained mice and sedentary ones—“they just look a little bit more like a couch potato,” says co-author Christiane Wrann, also of Harvard Medical School, of the latter’s plumper figures—the groups also showed neurological differences. The runners had more FNDC5 in their hippocampus, an area of the brain responsible for learning and memory.

Using mouse brain cells developing in a dish, the group next showed that increasing the levels of the co-activator PGC-1α boosts FNDC5 production, which in turn drives BDNF genes to produce more of the vital neuron-forming BDNF protein. They report these results online today in Cell Metabolism. Spiegelman says it was surprising to find that the molecular process in neurons mirrors what happens in muscles as we exercise. “What was weird is the same pathway is induced in the brain,” he says, “and as you know, with exercise, the brain does not move.”

So how is the brain getting the signal to make BDNF? Some have theorized that neural activity during exercise (as we coordinate our body movements, for example) accounts for changes in the brain. But it’s also possible that factors outside the brain, like those proteins secreted from muscle cells, are the driving force. To test whether irisin created elsewhere in the body can still drive BDNF production in the brain, the group injected a virus into the mouse’s bloodstream that causes the liver to produce and secrete elevated levels of irisin. They saw the same effect as in exercise: increased BDNF levels in the hippocampus. This suggests that irisin could be capable of passing the blood-brain barrier, or that it regulates some other (unknown) molecule that crosses into the brain, Spiegelman says.

Hempstead calls the findings “very exciting,” and believes this research finally begins to explain how exercise relates to BDNF and other so-called neurotrophins that keep the brain healthy. “I think it answers the question that most of us have posed in our own heads for many years.”

The effect of liver-produced irisin on the brain is a “pretty cool and somewhat surprising finding,” says Pontus Boström, a diabetes researcher at the Karolinska Institute in Sweden. But Boström, who was among the first scientists to identify irisin in muscle tissue, says the work doesn’t answer a fundamental question: How much of exercise’s BDNF-promoting effects come from irisin reaching the brain from muscle cells via the bloodstream, and how much are from irisin created in the brain?

Though the authors point out that other important regulator proteins likely play a role in driving BDNF and other brain-nourishing factors, they are focusing on the benefits of irisin and hope to develop an injectable form of FNDC5 as a potential treatment for neurological diseases and to improve brain health with aging.

http://news.sciencemag.org/biology/2013/10/how-exercise-beefs-brain

Thanks to Dr. Rajadhyaksha for bringing this to the attention of the It’s Interesting community.

After cardiac arrest, a final surge of brain activity could contain vivid experience, new research in rodents suggests.

On By A.P.In Allen Institute for Brain Science, brain, cardiac arrest, Christof Koch, death, EEG, electroencephalography, Jimo Borjigin, Kebmodee, near-death experiences, Neurology, Neuron, Neuroscience, neuroscientist, Proceedings of the National Academy of Sciences, Sam Parnia, Science, University of Michigan1 Comment

sn-brain

What people experience as death creeps in—after the heart stops and the brain becomes starved of oxygen—seems to lie beyond the reach of science. But the authors of a new study on dying rats make a bold claim: After cardiac arrest, the rodents’ brains enter a state similar to heightened consciousness in humans. The researchers suggest that if the same is true for people, such brain activity could be the source of the visions and other sensations that make up so-called near-death experiences.

Estimated to occur in about 20% of patients who survive cardiac arrest, near-death experiences are frequently described as hypervivid or “realer-than-real,” and often include leaving the body and observing oneself from outside, or seeing a bright light. The similarities between these reports are hard to ignore, but the conversation about near-death experiences often bleeds into metaphysics: Are these visions produced solely by the brain, or are they a glimpse at an afterlife outside the body?

Neurologist Jimo Borjigin of the University of Michigan, Ann Arbor, got interested in near-death experiences during a different project—measuring the hormone levels in the brains of rodents after a stroke. Some of the animals in her lab died unexpectedly, and her measurements captured a surge in neurochemicals at the moment of their death. Previous research in rodents and humans has shown that electrical activity surges in the brain right after the heart stops, then goes flat after a few seconds. Without any evidence that this final blip contains meaningful brain activity, Borjigin says “it’s perhaps natural for people to assume that [near-death] experiences came from elsewhere, from more supernatural sources.” But after seeing those neurochemical surges in her animals, she wondered about those last few seconds, hypothesizing that even experiences seeming to stretch for days in a person’s memory could originate from a brief “knee-jerk reaction” of the dying brain.

To observe brains on the brink of death, Borjigin and her colleagues implanted electrodes into the brains of nine rats to measure electrical activity at six different locations. The team anesthetized the rats for about an hour, for ethical reasons, and then injected potassium chloride into each unconscious animal’s heart to cause cardiac arrest. In the approximately 30 seconds between a rat’s last heartbeat and the point when its brain stopped producing signals, the team carefully recorded its neuronal oscillations, or the frequency with which brain cells were firing their electrical signals.

The data produced by electroencephalograms (EEGs) of the nine rats revealed a highly organized brain response in the seconds after cardiac arrest, Borjigin and colleagues report online today in the Proceedings of the National Academy of Sciences. While overall electrical activity in the brain sharply declined after the last heartbeat, oscillations in the low gamma frequency (between 25 and 55 Hz) increased in power. Previous human research has linked gamma waves to waking consciousness, meditative states, and REM sleep. These oscillations in the dying rats were synchronized across different parts of the brain, even more so than in the rat’s normal waking state. The team also noticed that firing patterns in the front of the brain would be echoed in the back and sides. This so-called top-down signaling, which is associated with conscious perception and information processing, increased eightfold compared with the waking state, the team reports. When you put these features together, Borjigin says, they suggest that the dying brain is hyperactive in its final seconds, producing meaningful, conscious activity.

The team proposed that such research offers a “scientific framework” for approaching the highly lucid experiences that some people report after their brushes with death. But relating signs of consciousness in rat brains to human near-death experiences is controversial. “It opens more questions than it answers,” says Christof Koch, a neuroscientist at the Allen Institute for Brain Science in Seattle, Washington, of the research. Evidence of a highly organized and connected brain state during the animal’s death throes is surprising and fascinating, he says. But Koch, who worked with Francis Crick in the early 1980s to hypothesize that gamma waves are a hallmark of consciousness, says the increase in their frequency doesn’t necessarily mean that the rats were in a hyperconscious state. Not only is it impossible to project any mental experience onto these animals, but their response was also “still overlaid by the anesthesiology,” he says; this sedation likely influenced their brain response in unpredictable ways.

Others share Koch’s concerns. “There is no animal model of a near-death experience,” says critical care physician Sam Parnia of Stony Brook University School of Medicine in New York. We can never confirm what animals think or feel in their final moments, making it all but impossible to use them to study our own near-death experiences, he believes. Nonetheless, Parnia sees value in this new study from a clinical perspective, as a step toward understanding how the brain behaves right before death. He says that doctors might use a similar approach to learn how to improve blood flow or prolong electrical activity in the brain, preventing damage while resuscitating a patient.

Borjigin argues that the rat data are compelling enough to drive further study of near-death experiences in humans. She suggests monitoring EEG activity in people undergoing brain surgery that involves cooling the brain and reducing its blood supply. This procedure has prompted near-death experiences in the past, she says, and could offer a systematic way to explore the phenomenon.

read more here: http://news.sciencemag.org/brain-behavior/2013/08/probing-brain%E2%80%99s-final-moments

Thanks to Kebmodee for bringing this to the attention of the It’s Interesting community.

Why music makes our brain sing

On By A.P.In brain, music, Neuroscience, neuroscientist, Robert J. Zatorre, SRWLeave a comment

music

By ROBERT J. ZATORRE and VALORIE N. SALIMPOOR
Published: June 7, 2013

Music is not tangible. You can’t eat it, drink it or mate with it. It doesn’t protect against the rain, wind or cold. It doesn’t vanquish predators or mend broken bones. And yet humans have always prized music — or well beyond prized, loved it.

In the modern age we spend great sums of money to attend concerts, download music files, play instruments and listen to our favorite artists whether we’re in a subway or salon. But even in Paleolithic times, people invested significant time and effort to create music, as the discovery of flutes carved from animal bones would suggest.

So why does this thingless “thing” — at its core, a mere sequence of sounds — hold such potentially enormous intrinsic value?

The quick and easy explanation is that music brings a unique pleasure to humans. Of course, that still leaves the question of why. But for that, neuroscience is starting to provide some answers.

More than a decade ago, our research team used brain imaging to show that music that people described as highly emotional engaged the reward system deep in their brains — activating subcortical nuclei known to be important in reward, motivation and emotion. Subsequently we found that listening to what might be called “peak emotional moments” in music — that moment when you feel a “chill” of pleasure to a musical passage — causes the release of the neurotransmitter dopamine, an essential signaling molecule in the brain.

When pleasurable music is heard, dopamine is released in the striatum — an ancient part of the brain found in other vertebrates as well — which is known to respond to naturally rewarding stimuli like food and sex and which is artificially targeted by drugs like cocaine and amphetamine.

But what may be most interesting here is when this neurotransmitter is released: not only when the music rises to a peak emotional moment, but also several seconds before, during what we might call the anticipation phase.

The idea that reward is partly related to anticipation (or the prediction of a desired outcome) has a long history in neuroscience. Making good predictions about the outcome of one’s actions would seem to be essential in the context of survival, after all. And dopamine neurons, both in humans and other animals, play a role in recording which of our predictions turn out to be correct.

To dig deeper into how music engages the brain’s reward system, we designed a study to mimic online music purchasing. Our goal was to determine what goes on in the brain when someone hears a new piece of music and decides he likes it enough to buy it.

We used music-recommendation programs to customize the selections to our listeners’ preferences, which turned out to be indie and electronic music, matching Montreal’s hip music scene. And we found that neural activity within the striatum — the reward-related structure — was directly proportional to the amount of money people were willing to spend.

But more interesting still was the cross talk between this structure and the auditory cortex, which also increased for songs that were ultimately purchased compared with those that were not.

Why the auditory cortex? Some 50 years ago, Wilder Penfield, the famed neurosurgeon and the founder of the Montreal Neurological Institute, reported that when neurosurgical patients received electrical stimulation to the auditory cortex while they were awake, they would sometimes report hearing music. Dr. Penfield’s observations, along with those of many others, suggest that musical information is likely to be represented in these brain regions.

The auditory cortex is also active when we imagine a tune: think of the first four notes of Beethoven’s Fifth Symphony — your cortex is abuzz! This ability allows us not only to experience music even when it’s physically absent, but also to invent new compositions and to reimagine how a piece might sound with a different tempo or instrumentation.

We also know that these areas of the brain encode the abstract relationships between sounds — for instance, the particular sound pattern that makes a major chord major, regardless of the key or instrument. Other studies show distinctive neural responses from similar regions when there is an unexpected break in a repetitive pattern of sounds, or in a chord progression. This is akin to what happens if you hear someone play a wrong note — easily noticeable even in an unfamiliar piece of music.

These cortical circuits allow us to make predictions about coming events on the basis of past events. They are thought to accumulate musical information over our lifetime, creating templates of the statistical regularities that are present in the music of our culture and enabling us to understand the music we hear in relation to our stored mental representations of the music we’ve heard.

So each act of listening to music may be thought of as both recapitulating the past and predicting the future. When we listen to music, these brain networks actively create expectations based on our stored knowledge.

Composers and performers intuitively understand this: they manipulate these prediction mechanisms to give us what we want — or to surprise us, perhaps even with something better.

In the cross talk between our cortical systems, which analyze patterns and yield expectations, and our ancient reward and motivational systems, may lie the answer to the question: does a particular piece of music move us?

When that answer is yes, there is little — in those moments of listening, at least — that we value more.

Robert J. Zatorre is a professor of neuroscience at the Montreal Neurological Institute and Hospital at McGill University. Valorie N. Salimpoor is a postdoctoral neuroscientist at the Baycrest Health Sciences’ Rotman Research Institute in Toronto.

Thanks to S.R.W. for bringing this to the attention of the It’s Interesting community.

Trouble With Math? Maybe You Should Get Your Brain Zapped

On By A.P.In Current Biology, developmental dyscalculia, electroshock therapy, Emily Underwood, Jacqueline Thompson, Math, Michael Weisend, Mind Research Network, near-infrared spectroscopy, neural prosthetics, neuroethicist, neuroethics, neuroplasticity, neuroprosthetic device, Neuroscience, neuroscientist, Peter Reiner, Roi Cohen Kadosh, Science, ScienceNOW, The Brain, The Singularity, University of British Columbia, University of OxfordLeave a comment

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by Emily Underwood
ScienceNOW

If you are one of the 20% of healthy adults who struggle with basic arithmetic, simple tasks like splitting the dinner bill can be excruciating. Now, a new study suggests that a gentle, painless electrical current applied to the brain can boost math performance for up to 6 months. Researchers don’t fully understand how it works, however, and there could be side effects.

The idea of using electrical current to alter brain activity is nothing new—electroshock therapy, which induces seizures for therapeutic effect, is probably the best known and most dramatic example. In recent years, however, a slew of studies has shown that much milder electrical stimulation applied to targeted regions of the brain can dramatically accelerate learning in a wide range of tasks, from marksmanship to speech rehabilitation after stroke.

In 2010, cognitive neuroscientist Roi Cohen Kadosh of the University of Oxford in the United Kingdom showed that, when combined with training, electrical brain stimulation can make people better at very basic numerical tasks, such as judging which of two quantities is larger. However, it wasn’t clear how those basic numerical skills would translate to real-world math ability.

To answer that question, Cohen Kadosh recruited 25 volunteers to practice math while receiving either real or “sham” brain stimulation. Two sponge-covered electrodes, fixed to either side of the forehead with a stretchy athletic band, targeted an area of the prefrontal cortex considered key to arithmetic processing, says Jacqueline Thompson, a Ph.D. student in Cohen Kadosh’s lab and a co-author on the study. The electrical current slowly ramped up to about 1 milliamp—a tiny fraction of the voltage of an AA battery—then randomly fluctuated between high and low values. For the sham group, the researchers simulated the initial sensation of the increase by releasing a small amount of current, then turned it off.

For roughly 20 minutes per day over 5 days, the participants memorized arbitrary mathematical “facts,” such as 4#10 = 23, then performed a more sophisticated task requiring multiple steps of arithmetic, also based on memorized symbols. A squiggle, for example, might mean “add 2,” or “subtract 1.” This is the first time that brain stimulation has been applied to improving such complex math skills, says neuroethicist Peter Reiner of the University of British Columbia, Vancouver, in Canada, who wasn’t involved in the research.

The researchers also used a brain imaging technique called near-infrared spectroscopy to measure how efficiently the participants’ brains were working as they performed the tasks.

Although the two groups performed at the same level on the first day, over the next 4 days people receiving brain stimulation along with training learned to do the tasks two to five times faster than people receiving a sham treatment, the authors reported in Current Biology. Six months later, the researchers called the participants back and found that people who had received brain stimulation were still roughly 30% faster at the same types of mathematical challenges. The targeted brain region also showed more efficient activity, Thompson says.

The fact that only participants who received electrical stimulation and practiced math showed lasting physiological changes in their brains suggests that experience is required to seal in the effects of stimulation, says Michael Weisend, a neuroscientist at the Mind Research Network in Albuquerque, New Mexico, who wasn’t involved with the study. That’s valuable information for people who hope to get benefits from stimulation alone, he says. “It’s not going to be a magic bullet.”

Although it’s not clear how the technique works, Thompson says, one hypothesis is that the current helps synchronize neuron firing, enabling the brain to work more efficiently. Scientists also don’t know if negative or unintended effects might result. Although no side effects of brain stimulation have yet been reported, “it’s impossible to say with any certainty” that there aren’t any, Thompson says.

“Math is only one of dozens of skills in which this could be used,” Reiner says, adding that it’s “not unreasonable” to imagine that this and similar stimulation techniques could replace the use of pills for cognitive enhancement.

In the future, the researchers hope to include groups that often struggle with math, such as people with neurodegenerative disorders and a condition called developmental dyscalculia. As long as further testing shows that the technique is safe and effective, children in schools could also receive brain stimulation along with their lessons, Thompson says. But there’s “a long way to go,” before the method is ready for schools, she says. In the meantime, she adds, “We strongly caution you not to try this at home, no matter how tempted you may be to slap a battery on your kid’s head.”

http://news.sciencemag.org/sciencenow/2013/05/trouble-with-math-maybe-you-shou.html?ref=hp

Cocaine Vaccine Passes Key Testing Hurdle of Preventing Drug from Reaching the Brain – Human Clinical Trials soon

On By A.P.In Addiction, brain, cocaine, cocaine vaccine, Cornell University, dopamine, Dr. Rajadhyaksha, Drugs, Kebmodee, National Institute on Drug Abuse, Neuropsychiatric Disease, Neuropsychopharmacology, Neuroscience, neuroscientist, neurotransmitter, NIDA, Ronald G. Crystal, The Future, Weill Cornell Medical College1 Comment

cocaine

Researchers at Weill Cornell Medical College have successfully tested their novel anti-cocaine vaccine in primates, bringing them closer to launching human clinical trials. Their study, published online by the journal Neuropsychopharmacology, used a radiological technique to demonstrate that the anti-cocaine vaccine prevented the drug from reaching the brain and producing a dopamine-induced high.

“The vaccine eats up the cocaine in the blood like a little Pac-man before it can reach the brain,” says the study’s lead investigator, Dr. Ronald G. Crystal, chairman of the Department of Genetic Medicine at Weill Cornell Medical College. “We believe this strategy is a win-win for those individuals, among the estimated 1.4 million cocaine users in the United States, who are committed to breaking their addiction to the drug,” he says. “Even if a person who receives the anti-cocaine vaccine falls off the wagon, cocaine will have no effect.”

Dr. Crystal says he expects to begin human testing of the anti-cocaine vaccine within a year.

Cocaine, a tiny molecule drug, works to produce feelings of pleasure because it blocks the recycling of dopamine — the so-called “pleasure” neurotransmitter — in two areas of the brain, the putamen in the forebrain and the caudate nucleus in the brain’s center. When dopamine accumulates at the nerve endings, “you get this massive flooding of dopamine and that is the feel good part of the cocaine high,” says Dr. Crystal.

The novel vaccine Dr. Crystal and his colleagues developed combines bits of the common cold virus with a particle that mimics the structure of cocaine. When the vaccine is injected into an animal, its body “sees” the cold virus and mounts an immune response against both the virus and the cocaine impersonator that is hooked to it. “The immune system learns to see cocaine as an intruder,” says Dr. Crystal. “Once immune cells are educated to regard cocaine as the enemy, it produces antibodies, from that moment on, against cocaine the moment the drug enters the body.”

In their first study in animals, the researchers injected billions of their viral concoction into laboratory mice, and found a strong immune response was generated against the vaccine. Also, when the scientists extracted the antibodies produced by the mice and put them in test tubes, it gobbled up cocaine. They also saw that mice that received both the vaccine and cocaine were much less hyperactive than untreated mice given cocaine.

In this study, the researchers sought to precisely define how effective the anti-cocaine vaccine is in non-human primates, who are closer in biology to humans than mice. They developed a tool to measure how much cocaine attached to the dopamine transporter, which picks up dopamine in the synapse between neurons and brings it out to be recycled. If cocaine is in the brain, it binds on to the transporter, effectively blocking the transporter from ferrying dopamine out of the synapse, keeping the neurotransmitter active to produce a drug high.

In the study, the researchers attached a short-lived isotope tracer to the dopamine transporter. The activity of the tracer could be seen using positron emission tomography (PET). The tool measured how much of the tracer attached to the dopamine receptor in the presence or absence of cocaine.

The PET studies showed no difference in the binding of the tracer to the dopamine transporter in vaccinated compared to unvaccinated animals if these two groups were not given cocaine. But when cocaine was given to the primates, there was a significant drop in activity of the tracer in non-vaccinated animals. That meant that without the vaccine, cocaine displaced the tracer in binding to the dopamine receptor.

Previous research had shown in humans that at least 47 percent of the dopamine transporter had to be occupied by cocaine in order to produce a drug high. The researchers found, in vaccinated primates, that cocaine occupancy of the dopamine receptor was reduced to levels of less than 20 percent.

“This is a direct demonstration in a large animal, using nuclear medicine technology, that we can reduce the amount of cocaine that reaches the brain sufficiently so that it is below the threshold by which you get the high,” says Dr. Crystal.

When the vaccine is studied in humans, the non-toxic dopamine transporter tracer can be used to help study its effectiveness as well, he adds.

The researchers do not know how often the vaccine needs to be administered in humans to maintain its anti-cocaine effect. One vaccine lasted 13 weeks in mice and seven weeks in non-human primates.

“An anti-cocaine vaccination will require booster shots in humans, but we don’t know yet how often these booster shots will be needed,” says Dr. Crystal. “I believe that for those people who desperately want to break their addiction, a series of vaccinations will help.”

Co-authors of the study include Dr. Anat Maoz, Dr. Martin J. Hicks, Dr. Shankar Vallabhajosula, Michael Synan, Dr. Paresh J. Kothari, Dr. Jonathan P. Dyke, Dr. Douglas J. Ballon, Dr. Stephen M. Kaminsky, Dr. Bishnu P. De and Dr. Jonathan B. Rosenberg from Weill Cornell Medical College; Dr. Diana Martinez from Columbia University; and Dr. George F. Koob and Dr. Kim D. Janda from The Scripps Research Institute.

The study was funded by grants from the National Institute on Drug Abuse (NIDA).

Thanks to Kebmodee and Dr. Rajadhyaksha for bringing this to the attention of the It’s Interesting community.

Brain implants: Restoring memory with a microchip

On By A.P.In brain, brain computer interface, Constantine Lyketsos, Doug Brown, hippocampus, Inventions, Johnny Mnemonic, memory, neural activity, neural prosthetics, Neurology, neuroplasticity, neuroprosthetic device, Neuroscience, neuroscientist, neurosurgery, Rob Hampson, Science, Technology, Ted Berger, The Brain, The Future, The Singularity, University of Southern California, Wake Forest University1 Comment

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William Gibson’s popular science fiction tale “Johnny Mnemonic” foresaw sensitive information being carried by microchips in the brain by 2021. A team of American neuroscientists could be making this fantasy world a reality. Their motivation is different but the outcome would be somewhat similar. Hailed as one of 2013’s top ten technological breakthroughs by MIT, the work by the University of Southern California, North Carolina’s Wake Forest University and other partners has actually spanned a decade.

But the U.S.-wide team now thinks that it will see a memory device being implanted in a small number of human volunteers within two years and available to patients in five to 10 years. They can’t quite contain their excitement. “I never thought I’d see this in my lifetime,” said Ted Berger, professor of biomedical engineering at the University of Southern California in Los Angeles. “I might not benefit from it myself but my kids will.”

Rob Hampson, associate professor of physiology and pharmacology at Wake Forest University, agrees. “We keep pushing forward, every time I put an estimate on it, it gets shorter and shorter.”

The scientists — who bring varied skills to the table, including mathematical modeling and psychiatry — believe they have cracked how long-term memories are made, stored and retrieved and how to replicate this process in brains that are damaged, particularly by stroke or localized injury.

Berger said they record a memory being made, in an undamaged area of the brain, then use that data to predict what a damaged area “downstream” should be doing. Electrodes are then used to stimulate the damaged area to replicate the action of the undamaged cells.

They concentrate on the hippocampus — part of the cerebral cortex which sits deep in the brain — where short-term memories become long-term ones. Berger has looked at how electrical signals travel through neurons there to form those long-term memories and has used his expertise in mathematical modeling to mimic these movements using electronics.

Hampson, whose university has done much of the animal studies, adds: “We support and reinforce the signal in the hippocampus but we are moving forward with the idea that if you can study enough of the inputs and outputs to replace the function of the hippocampus, you can bypass the hippocampus.”

The team’s experiments on rats and monkeys have shown that certain brain functions can be replaced with signals via electrodes. You would think that the work of then creating an implant for people and getting such a thing approved would be a Herculean task, but think again.

For 15 years, people have been having brain implants to provide deep brain stimulation to treat epilepsy and Parkinson’s disease — a reported 80,000 people have now had such devices placed in their brains. So many of the hurdles have already been overcome — particularly the “yuck factor” and the fear factor.

“It’s now commonly accepted that humans will have electrodes put in them — it’s done for epilepsy, deep brain stimulation, (that has made it) easier for investigative research, it’s much more acceptable now than five to 10 years ago,” Hampson says.

Much of the work that remains now is in shrinking down the electronics.

“Right now it’s not a device, it’s a fair amount of equipment,”Hampson says. “We’re probably looking at devices in the five to 10 year range for human patients.”

The ultimate goal in memory research would be to treat Alzheimer’s Disease but unlike in stroke or localized brain injury, Alzheimer’s tends to affect many parts of the brain, especially in its later stages, making these implants a less likely option any time soon.

Berger foresees a future, however, where drugs and implants could be used together to treat early dementia. Drugs could be used to enhance the action of cells that surround the most damaged areas, and the team’s memory implant could be used to replace a lot of the lost cells in the center of the damaged area. “I think the best strategy is going to involve both drugs and devices,” he says.

Unfortunately, the team found that its method can’t help patients with advanced dementia.

“When looking at a patient with mild memory loss, there’s probably enough residual signal to work with, but not when there’s significant memory loss,” Hampson said.

Constantine Lyketsos, professor of psychiatry and behavioral sciences at John Hopkins Medicine in Baltimore which is trialing a deep brain stimulator implant for Alzheimer’s patients was a little skeptical of the other team’s claims.

“The brain has a lot of redundancy, it can function pretty well if loses one or two parts. But memory involves circuits diffusely dispersed throughout the brain so it’s hard to envision.” However, he added that it was more likely to be successful in helping victims of stroke or localized brain injury as indeed its makers are aiming to do.

The UK’s Alzheimer’s Society is cautiously optimistic.

“Finding ways to combat symptoms caused by changes in the brain is an ongoing battle for researchers. An implant like this one is an interesting avenue to explore,” said Doug Brown, director of research and development.

Hampson says the team’s breakthrough is “like the difference between a cane, to help you walk, and a prosthetic limb — it’s two different approaches.”

It will still take time for many people to accept their findings and their claims, he says, but they don’t expect to have a shortage of volunteers stepping forward to try their implant — the project is partly funded by the U.S. military which is looking for help with battlefield injuries.

There are U.S. soldiers coming back from operations with brain trauma and a neurologist at DARPA (the Defense Advanced Research Projects Agency) is asking “what can you do for my boys?” Hampson says.

“That’s what it’s all about.”

http://www.cnn.com/2013/05/07/tech/brain-memory-implants-humans/index.html?iref=allsearch

New Study Ties Autism Risk to Creases in Placenta

On By A.P.In autism, Biological Psychiatry, Center for Autism Research at Children’s Hospital of Philadelphia, Cheryl K. Walker, Chris Mann Sullivan, Dr. Rajadhyaksha, Harvard Medical School, Harvey J. Kliman, Jonathan L. Hecht, Marbles, Medicine, MIND Institute, Neuropsychiatric Disease, Neuroscience, neuroscientist, New York Times, Placenta, Science, Tara Wenger, The Brain, trophoblast inclusions, UC Davis, University of California, Yale UniversityLeave a comment

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After most pregnancies, the placenta is thrown out, having done its job of nourishing and supporting the developing baby.

But a new study raises the possibility that analyzing the placenta after birth may provide clues to a child’s risk for developing autism. The study, which analyzed placentas from 217 births, found that in families at high genetic risk for having an autistic child, placentas were significantly more likely to have abnormal folds and creases.

“It’s quite stark,” said Dr. Cheryl K. Walker, an obstetrician-gynecologist at the Mind Institute at the University of California, Davis, and a co-author of the study, published in the journal Biological Psychiatry. “Placentas from babies at risk for autism, clearly there’s something quite different about them.”

Researchers will not know until at least next year how many of the children, who are between 2 and 5, whose placentas were studied will be found to have autism. Experts said, however, that if researchers find that children with autism had more placental folds, called trophoblast inclusions, visible after birth, the condition could become an early indicator or biomarker for babies at high risk for the disorder.

“It would be really exciting to have a real biomarker and especially one that you can get at birth,” said Dr. Tara Wenger, a researcher at the Center for Autism Research at Children’s Hospital of Philadelphia, who was not involved in the study.

The research potentially marks a new frontier, not only for autism, but also for the significance of the placenta, long considered an after-birth afterthought. Now, only 10 percent to 15 percent of placentas are analyzed, usually after pregnancy complications or a newborn’s death.

Dr. Harvey J. Kliman, a research scientist at the Yale School of Medicine and lead author of the study, said the placenta had typically been given such little respect in the medical community that wanting to study it was considered equivalent to someone in the Navy wanting to scrub ships’ toilets with a toothbrush. But he became fascinated with placentas and noticed that inclusions often occurred with births involving problematic outcomes, usually genetic disorders.

He also noticed that “the more trophoblast inclusions you have, the more severe the abnormality.” In 2006, Dr. Kliman and colleagues published research involving 13 children with autism, finding that their placentas were three times as likely to have inclusions. The new study began when Dr. Kliman, looking for more placentas, contacted the Mind Institute, which is conducting an extensive study, called Marbles, examining potential causes of autism.

“This person came out of the woodwork and said, ‘I want to study trophoblastic inclusions,’ ” Dr. Walker recalled. “Now I’m fairly intelligent and have been an obstetrician for years and I had never heard of them.”

Dr. Walker said she concluded that while “this sounds like a very smart person with a very intriguing hypothesis, I don’t know him and I don’t know how much I trust him.” So she sent him Milky Way bar-size sections of 217 placentas and let him think they all came from babies considered at high risk for autism because an older sibling had the disorder. Only after Dr. Kliman had counted each placenta’s inclusions did she tell him that only 117 placentas came from at-risk babies; the other 100 came from babies with low autism risk.

She reasoned that if Dr. Kliman found that “they all show a lot of inclusions, then maybe he’s a bit overzealous” in trying to link inclusions to autism. But the results, she said, were “astonishing.” More than two-thirds of the low-risk placentas had no inclusions, and none had more than two. But 77 high-risk placentas had inclusions, 48 of them had two or more, including 16 with between 5 and 15 inclusions.

Dr. Walker said that typically between 2 percent and 7 percent of at-risk babies develop autism, and 20 percent to 25 percent have either autism or another developmental delay. She said she is seeing some autism and non-autism diagnoses among the 117 at-risk children in the study, but does not yet know how those cases match with placental inclusions.

Dr. Jonathan L. Hecht, associate professor of pathology at Harvard Medical School, said the study was intriguing and “probably true if it finds an association between these trophoblast inclusions and autism.” But he said that inclusions were the placenta’s way of responding to many kinds of stress, so they might turn out not to be specific enough to predict autism.

Dr. Kliman calls inclusions a “check-engine light, a marker of: something’s wrong, but I don’t know what it is.”

That’s how Chris Mann Sullivan sees it, too. Dr. Sullivan, a behavioral analyst in Morrisville, N.C., was not in the study, but sent her placenta to Dr. Kliman after her daughter Dania, now 3, was born. He found five inclusions. Dr. Sullivan began intensive one-on-one therapy with Dania, who has not been given a diagnosis of autism, but has some relatively mild difficulties.

“What would have happened if I did absolutely nothing, I’m not sure,” Dr. Sullivan said. “I think it’s a great way for parents to say, ‘O.K., we have some risk factors; we’re not going to ignore it.’ ”

Thanks to Dr. Rajadhyaksha for bringing this to the attention of the It’s Interesting community.

Documentary on Sleep Paralysis this May

On By A.P.In brain, Brazil, Carla MacKinnon, demon, dream, incubus, LiveScience, lucid dreaming, Medicine, narcolepsy, Neuroscience, neuroscientist, Royal College of Arts in London, Sleep, sleep paralysis, Stephanie Pappas, succubus, Wellcome TrustLeave a comment

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Stephanie Pappas, LiveScience Senior Writer

When filmmaker Carla MacKinnon started waking up several times a week unable to move, with the sense that a disturbing presence was in the room with her, she didn’t call up her local ghost hunter. She got researching. Now, that research is becoming a short film and multiplatform art project exploring the strange and spooky phenomenon of sleep paralysis. The film, supported by the Wellcome Trust and set to screen at the Royal College of Arts in London, will debut in May.

Sleep paralysis happens when people become conscious while their muscles remain in the ultra-relaxed state that prevents them from acting out their dreams. The experience can be quite terrifying, with many people hallucinating a malevolent presence nearby, or even an attacker suffocating them. Surveys put the number of sleep paralysis sufferers between about 5 percent and 60 percent of the population. “I was getting quite a lot of sleep paralysis over the summer, quite frequently, and I became quite interested in what was happening, what medically or scientifically, it was all about,” MacKinnon said.

Her questions led her to talk with psychologists and scientists, as well as to people who experience the phenomenon. Myths and legends about sleep paralysis persist all over the globe, from the incubus and succubus (male and female demons, respectively) of European tales to a pink dolphin-turned-nighttime seducer in Brazil. Some of the stories MacKinnon uncovered reveal why these myths are so chilling.

One man told her about his frequent sleep paralysis episodes, during which he’d experience extremely realistic hallucinations of a young child, skipping around the bed and singing nursery rhymes. Sometimes, the child would sit on his pillow and talk to him. One night, the tot asked the man a personal question. When he refused to answer, the child transformed into a “horrendous demon,” MacKinnon said.

For another man, who had the sleep disorder narcolepsy (which can make sleep paralysis more common), his dream world clashed with the real world in a horrifying way. His sleep paralysis episodes typically included hallucinations that someone else was in his house or his room — he’d hear voices or banging around. One night, he awoke in a paralyzed state and saw a figure in his room as usual. “He suddenly realizes something is different,” MacKinnon said. “He suddenly realizes that he is in sleep paralysis, and his eyes are open, but the person who is in the room is in his room in real life.” The figure was no dream demon, but an actual burglar.

Sleep paralysis experiences are almost certainly behind the myths of the incubus and succubus, demons thought to have sex with unsuspecting humans in their sleep. In many cases, MacKinnon said, the science of sleep paralysis explains these myths. The feeling of suffocating or someone pushing down on the chest that often occurs during sleep paralysis may be a result of the automatic breathing pattern people fall into during sleep. When they become conscious while still in this breathing pattern, people may try to bring their breathing under voluntary control, leading to the feeling of suffocating. Add to that the hallucinations that seem to seep in from the dream world, and it’s no surprise that interpretations lend themselves to demons, ghosts or even alien abduction, MacKinnon said.

What’s more, MacKinnon said, sleep paralysis is more likely when your sleep is disrupted in some way — perhaps because you’ve been traveling, you’re too hot or too cold, or you’re sleeping in an unfamiliar or spooky place. Those tendencies may make it more likely that a person will experience sleep paralysis when already vulnerable to thoughts of ghosts and ghouls. “It’s interesting seeing how these scientific narratives and the more psychoanalytical or psychological narratives can support each other rather than conflict,” MacKinnon said.

Since working on the project, MacKinnon has been able to bring her own sleep paralysis episodes under control — or at least learned to calm herself during them. The trick, she said, is to use episodes like a form of research, by paying attention to details like how her hands feel and what position she’s in. This sort of mindfulness tends to make scary hallucinations blink away, she said. “Rationalizing it is incredibly counterintuitive,” she said. “It took me a really long time to stop believing that it was real, because it feels so incredibly real.”

http://www.livescience.com/28325-spooky-film-explores-sleep-paralysis.html