Friday, September 28, 2012

Drugs Live: how to take ecstasy in a brain scanner

(c) Matt Herring London is a city with lots of things you should do, but sadly it is also a city where there can be very little time to do them in. Given these restrictions, what chance have you got of ever getting round to the things you shouldn’t do? None. But it’s okay, every week Michael Hodges is going to do one of them for you.

This week, our intrepid Executive Editor took part in a drugs trial partly funded by Channel 4 for inclusion in Drugs Live. The first half of the show was broadcast last night, the second part is tonight. Michael Hodges was going to be filmed after taking MDMA but withdrew halfway through the process after it was suggested that he take MDMA on the evening of the show rather than the morning. Thus sparing viewers footage of a gurning columnist. As it won’t be shown on TV, here’s what happened…

‘I am lying on a gurney with my head in a restraining bracket, wearing green scrubs, a plastic face mask and a protective helmet. Half an hour ago I took a red capsule which either contained an 80mg dose of pharmaceutical-quality MDMA (known in some circles as ‘the good stuff’) or an 80mg dose of vitamin C (known in all circles as ‘vitamin C’). MDMA – for those too young to remember the late ’80s, or indeed those who were old enough to be there and for whom the era is now a total blank – is the active ingredient in ecstasy.

None of the medical professionals currently scurrying around my body attaching tubes and taking notes knows which it is. Neither do I. If it’s vitamin C, I should remain sniffle-free for a week. If it’s MDMA, there is a strong chance of face-pulling, a cascade of my deepest psychosexual secrets and, inevitably, dancing. All of which will be a little bit trickier because I will be inside a functional magnetic resonance imaging machine, or brain scanner, when the dose kicks in.

I am taking part in a research project led by Professor David Nutt, former chairman of the Advisory Council on the Misuse of Drugs, looking into the effects of MDMA on the ‘resting human brain’. I will be visiting the Neuropsychopharmacology Unit at Imperial College London twice. Once to take MDMA while his team look at my brain. And once to take the vitamin C placebo while his team look at my brain.

On each visit I will be placed in the functional magnetic resonance imaging machine for one hour and 20 minutes. I have yet to be extensively briefed, but I do know that the machines are extremely loud, and that I will be completing a series of psychological tests and emotional assessments. ‘Make a list,’ I was told, ‘of the six best and six worst things that have ever happened to you.’ These memories will act as triggers which will fire my mind into action, enabling the researchers watching my brain to quite literally follow my thoughts.

For the sake of privacy, it was suggested I put this list into a code that only I understood. I took my time over this coding. Perhaps too much time, as now I realise that my codes are so cryptic I have forgotten what they mean. Just what, I wonder, does ‘beware of the chair’ signify? Why did I fear ‘the tree in Eltham’? Who was ‘Mc T’ and what was it that happened to him? Or her?

Too late: the gurney rises ominously then slides along until I am encased in a white plastic tube. Immediately I get a little claustrophobic. My head is pretty much immobile and all I can see is a screen with the flashing message ‘Close your eyes’. Why? What is going to happen?

Before I can consider this further, the functional magnetic resonance imaging machine, until now throbbing quietly, breaks into angry life. Huge magnets rotate around my head and every discordant noise in the world happens at the same time. Several hundred furious men with hammers set about the side of HMS Belfast. Fifty-seven of those tiny mopeds that kids ride around estates start up. An anvil is dropped in a skip. Eventually the noise stops and a disembodied voice says: ‘Open your eyes.’ The memories flash in front of me. Then the noise begins again. Then more questions. Then the noise begins again. I am caught in a loop. I feel strange sensations. I start to slip away.

An hour later the gurney slides out. I slump on to the floor. Shaky and dry-mouthed, I beg for a glass of water. It’s too early to present the findings of Professor Nutt’s research, but I can tell you this – there’s some pretty mean vitamin C out there.’

Also not recommended: Top five drugs to avoid

2CB
Also known as 2CT-7, this drug made its UK debut at this summer’s festivals, arriving from the Continent. The effects of this hallucinogenic stimulant fall between ecstasy and LSD.
KETAMINE
Better known as an animal tranquilliser, ketamine can make you feel floaty but paralyse you at the same time. Reports link usage with bladder problems, in some cases resulting in removal.
MEPHEDRONE
Also called meow meow, this belongs to the cathinone family of stimulants. Like ecstasy, it brings on euphoria and love for one and all, but overuse can lead to heart attacks and fits.
APB
A legal stimulant found in overthe-internet product Benzo Fury. Tests on Benzo Fury reveal a worrying inconsistency of active ingredients. If it works, it’s like speed (amphetamine).
PMA
PMA acts like MDMA, but is far stronger. It is sometimes sold as ecstasy. A batch of pink tablets with ‘M’ on them was mistaken for E by users earlier this year, and several were hospitalised.

Thursday, September 27, 2012

Studies Show How Physical, Emotional Neglect Harms Children’s Brains

It’s not surprising but it is alarming: physical and emotional neglect has a harmful effect on children’s developing brains, new research shows.

Children’s Hospital Boston’s blog Vector pulls together several studies that detail the various levels of damage that can be done to children’s brains when they are subject to trauma, neglect and social isolation:
Sheridan, Nelson and colleagues obtained brain MRIs from three groups of 8- to 11-year old children: 29 had been reared in an institution, 25 had left the institution for a high-quality foster home (where they spent 6 to 9 years), and 20 typically developing children who were never institutionalized served as controls.

The findings were mixed:
–Children who had spent their entire lives in an institution had significantly lower volumes of white matter—necessary for making connections in the brain—in the cortex of the brain than did the controls. But if they were transferred into foster care, their white matter volume became indistinguishable from that in controls.

–Children spending any amount of time in an institution—even if later placed in foster care—had significantly smaller gray matter volumes in the cortex.
“White matter, which forms the ‘information superhighway’ of the brain, shows some evidence of ‘catch up,’” says Sheridan.
An earlier study in mice made the connection between neglect and social isolation and cognitive impairment on a cellular level. Again, from the Vector blog:
Earlier this month, the journal Science reported findings from the Boston Children’s Hospital lab of Gabriel Corfas, PhD, showing how neglect and social isolation lead to cognitive impairment at the cellular level.
The team, led by Corfas and postdoctoral fellow Manabu Makinodan, MD, PhD, simulated neglect in mice by placing them in isolation early in life.
The results were striking. Cells that make up the brain’s white matter, known as oligodendrocytes, failed to mature, and failed to produce proper amounts of myelin, the fatty “insulation” on nerve fibers that boosts the speed and efficiency of communication between different areas of the brain. This was especially true in the prefrontal cortex. The mice, for their part, showed reduced sociability and deficits in working memory.
Confirming the earlier research, Corfas’s team showed that the effects of social isolation are timing-dependent. If mice were isolated during a specific period in their development, they failed to recover sociability and memory function even when they were put back in a social environment. Conversely, if they were isolated after this so-called critical period, they remained normal.

Many female brains contain male DNA

brain neuron

In the first study of its kind, researchers have discovered that male DNA is commonly found in the brains of women – a finding that could hold important implications for diseases like Alzheimer’s disease and cancer.
Male DNA is likely transferred to female brains during pregnancy, according to researchers from the Fred Hutchinson Cancer Research Center in Seattle.  During this time, mothers and fetuses exchange and harbor genetic material and cells in a phenomenon called microchimerism.

This means, if a mother is pregnant with a boy, she will end up with male DNA in her system – potentially for the rest of her life. If the fetus is female, the mother will end up with genetic material from her daughter, though it is difficult for researchers to distinguish between two sets of female DNA in microchimerism studies.
What this means for treating diseases
Prior studies have observed fetal DNA in many other of the mother’s tissues and organs, but this is the first to confirm fetal cells can cross the blood-brain barrier and reside in the mother’s brain beyond pregnancy.
“We were interested in looking at the human brain because it’s never been looked at before, and it was really unknown if the cells of fetal origin could reach the brain,” study senior author Dr. Lee Nelson, a member of the Fred Hutchinson Cancer Research Center and professor of medicine at the University of Washington, told FoxNews.com.  Nelson and her colleagues performed autopsies on 59 brains of deceased females and detected male microchimerism in 63 percent of them.

Male microchimerism was distributed across multiple regions of the female brain, including those affected by dementia, and could persist for decades – potentially even an entire human lifespan.  According to the study, the oldest female with microchimerism detected in her brain was 94.

“The question naturally arises what role might the cells have in benefiting health and what role they play in diseases,” Nelson added.

The researchers hope further studies on microchimerism might shed new light on various diseases that affect the brain, such as Alzheimer’s, Parkinson’s or even brain tumors.

“These cells have access to the brain could help us understand different treatment options for diseases that aren’t well treated,” Nelson said.  “It’s a very exciting new area that opens up different possibilities, such as, what if these cells have anti-tumor potential?  For example, glioblastomas are deadly tumors, (which) have poor treatment options.  We’re very much in need of new potential options.”

The researchers also examined rates of Alzheimer’s disease in women with and without male microchimerism in their brains.  In previous studies, it has been suggested that Alzheimer’s may be more prevalent in women who have had children.  However, data from this study found the women who had been diagnosed with Alzheimer’s had lower rates, or concentrations, of microchimerism in their brains than those without dementia.

Studies of other tissues and organs have suggested both protective benefits and risks associated with male microchimerism in mothers.  In a study of breast cancer, male microchimerism appeared to play a protective role: Women with male DNA had a lower rate of the disease than those without.

But –  a colon cancer study showed the opposite: Mothers with microchimerism had higher rates of the disease.

Researchers have a theory behind the protective benefits of microchimerism: They believe the ‘outsider’ DNA may boost the capacity of the mother’s immune system to seek out and destroy antigens.

“The theory is because the cells persisting after pregnancy are half-genetically different, they have another small window to recognize antigens, or cells that are either malignant or pre-malignant,” Nelson said.  “They can look at the cells with a slightly different perspective.”

The researchers said the next steps are to further define the role of microchimerism in health and disease, and see if the fetal cells are able to differentiate into other cells and perform other functions in the mother’s body.

Military’s new binoculars read brain waves to find danger

brainwave binoculars.jpg A brainwave-reading cap and a prototype binocular system combine to monitor threats far more effectively than a human acting alone.

By reading a soldier’s brain waves, new binoculars can detect a threat his brain has registered before he’s even conscious of it.

The Defense Advanced Research Projects Agency (DARPA) set out five years ago to provide the military with a far better device to visually detect threats. After all, the human eye’s limited field of view, breadth of area and the effects of fatigue can make relying on vision alone difficult.

They came up with the Cognitive Technology Threat Warning System program (CT2WS), binoculars paired that harness thoughts in the soldier’s brain.

It sounds like the stuff of science fiction, but CT2WS is based on real science: Humans are naturally skilled at detecting the out-of-the-ordinary -- and complex algorithms can interpret even subconscious human thoughts for computers to understand.

When the brain detects potentially threatening things like unexpected movements, it triggers a P-300 brain wave, a signal believed to connect with stimulus evaluation and categorization. The CT2WS system picks up those signals, translates them, and alerts the wearer of a threat through three key components.

The first is an electroencephalogram (EEG) cap that monitors the user’s brain signals. When the brain detects a threat, as seen through a tripod-mounted, 120-megapixel video camera with a 120-degree field of view, the cap records it. It's hardly the bird-watching binoculars you may be familiar with, but the system gets the job done.

The final part is complex visual processing algorithms that can run on a laptop, identifying potential targets and cuing images for the user to evaluate.

Testing revealed that while users were shown a rapid sequence of about ten images per second, their brains were still able to send signals flagging the relevant images, signals that could be read by the computer.

What about the classic rustle in the brush, however -- is it a bird or the enemy? The agency claims these cognitive algorithms have become so good that leaves rustling or wildlife movement that could be written off as typical nature will still be tagged as revealing potential threats.

Yet false alarm rates are greatly reduced through the EEG-based human filtering system.

Without a human and her brainwaves in the loop, the entire CT2WS system was tested and produced 810 false alarms per hour out of 2,304 events. But when a war fighter wears the EEG cap and contributes her brainpower to the system, false alarms were reduced to only 5 out of 2,304 events.

That’s a 91 percent improvement, thanks to those brain waves.

And target detection can reach 100 percent when commercial radar like Cerberus Scout is also deployed.
DARPA has been working with HRL Laboratories; Advanced Brain Monitoring; Quantum Applied Science & Research, Inc. and the University of California San Diego to create the system.

HRL Laboratories helped develop the sensor, cognitive and EEG decoding technologies. These sorts of advances are critical to harvesting an operator’s thought for the system.

Last year, the CT2WS was field-tested in a range of real environments including open desert at Arizona’s Yuma Proving Ground and tropical terrain in Hawaii, as well as open ground at California's Camp Roberts.
The results revealed the system can outperform trained humans, who detected about 60 percent of threats with binoculars. CT2WS wiped the floor with them, catching about 91 percent of risks.

Goals for this year included improving algorithms to increase frame rate and extending algorithms to handle imagery from Army and Marine Corps systems that generate visible, IR, and radar imagery from mast-mounted systems like Cerebus Scout.

Another critical aim for this year was to implement dry wearable EEG sensors that would not require conductive gels. DARPA awarded a contract to Quasar last September.

DARPA allocated $8.5 million last year and $1.75 million this year, providing a final demonstration to Army officials recently at Fort Belvoir, Va.

The CT2WS technology is currently being transitioned to the Night Vision and Electronic Sensors Directorate (NVEDS) in Fort Belvoir, where the first night vision goggles were created.

Since debuting those groundbreakers, NVEDS claimed to "own the night." Will they soon own the brain waves, too?

Sunday, September 23, 2012

Normal brains, waning with age

Some elderly become vulnerable to scams. The losses can be high.

Murray Grossman, left, studies degeneration of the brain's frontal and temporal lobes at Penn.
Murray Grossman, left, studies degeneration of the brain
The patient was in his 80s. He didn't have dementia, but this smart, sophisticated man had made a series of baffling, devastatingly bad financial decisions of a sort that are all too common at his age.

He had been told he'd won a contest and would get a big prize if he sent some money in first. His daughter caught on after the man had lost "tens of thousands of dollars," said Murray Grossman, a University of Pennsylvania neurologist who studies degeneration of the brain's frontal and temporal lobes.

Even after the patient's daughter changed his phone numbers and took control of his bank account, even after he knew the contest was a scam, he tried to give the con artists more money. "The guy would literally call the scammer and give him the new phone number," Grossman said.

As far as Grossman could tell, the man had "normal" aging, which is cold comfort. Just as our muscles and eyes typically decline with age, so too do our brains. They shrink and show other signs of wear. And that process often plays disproportionate hell with the frontal lobes.

Located behind your forehead and above your eyes, the frontal lobes are the seat of what doctors call executive function - abilities that help you assess new situations, perform complex, multistep tasks, and make decisions.

Jason Karlawish, a geriatrician and bioethicist at the Penn Memory Center, said there's growing interest in changes in judgment and decision-making that go along with aging but "right now don't map onto any disease."

Last year, the FINRA Investor Education Foundation and Stanford University's Center on Longevity jointly launched the Research Center on the Prevention of Financial Fraud. The National Endowment for Financial Education met with researchers this month to lay groundwork for a project on diminished financial capacity and cognitive decline.

University of Iowa researchers recently published a study showing that people with damage in the ventromedial prefrontal cortex - a part of the frontal lobe that often degrades in the elderly - were more vulnerable to misleading advertising. A Vanderbilt University study this year traced older people's problems with making decisions in novel situations to a decline in the white matter that connects the medial prefrontal cortex with the striatum deeper in the brain.

Another group from Harvard and New York Universities and the Federal Reserve Bank and Board studied real-world decisions involving mortgages and credit cards. The quality of decisions peaked at age 53.

"This kind of research," said David Laibson, a Harvard behavioral economist and one of the authors of that study, "is . . . going to be an explosively important topic."

The obvious reason is demographics. Baby boomers are getting old. The rise in obesity and diabetes also does not bode well. Both increase the odds of dementia caused by vascular problems, which not only lead to more frontal lobe dysfunction than Alzheimer's, but also make Alzheimer's worse.

Laibson said the demise of pensions is another reason the research is important. In the old days, a con artist could steal only so much at a time. Now, older people can easily have retirement accounts with half a million dollars in them. "Boy, is that a juicy target," he said.

Laibson is worried about fraud, but he's even more concerned about bad, but legal, investments.

As scientific studies of the aging brain reveal more about how structural damage affects thinking, they raise thorny, as-yet-unanswered questions. How do we protect the vulnerable elderly? How do we make sure that aging CEOs, investment managers, and politicians can handle their demanding jobs? One researcher recommends annual cognitive tests, a slippery slope if ever there was one.

There's ample evidence that people can make stupid decisions or be victims of fraud at any age.

"All of us can be taken," said Anthony Pratkanis, a University of California Santa Cruz psychology professor who studies persuasion.

Laura Carstensen, director of Stanford's Center on Longevity, said the trick will be finding ways to safeguard the vulnerable without restricting people who can still make their own financial decisions. "There are a lot of older people who I would turn to in a heartbeat for financial advice," she said, including her 92-year-old father. Suggesting she should take over for him would be "truly offensive and ridiculously stupid."

Researchers on all sides, though, agree that older people are disproportionately targeted, in part because they have more assets.

Those who study the aging brain, however, think some older people are at special risk. About half of adults in their 80s, Laibson said, suffer from either dementia or cognitive impairment without dementia.

"People who throughout their life have not been vulnerable to scams do become vulnerable in their later years," said Daniel Marson, a neuropsychologist and lawyer who runs the University of Alabama at Birmingham's Alzheimer's Disease Center. "We think that financial abilities are exquisitely vulnerable to early cognitive changes."

Psychologists have known for decades that executive function declines with age. Some aspects peak in the 20s. Luckily, the decline is balanced by wisdom. Overall knowledge rises throughout adulthood. As Scott Huettel, a neuroscientist at Duke University, put it, older people can't respond as fast to a changing streetlight, but they're less likely to put themselves in situations where they make mistakes.

The question of what's normal and what's an early symptom of dementia has taken on more urgency as doctors have come to realize that Alzheimer's and other dementias may start decades before symptoms become disabling.

The aging brain remains a vast frontier, vulnerable to time, vascular problems that can rob it of vital energy, and errant proteins associated with Alzheimer's disease and, Grossman's specialty, frontotemporal dementia. These conditions can occur alone or together in a complex mishmash. Some of the "normal" changes doctors see may, in fact, be early signs of dementia. A recent Penn study found that the first symptoms of Alzheimer's in patients with a particular genetic profile were problems with attention, language, and executive function.

If you look at average performance on tests of what Laibson calls fluid intelligence - the ability to solve new problems - by age group, the changes are striking. The average for all age groups would be at the 50th percentile, meaning that half are above and half below. The average 20-year-old is at the 75th percentile on that scale, Laibson said. The average 80-year-old is at the 25th.

"That's just a huge change," he said.

The "normal" changes, however, are highly variable. Some 80-year-olds still have better executive function than some 20-year-olds. People with more "cognitive reserve" - typically the better-educated - can decline a fair amount before they get into trouble. Doctors suspect that everyone declines.

William Milberg, a neuropsychologist at Harvard, thinks people with high blood pressure and diabetes likely accelerate the process of deterioration by damaging blood vessels that supply the brain.

What signs indicate executive function problems?

Karlawish said doctors talk about an easy test: "Ask your older patients when was the last time they were able to organize a dinner party."

Frontal lobe damage does indeed impair organization. It also affects working memory, or the ability to hold multiple ideas in your head while you work with them. Inhibiting an extraneous thought while trying to focus on another becomes harder, as in attention deficit disorder. People with damaged frontal lobes are more likely to do risky things.

Here are some tests that people find more difficult as they age: hearing a list of numbers and then reciting them backward, saying the color of letters used to spell the name of a different color (think the letters RED written in yellow ink) or ordering the 13 digits in your phone number from smallest to largest in your head.

Frontal lobe decline can also make people more impulsive and prone to false memories. The elderly are less likely to remember where they learned something, a problem if the source was shady.

Marson cites these danger signs of diminished financial capacity: new memory lapses about bills, new disorganization of financial paperwork, trouble doing math such as figuring tips and less understanding of things like fluctuating interest rates or reverse mortgages. This is the most important one: a new interest in get-rich schemes.

The National Institute of Aging has made understanding normal aging one of its initiatives. Molly Wagster, chief of the behavioral systems neuroscience branch, is interested in how older brains compensate for some of the negative changes. The NIA has funded small pilot studies that look at whether cognitive aging can be affected by exercise, brain training, and diet.

"I don't think that this is an irreversible course that everyone is on," she said.

Connecting Autistic Behavior to Brain Function

Autism is a disorder that is well known for its complex changes in behavior -- including repeating actions over and over and having difficulty with social interactions and language. Connecting these behavioral patterns to an underlying neural deficiency is imperative for understanding what gives rise to autism, to developing better measures for diagnosing those along the Autism Spectrum Disorder and designing more effective treatments.

However, even given our significant advances in understanding how the brain works, there hasn't been evidence to tie autistic behavioral patterns together with corresponding neural functions. Until now.

A team of researchers -- including myself and colleagues from Carnegie Mellon University, the University of Pittsburgh, New York University and the Weizmann Institute of Science -- were interested in trying to understand on a basic neural level what happens inside the brain that might give rise to the altered behaviors in autism. Instead of focusing on the more complex behaviors, we set out to uncover and measure fundamental neural responses -- the patterns of brain activation in individuals with autism compared to those without.

Using an fMRI at Carnegie Mellon's Scientific Imaging and Brain Research Center, we scanned the brains of 14 adults with autism and 14 without while these individuals responded separately to visual, auditory and touch stimuli. We looked at the way the most elemental part of the brain's cortex responded to these simple stimuli.

In typical individuals, every time they saw the same visual stimulus, they had an almost identical response in the primary visual system. The stimulus drove normal visual systems in the same way time and time again. So, the question was whether we would see the same kind of consistent responses in the visual, auditory and somatosensory, or touch, cortices and within autism. It was our belief that any alteration in brain response we saw would be a very powerful indication of a major characteristic of autism.

It turns out that in all three of the primary cortices -- visual, auditory and somatosensory -- we did not see the typical response trial after trial in the individuals with autism. Instead, we saw considerable variability -- sometimes a strong response, sometimes a weak response. The fact that we did not see precise responses in autism was a really important result. It suggests that there is something fundamental that is altered in the cortical responses in autism. This variability in the brain response might also possibly explain why individuals with autism find visual stimulation, touch and sound to be so strong and overwhelming.

We know from genetic research that many of the neurobiological changes that occur in autism have to do with changes at the level of the synapse, the way that information is transmitted from one neuron to another. What these results -- that autistic adults have unreliable neural responses -- does is begin to allow us to build a bridge between the kind of genetic changes that may have given rise to autism in the first place. It cracks open a new avenue of research which has a good potential to be highly informative in understanding the connection between the neurophysiology and the behavioral patterns in autism.

While this particular study involved high functioning autistic adults and fMRI, we are now running follow-up experiments using EEG. This method which will give us even more detailed information about the neural responses and will allow us to test individuals across the autism spectrum and across different age groups so that we can gain further understanding of this unreliable neural response profile. And, because unreliable neural activity is a general property that could have a profound impact on how many brain systems function, it could underlie not only autism but a range of cognitive and social abnormalities including epilepsy and schizophrenia.

We are at the tip of a huge iceberg here; further research to fill in the details of exactly how this unreliability happens is essential for accurately diagnosing and treating autism and other disorders. At places like Carnegie Mellon University, which established a Brain, Mind and Learning initiative to build from its excellence in psychology, computer science and computation to continue to solve real world problems, these types of research projects are a priority. Our ongoing collaborations with Center for Autism Research at the University of Pittsburgh, and with ABIDE, which shares autism imaging data from top research facilities around the world, are crucial for working together to make sure we have all of the scientific resources possible to conduct high quality research.

What is Creativity? Art as a Symptom of Brain Disease

Van Gogh
We don’t normally associate creativity with brain disease, but a recent paper published in Brain suggests that maybe we should. When we think of someone affected by a serious brain disorder, we imagine deterioration and loss of function, but a surprising new study shows that some people may actually develop artistic talent as a result of their brain disorder, and that in turn, their art can tell us about the nature of their brain disorder.

This recent review by Schott brings together cases of individuals with neurological conditions, who with no previous artistic motivations suddenly become compelled to make art, and the art is good!

The authors describe a case of an epileptic man with no artistic ability who began to suffer recurring epileptic attacks in which he acted aggressively, could not speak or focus his eyes, and acted out of character. During these attacks, the patient began to draw spontaneously and compulsively, and with remarkable skill. In another case, a 68 year-old man had begun to paint at age 56 with the onset of dementia, despite never being interested in art before. In the ten years that passed after the onset of his dementia, his paintings became more and more detailed, colorful, precise and realistic, and he even began to win awards for his art.

Both these cases highlight the importance of context in understanding how art can tell us about brain disorders. The onset of uncharacteristic artistic behavior or the compulsive desire to create art where there has been no desire before might indicate an emerging neurological abnormality. Similarly, in people who already have creative ability, dramatic changes in style (e.g. from abstract to realistic) can indicate the onset or progression of brain dysfunction.

But how can these unusual events tell doctors about the patient’s underlying condition? In these and most other cases of emerging artistry, involvement of the left anterior temporal lobe appears to be crucial. The temporal lobe and frontal brain regions work together and are involved in creativity. Damage or degeneration of temporal regions can release the temporal lobe’s inhibitory influence on the frontal cortex, resulting in enhanced creativity. For example, a magnetic resonance imaging (MRI) scan of the elderly man with dementia revealed severe damage to the temporal lobe, while his frontal brain regions remained intact.

Similarly, an imbalance between left and right hemisphere activity appears to affect creativity. For example, in the case of the epileptic patient, based on his unusual behavior, neurologists deduced that the seizures were originating in the left frontal hemisphere. Depression of the dominant, logical left-brain regions during his seizure had caused the “release” of the more creative right brain, resulting in his unusual artistic ability.

These interesting case studies offer a new perspective on the way we study brain disorders, and challenge our understanding of creativity. The neural networks involved in creativity are delicately balanced. Disruption of this network can lead to the surprising and counter-intuitive emergence of new artistic talent; talent that is regarded by many to be a skill that is learned over years of practice. What makes some people artistically talented and others not? Practice or innate ability? The relevance of the age-old debate, ‘nature versus nurture?’ is brought to the fore by these cases, and points to the emergence of an exciting new, interdisciplinary field of neuroscience research.

Fast-food logos light up kids’ brains

 Fast-food logos light up kids’ brains London: The brains of children are ‘imprinted’ with logos of fast-food companies, according to a new study.

The study, conducted at the University of Missouri-Kansas City and the University of Kansas Medical Center, found that the pleasure and appetite centres of the brains light up when children are shown advertising images such as the McDonald’s logo.

But the same areas do not respond to well-known logos that are not to do with food, the Independent reported.

Scientists suggest fast-food firms are tapping into the reward areas of the brain, and that these develop before the regions that provide self-control, leading to unhealthy choices.

“Research has shown children are more likely to choose those foods with familiar logos. That is concerning because the majority of foods marketed to children are unhealthy, calorifically-dense foods high in sugars, fat, and sodium,” said Dr Amanda Bruce, who led the study.

The study selected 120 popular food and non-food brands, including McDonald’s and Rice Krispies, and BMW and FedEx.

They used a type of MRI scanner – functional magnetic resonance imaging – which homes in on changes in blood flow: when areas of the brain become more active, blood flow increases.

Scans were carried out on children aged 10 to 14 as they were exposed to 60 food and 60 non-food logos. The results showed the food logos triggered increased activity in areas of the brain known to be involved in reward processing and in driving and controlling appetite.

The finding comes in the wake of research which showed advertising had a pronounced effect on children’s eating habits. Children who tasted two identical burgers, one in a plain box and one labelled McDonald’s, preferred the latter.

It`s the brain that draws you to chocolate

It`s the brain that draws you to chocolate Washington: What makes chocolate so irresistible? Scientists have traced the lure of chocolate to a part of the brain called neostriatum, and its production of a natural, opium-like chemical, enkephalin.

The findings reveal a surprising extension of the neostriatum`s role, as Alexandra DiFeliceantonio, from the University of Michigan, Ann Arbor and her team made the discovery.

DiFeliceantonio notes that the brain region had primarily been linked to movement. And there is reason to expect that the findings in rats can tell us a lot about our own binge-eating tendencies, the jounral "Current Biology" reports.

The researchers also found that enkephalin surged when rats began to eat the candy-coated morsels, according to a Michigan statement.

It`s not that enkephalins or similar drugs make the rats like the chocolates more, the researchers say, but rather that the brain chemicals increase their desire and impulse to eat them.

"This means that the brain has more extensive systems to make individuals want to over consume rewards than previously thought," said DiFeliceantonio. "It may be one reason why over consumption is a problem today."

"The same brain area we tested here is active when obese people see foods and when drug addicts see drug scenes," she says.

"It seems likely that our enkephalin findings in rats mean that this neurotransmitter may drive some forms of over consumption and addiction in people," she said.

Saturday, September 22, 2012

Kangaroo Care’ Positively Impacts Preemies’ Brain Development

'Kangaroo Care' Positively Impacts Preemies' Brain Development  Kangaroo Mother Care — in which a premature infant remains in skin-to-skin contact with the parent’s chest rather than being placed in an incubator — may have lasting positive benefits on brain development, according to a new study.

Researchers at Université Laval found that premature infants who benefited from this technique had better brain functioning in adolescence than premature infants placed in incubators.

Earlier research showed that infants born before the 33rd week of pregnancy experienced more cognitive and behavioral problems during childhood and adolescence.

In the new study, researchers compared brain functions of 18 premature infants kept in incubators, 21 held in Kangaroo contact for an average of 29 days, and nine full-term infants.

To assess the brain functions of the children — now aged 15 — the researchers used transcranial magnetic stimulation. With this non-invasive and painless technique they could activate brain cells in targeted areas, namely the primary motor cortex that controls muscles. 

By measuring muscle responses to the stimulation, they were able to assess brain functions such as the level of brain excitability and inhibition, cell synchronization, neural conduction speed, and coordination between the two cerebral hemispheres.

The researchers found that all brain functions of the adolescent Kangaroo group were comparable to those of the full-term infant group. 

On the other hand, premature infants placed in incubators significantly deviated from the other two groups 15 years after their birth, the researchers said.

“Thanks to Kangaroo Mother Care, infants benefited from nervous system stimulation — the sound of the parent’s heart and the warmth of their body — during a critical period for the development of neural connections between the cerebral hemispheres,” said neurophysiologist Dr. Cyril Schneider.
“This promoted immediate and future brain development.”

Psychology researcher Dr. Réjean Tessier added that “infants in incubators also receive a lot of stimulation, but often the stimulation is too intense and stressful for the brain capacity of the very premature.”

“The Kangaroo Mother Care reproduces the natural conditions of the intrauterine environment in which the infants would have developed had they not been born premature. These beneficial effects on the brain are in evidence at least until adolescence and perhaps beyond.”

How fear can be erased from the brain



Researchers at Uppsala University in Sweden have determined that emotional memories can be effectively erased from the human brain.



"When a person learns something, a lasting long-term memory is created with the aid of a process of consolidation, which is based on the formation of proteins. When we remember something, the memory becomes unstable for a while and is then re-stabilized by another consolidation process," explained Thomas Ã…gren, a doctoral candidate at the Department of Psychology.





"In other words, it can be said that we are not remembering what originally happened, but rather what we remembered the last time we thought about what happened. By disrupting the re-consolidation process that follows upon remembering, we can affect the content of memory."

Ã…gren's team reached the above-mentioned conclusion by conducting an experiment in which subjects were shown a neutral picture while simultaneously administering an electric shock.



"In this way the picture came to elicit fear in the subjects which meant a fear memory had been formed. In order to activate this fear memory, the picture was then shown without any accompanying shock," he said.



For one experimental group the re-consolidation process was disrupted with the aid of repeated presentations of the picture. For a control group, the re-consolidation process was allowed to complete before the subjects were shown the same repeated presentations of the picture.

Because the experimental group was not allowed to reconsolidate the fear memory, the panic they previously associated with the picture dissipated.

Essentially, by disrupting the re-consolidation process, the memory was rendered neutral and no longer incited fear. 

Additional research, bolstered with the use of an MR-scanner, showed that traces of a specific "fear" memory also disappeared from the part of the brain that normally stores fearful memories, the nuclear group of amygdala in the temporal lobe.

"These findings may be a breakthrough in research on memory and fear. Ultimately the new findings may lead to improved treatment methods for the millions of people in the world who suffer from anxiety issues like phobias, post-traumatic stress, and panic attacks," added Ã…gren.

U-M Researchers Identify Brain Mechanism That Causes People To Overeat

istockphoto

A part of the brain usually thought to control movement also may cause people to overeat, say University of Michigan researchers.

A new study appearing in the current issue of the journal Current Biology indicates that a new brain mechanism in the neostriatum produces intense motivation to overeat tasty foods.

The neostriatum, located near the middle and front of the brain, has traditionally been thought to control only motor movements (this is the part of the brain that is damaged in patients with Parkinson’s disease and Huntington’s disease).

Yet for several years, it has been known that the neostriatum is active in brains of obese people when viewing or tasting foods, and in brains of drug addicts when viewing photos of drug-taking.

The research showed that an opium-like chemical — enkaphalin — produced naturally in the brain is a mechanism that generates intense motivation to consume pleasant rewards, said Alexandra DiFeliceantonio, a doctoral student in psychology and the study’s lead author.

When researchers gave extra morphine-like drug stimulation to the top of the neostriatum in rats, it caused the animals to eat twice the normal amount of sweet fatty food. For this study, that food was M&M milk chocolate candies.

“The same brain area we tested here is active when obese people see foods and when drug addicts see drug scenes,” DiFeliceantonio said. “So it seems likely that our enkephalin findings in rats mean that this neurotransmitter may drive some forms of overconsumption and addiction in people.”

Researchers measured levels of enkephalin using a painless microdialysis probe while rats were allowed to eat as much chocolate as they wanted. They found that enkephalin levels surged dramatically as soon as the rats started to eat, and remained high as long as they ate.

In addition, when researchers gave a painless microinjection of an opioid-stimulating drug in the rats’ neostriatum, the rats ate double the amount of chocolate.

DiFeliceantonio and colleagues mapped where extra drug stimulation of opioid receptors affected eating habits. They found that overeating was only caused in one region at the front and center part of the neostriatum (called the anterior-medial region of dorsal neostriatum).

“Finding the brain mechanisms for overconsumption is a step towards designing better biological-based treatments for obesity and binge eating disorders,” DiFeliceantonio said.

The study’s other researchers were Omar Mabrouk, a postdoctoral research fellow in pharmacology and chemistry; Robert Kennedy, the Hobart H. Willard Collegiate Professor of Chemistry and professor of pharmacology; and Kent Berridge, the James Olds Collegiate Professor of Psychology and Neuroscience.

Dark matter DNA active in brain during day/night cycle

Long stretches of DNA once considered inert dark matter appear to be uniquely active in a part of the brain known to control the body’s 24-hour cycle, according to researchers at the National Institutes of Health. 

Working with material from rat brains, the researchers found some expanses of DNA contained the information that generate biologically active molecules. The levels of these molecules rose and fell, in synchrony with 24-hour cycles of light and darkness. Activity of some of the molecules peaked at night and diminished during the day, while the remainder peaked during the day and diminished during the night. 

The material came from the brain structure known as the pineal gland. Located in the center of the human brain, the pineal gland helps regulate the body’s responses to day and night cycles, the researchers explained. In the evenings and at night, the pineal gland increases production of melatonin, a hormone that synchronizes the body’s rhythms with the cycle of light and dark. In many species, the pineal gland also plays a role in seasonally associated behaviors, such as hibernation and mating, as well as in sexual maturation.

The biologically active material arising from the pineal gland DNA is called long noncoding RNA (lncRNA). The lncRNA is distinct from the better-known messenger RNA (mRNA), which serves as a kind of template to translate the information contained in DNA for the manufacturing of proteins. The lncRNAs appear instead to be involved in activating, blocking or altering the activity of genes or influencing the function of the proteins, or acting as scaffolds for the organization of complexes of proteins. The researchers’ use of next-generation sequencing methods detected the lncRNA activity in addition to the mRNA they originally targeted, which helped them in making their discovery. 
 
"These lncRNAs come from areas of the genome that we thought were quiet," said senior author David Klein, Ph.D., head of the Section on Neuroendocrinology at the NIH's Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), in much of the research was conducted. "But current research in the field makes it unequivocally clear that the information-carrying capacity of the genome is a lot greater than we realized previously."

The study was a collaboration between Dr. Klein and NIH colleagues at the NICHD; the National Human Genome Research Institute (NHGRI); the NIH Intramural Sequencing Center, administered by NHGRI and the Center for Information Technology. In addition, researchers from King’s College London; the University of Copenhagen, in Denmark; the Genomatix Software company, in Munich contributed to the study.

Their findings appear online in the Proceedings of the National Academy of Sciences.
To conduct their analysis, the researchers examined RNA from the pineal glands of rats exposed to cycles of 14 hours of light and 10 hours of darkness. The researchers identified 112 lncRNAs with 24 hour cycles. For nearly 60 percent of these lncRNAs, the rats' DNA produced twice as many lncRNA molecules at night as during the day. In addition, nearly 90 percent of the lncRNAs were produced in significantly greater quantities in the pineal gland than in other tissues of the body, most of which did not have detectable levels of these lncRNAs. 

The researchers also disrupted the rats' regular day–night light cycle by turning on a light during a typical dark period. Within 30 minutes of the light going on, most of the lncRNAs decreased by half.
The role of the pineal gland lncRNAs is unclear; however, they have circadian patterns of activity. Dr. Klein previously documented hundreds of genes in the pineal gland with consistent day–night cycles of activity.

"The lncRNAs show such strong activity, they obviously have something to tell us about the biology of daily body rhythms," Dr. Klein said. "We are only beginning to understand how the pineal gland helps maintain the body's 24 hour rhythms."

DARPA's Cybernetic Binoculars Tap Soldiers' Brains To Spot Threats

The U.S. Army and DARPA have concluded field tests on next-generation binocular replacements that read human brain signals and have a 91% threat detection success rate. They might just help you control your car with your thoughts too (seriously).

Binoculars on the battlefield are fine, as long as soldiers know what they're looking at. But when a target's not so clear or, say, a shopkeeper with a broom could easily be mistaken for an insurgent with an RPG, the eyes--even the conscious, rational mind--might not be the best tool for threat-spotting and quick reaction.
So a new system from military think tank DARPA is instead going straight to soldiers' brainwaves to spot real threats--from far away, or amid a crowded landscape.

The concept might sound familiar to science fiction readers: Augmenting human soldiers with brainwave-reading computers. The Cognitive Technology Threat Warning System (CT2WS) is a threat detection system for troops in the field that simultaneously scans warfighters' brainwaves while a camera surveys the area. The binocular replacement system detects a specific kind of brainwave (the P300, which is involved in stimulus evaluation and categorization), combines that info with a camera feed, and processes it all through an algorithm in near-real time to feed back an almost-instant threat assessment. (Think: every cyborg POV shot in every Terminator movie ever made.) Sounds pretty out there, but testing indicates 91% of enemy targets were identified in the field, compared with the 47% spotted by U.S. warfighters in action today who aren't using the new system.

The CT2WS project started in 2008, with the goal of developing next-generation portable visual threat detection devices for use in warzones. The University of California San Diego's bioengineering department and several California biotech and hardware firms partnered with DARPA to develop the brain-scanning enemy detection device.

As currently developed, CT2WS consists of three parts. There is an electroencephalogram (EEG) headset (below) worn by the user which records electrical activity in the brain and sends a ping to an outside computer system when the subconscious evaluates a visual threat.


Additionally, there is a separate 120 megapixel electro-optical video camera with a 120-degree field of view (below).



Lastly, both the camera and EEG unit are connected to a computer system that uses proprietary algorithms to identify potential targets and cue images for review. The software behind CT2WS can be run on a laptop as well, according to DARPA.


HRL Laboratories is a Malibu-based R&D house jointly owned by Boeing and General Motors which worked on CT2WS. One of HRL's specialties is developing cognitive-neural algorithms that allow computers to interpret human thoughts. According to HRL, the end result is far superior to conventional enemy-spotting technologies like binoculars. “CT2WS automatically scans a field of view more than ten times as wide as that is available using standard army binoculars. This is coupled with digital techniques that provide far higher resolution and greater effective visual distance than today's binoculars,” HRL's Deepak Khosla tells Fast Company.

In testing for desert, tropical, and open terrain, CT2WS was able to identify 91% of targets successfully. DARPA is also considering combining the system with a commercial radar--during field tests, the combination of CT2WS and a commercial system, the Cerberus Scout surveillance system, was able to identify 100% of the targets encountered.

The EEG sensor component of CT2WS was developed by San Diego's Quasar. Quasar used special wireless EEG sensors for the project that don't require the use of conductive gels and which don't cause skin abrasion. The lightweight EEG sensors and accompanying headset are small enough to wear under a bike helmet, according to Quasar's Walid Soussou. The CT2WS headset is also designed for easy cleaning, and meets the blunt and ballistic impact safety requirements for a military helmet.

DARPA, for their part, is playing up the fact that human and machine can complement each other on the battlefield. Project literature claims that “humans are inherently adept at detecting the unusual,” while algorithms are successful at detecting commonplace phenomena that are potential indicators of threats or targets--such as birds in flight or tree branches swaying. When the camera and sensor were tested, sensor and cognitive algorithms returned 810 false alarms per hour. However, once a testee began wearing an EEG cap and feeding in results, false alarms dropped to only five per hour.

Development of CT2WS is currently being transitioned from DARPA to the U.S. Army Night Vision and Electronic Sensors Directorate. According to HRL, the military is interested in CT2WS for situational awareness in reconnaissance, force protection surveillance, and standard infantry tactical fighting. The transfer of CT2WS technology to the U.S. Army indicates that the brain-wave-reading binoculars have progressed past testing and into the sweet spot of Pentagon bureaucracy.

Of course, CT2WS also has civilian applications: According to Khosla, HRL (which, again, is partly owned by General Motors) believes that the EEG decoding and cognitive algorithms used by CT2WS can also be used for controlling buttons inside cars or breaking in sudden emergencies--all using, well, human thought.

I Kissed A Girl With My Brain… The Results Weren’t So Good


Find out if you really like each other by testing your brain waves. That's what the Brain Kiss app tests to see.

By wearing a brain wave scanner and looking into each other's eyes for 15 seconds, you can get the results of how you really feel about the person you're looking at in 5 levels of attraction: Like very much, Like, So-so, Not very, and No interest.

I got a chance to try it out at the Architect Co., Ltd. booth at Tokyo Game Show 2012. The companion at the desk fitted the brain wave scanner onto my head and started the app. We then looked into each other's eyes for 15 seconds which was pretty embarrassing (she was pretty cute), and got out results.

According the app screens, her feelings for me were "Like very much," but my feelings for her were "No interest..." (Above image) I would swear it wasn't true, but it's kind of hard to argue with science.

It might be fun to try Brain Kiss with my friends, but while the app is free, the brain wave scanner costs ¥9,500 (US$121.5), which is a little steep for what is kind of a novelty game... There is also a brain training app that utilizes the brain wave scanner, Zone Trainer, that is scheduled for release in fall, 2012.

I should go back and ask that companion out for some coffee after the game show...

Vitamin D during pregnancy may boost baby’s brain health, says study

LOS ANGELES, Sept 22 — A new study published this week finds that when moms get enough vitamin D during pregnancy, their babies score higher on developmental tests.
Vitamin D during pregnancy may boost a baby’s brain health, according to a new Spanish study. 
Researchers from the Centre for Research in Environmental Epidemiology in Barcelona studied 1,820 mothers and their babies and found that babies of moms who had optimal levels of vitamin D during pregnancy scored slightly higher than babies of moms who were vitamin D deficient. The study was published September 17 in the journal Pediatrics.

While experts say that this shouldn’t cause alarm for healthy women, this study could “open the door” for “advocating a stronger stance on vitamin D recommendations for pregnancy and pre-pregnancy,” Valencia Walker, MD, a neonatologist at Mattel Children’s Hospital UCLA, told WebMD. She was not involved in the study.

While clinical recommendations for vitamin D are unclear, researcher Eva Morales, MD, PhD, MPH, notes that trials are underway to make determinations.

Meanwhile, Walker told WebMD that women may face a higher risk of vitamin D deficiency if they are overweight or obese, have darker skin, or live in northern locations, especially during wintertime. Prenatal vitamins often provide 400 IU of vitamin D, but WebMD adds that there is not enough research yet to conclude that supplementing with more vitamin D would be beneficial.

According to BabyCenter.com, the National Academy of Sciences currently recommends 200 IUs of vitamin D every day if you’re not exposed to a lot of sunlight, but many experts believe this isn’t enough. Access BabyCenter for tips on food sources packed with vitamin D, such as fatty fish and fortified milk

Brain Fluid Changes Predict Alzheimer’s 10 Years in Advance

Brain Fluid Changes Predict Alzheimer's 10 Years in AdvanceNew signs of future Alzheimer’s disease have been identified by researchers at Lund University and Skane University in Sweden. Dr. Peder Buchhave and his team explain that disease-modifying treatments are more beneficial if started early, so it is essential identify Alzheimer’s disease patients as quickly as possible.

Alzheimer’s disease accounts for most cases of dementia worldwide. Its development may start up to 20 years before symptoms appear. The so-called amyloid plaques which form in the brains of people with Alzheimer’s disease contain substances known as beta-amyloid and tangles made of tau proteins.

The team followed 137 patients with mild cognitive impairment for about nine years. At the start of the study, all patients underwent lumbar puncture, in order to collect a sample of cerebrospinal fluid. During the nine years of the study, 54 percent developed Alzheimer’s disease. Sixteen percent developed other forms of dementia.

Patients’ levels of beta-amyloid 1-42, T-tau and P-tau were measured at the study’s start. Those who went on to develop Alzheimer’s disease had reduced levels of beta-amyloid 1-42 five to 10 years in advance of the disease. Raised levels of the other spinal fluids seemed to be associated with the disease, but the link occurred later on.

Findings appear in the January 2012 issue of Archives of General Psychiatry. The authors predict that:
Approximately 90 percent of patients with mild cognitive impairment and pathologic [disease-indicating] cerebrospinal fluid biomarkers will develop Alzheimer’s disease within 9.2 years. Therefore, these markers can identify individuals at high risk for future Alzheimer’s disease least five to ten years before conversion to dementia.
In conclusion, the cerebrospinal fluid levels of tau and beta-amyloid seem to be substantially altered very early in the disease process of Alzheimer’s disease.
Hopefully, new therapies that can retard or even halt progression of the disease will soon be available. Together with an early and accurate diagnosis, such therapies could be initiated before neuronal degeneration is too widespread and patients are already demented.”
They say these results support the theory that beta-amyloid metabolism is altered before the brain begins to degenerate. This may help to shape future research studies. Furthermore, once Alzheimer’s disease symptoms begin, a patient’s beta-amyloid and tau levels in their cerebrospinal fluid stay relatively constant, so might serve as markers for the efficiency of treatment, the researchers add.

But other researchers believe that, by the time the clinical symptoms of Alzheimer’s disease appear, so much neurodegeneration has occurred that disease-modifying therapy may not be effective.

This is why it is so important the underlying pathology is better understood, possibly by measuring cerebrospinal fluid levels. Experts led by Dr. Niklas Mattsson of the University of Gothenburg, Sweden, looked at this question in a large study of 750 adults with mild cognitive impairment, 529 with Alzheimer’s disease, and 304 healthy adults.
They found that, over two years, levels of beta-amyloid, T-tau, and P-tau predicted patient outcomes, suggesting that these markers “may be useful in identifying patients for clinical trials and possibly screening tests in memory clinics.”

This group of investigators has been studying these issues for several years, and their study has been described as “a tour de force” of clinical and laboratory data collections. The markers are now confirmed as being useful indicators for Alzheimer’s disease.

But Ronald C. Petersen, professor of neurology at the Mayo Clinic in Rochester, Minn., who is involved with the Study of Aging, says “it is premature to recommend application of these techniques in clinical practice.” He believes that “significant refinement of the testing procedures is necessary before these techniques can be recommended for general clinical use.”

Efforts in this direction are under way in a study based at 57 centers in the U.S. and Canada which was designed to look at biomarkers for predicting Alzheimer’s disease. A major focus of the study is to decide on standard, reliable clinical, neuroimaging and laboratory procedures.

But Prof. Petersen says, “Of critical importance, however, is what the clinician and patient will do with such results. Alzheimer disease has no treatment to prevent or alter the course of the disease, so making the diagnosis with good accuracy may aid in planning but also could be devastating news for some patients and families.

“Furthermore, false positives and false negatives occur as with any screening test. However, as biomarkers become more sophisticated, they are likely to take on an increasingly important role in the diagnosis and management of Alzheimer disease.”

Brain power? It's the lust thing on our minds

Lust 'tends to focus our minds on the present and on detail'.
Lust 'tends to focus our minds on the present and on detail'. 

LUST is good for you, not just because it gets you laid, but because it boosts your brain, according to University of Melbourne experimental psychologist Simon Laham.

''Because lust is there to essentially lead us to pursue people into bed, which is a very current goal, it tends to focus our minds on the present and on detail,'' he says. ''People in a lustful state are more detailed [in their thinking], focused on the trees rather than the forest'', which leads to ''decomposition of a problem into smaller pieces'', he says.

Even a relatively tepid form of lust, induced by nude pictures or certain words, causes people in experiments to perform better on analytic reasoning problems that involve working through details step by step, he says.

His book, The Joy of Sin, musters evidence from psychology experiments by researchers worldwide to argue that the seven deadly sins (lust, gluttony, greed, sloth, wrath, envy and pride) are not necessarily bad.

''Under certain circumstances these things can bring about a range of benefits, including making one happier, smarter, more creative and increasing pro-social behaviour,'' he says.

People feeling proud of themselves will stick at a task longer and achieve greater success. People with time to spare are more sensitive to the needs of others and more likely to help.

Dr Laham said he did not feel the need to amplify the point that the seven deadly sins can be bad for you, too. Most people already have a sense of that, he believes.

Research also shows, for example, that high lust levels can trigger risk-taking sexual behaviour and sexual aggression.

This Brain Chemical Could Be Why We Binge Eat

brain chemical molecule enkephalin
This is enkephalin, which may be responsible for over eating. 

 The slogan for Pringles, "once you pop, you can’t stop," may be true, and not just because they are delicious. Scientists have found that something in our brains makes us indulge in food as well as drugs and alcohol. 

Scientists from the University of Michigan decided to study a part of the brain called the neostriatum that may be involved in providing reward signals when we engage in pleasurable tasks.

The main player in this brain area is enkephalin, a chemical that turns up brain activity. It was discovered in 1975, and is known as a painkiller and a possible neurotransmitter. Enkephalin is produced in the brain and binds to the same receptors as many anesthetic and psychoactive drugs.

To find out how enkephalin acts in the brain, the researchers offered rats an unlimited amount of M&M’s. The average rat ate 10 candies in 20 minutes, which is a lot of candy for their small size.

Researchers found that levels of enkephalin spiked in the neostriatum, and the rats that ate the most M&M’s had the quickest and highest spike of enkephalin.

The spike in enkephalin could have been a result or the cause of the binge eating. To figure this out, the experiment was repeated, but this time the researchers injected the rats' brains with enkephalin. With the extra brain stimulants, the rats ate twice as much candy — so the chemical seems to be the cause of the overeating, not the result of it.

It could be that the rats overeat because enkephalin makes food taste better. Although it may sound ridiculous, the researchers watched the rats’ facial expressions to see how happy the were during the binge. The more they lick their lips and stick out their tongues, the tastier the food.

But, the dosed rats didn't show this.

Lead author, Alexandra DiFeliceantonio of the University o Michigan, tells Smithsonian.com's Surprising Science blog “that the brain has more extensive systems to make individuals want to over-consume rewards than previously thought.”

She concluded: “It may be one reason why over-consumption is a problem today.”

Just remember: Once you pop, try to stop before you eat the entire can. 

Blowhard silencer, dead-fish brain science win spoof Nobel prizes


Psychologists who discovered that leaning to the left makes the Eiffel Tower seem smaller, neuroscientists who found brain activity in a dead salmon, and designers of a device that can silence blowhards are among the winners of Ig Nobel prizes for the oddest and silliest real discoveries.

The annual prizes are awarded by the Annals of Improbable Research as a whimsical counterpart to the Nobel prizes, which will be announced early next month.

Former winners of the real Nobels hand out the Ig Nobel Awards at a ceremony held at Harvard University in Massachusetts.

Ig Nobels for 2012 also went to US researchers who discovered that chimps can recognise other chimps by looking at snapshots of their backsides, and to a Swedish researcher for solving the puzzle of why people’s hair turned green while living in certain houses in the town of Anderslöv, Sweden. (The culprit was a combination of copper pipes and hot showers.)

Marc Abrahams, editor of the Annals and architect of the Ig Nobels who announced the winners on Thursday, said one of his personal favourites was this year’s Acoustics Prize. reuters

Other Winners :

Physicists at Unilever led by Dr Patrick Warren and at Stanford University led by Professor Joe Keller for their use of mathematics to explain why ponytails take on their distinctive “tail” shape. The Ig Nobel is Keller’s second.

Igor Petrov and colleagues at the SKN Company in Russia for using technology to convert old Russian ammunition into new diamonds.

Rouslan Krechetnikov and Hans Mayer of the University of California, Santa Barbara, for illuminating why carrying a cup of coffee often ends up in a spill.

French researcher Emmanuel Ben-Soussan on how doctors performing colonoscopies can minimise the chance of igniting gasses that make their patients explode.

The US Government General Accountability Office, for issuing a report recommending the preparation of a report to discuss the impact of reports about reports.

Wipe away fearful memories from brain

WASHINGTON: And you thought it just happens in sci-fi movies!

Scientists have found that newly formed emotional memories can be erased from the human brain, a breakthrough that could lead to new treatments for phobias and post-traumatic stress, with researcher Thomas Agren from Uppsala University leading the research.

"The findings may be a breakthrough in research on memory and fear. Ultimately the new findings may lead to improved treatment methods for the millions of people in the world who suffer from anxiety issues like phobias, post-traumatic stress, and panic attacks," said Agren.

When a person learns something, a long-term memory is created with the aid of a process of consolidation, which is based on the formation of proteins. As we remember something, the memory becomes unstable for a while and is then restabilized by another consolidation process.

In other words, we are not remembering what originally happened, but rather what we remembered the last time we thought about what happened.

By disrupting the reconsolidation process that follows upon remembering, we can affect the content of memory.

Researchers showed subjects a neutral picture and simultaneously administered an electric shock. In this way the picture came to elicit fear in the subjects which meant a fear memory had been formed. To activate this fear memory, the picture was then shown without any shock. For one experimental group the reconsolidation process was disrupted with the aid of repeated presentations of the picture.

Brain’s gene map shows striking similarities

EDINBURGH, UK: Human brains follow the same basic molecular pattern despite different individual personalities, a 3D map of where our genes are expressed suggests.
The map draws on more than 100 million gene expression measurements found in three human brains cut into 900 pieces.Researchers from the Allen Institute for Brain Science in Seattle and Edinburgh University said the project might help understand how genetic disorders cause brain disease. The study appears in Nature journal. The human brain is the most complex structure in the world, composed of 100 billion cells, but it is still not fully understood.

Prof Ed Lein, from the Allen Institute for Brain Science, one of the authors of the paper, said this atlas could provide vital information in the general understanding of “brain function, development, evolution and disease”.

The teams says that the majority of genes in the human brain are expressed in patterns very similar from one brain to another - showing that despite different individual personalities, our brains are in fact strikingly similar.

Thursday, September 20, 2012

Alzheimer`s sabotages brain wiring?


Alzheimer`s sabotages brain wiring?
Washington: Alzheimer`s could actually sabotage the working of several of the brain`s networks, says a study.

Beau Ances, assistant professor of neurology, Washington University School of Medicine in St. Louis, who led the study said: "Communications within and between networks are disrupted, but it doesn`t happen all at once."

"There`s even one network that has a momentary surge of improved connections before it starts dropping again.

"That`s the salience network, which helps you determine what in your environment you need to pay attention to," added Ances, The Journal of Neuroscience reported.

Ances and colleagues analyzed brain scans of 559 subjects.

Some of these subjects were cognitively normal, while others were in the early stages of very mild to mild Alzheimer`s disease.

 Scientists found that all of the networks they studied eventually became impaired during the initial stages of Alzheimer`s, according to a university statement.

Scientists also examined Alzheimer`s effects on a brain networking property known as anti-correlations.

Researchers identify networks by determining which brain areas frequently become active at the same time, but anti-correlated networks are noteworthy for the way their activities fluctuate: when one network is active, the other network is quiet.

This ability to switch back-and-forth between networks is significantly diminished in participants with mild to moderate Alzheimer`s disease.

The default mode network, previously identified as one of the first networks to be impaired by Alzheimer`s, is a partner in two of the three pairs of anti-correlated networks scientist studied.

"There are, however, a number of additional networks besides the default mode network that become active when the brain is idling and could tell us important things about Alzheimer`s effects," said Ances.

It`s not practical to use these network breakdowns to clinically diagnose Alzheimer`s disease, Ances notes, but they may help track the development of the disease and aid efforts to better understand its spread through the brain.

Ances plans to look at other markers for Alzheimer`s disease in the same subjects, such as levels in the cerebrospinal fluid of amyloid beta, a major component of Alzheimer`s plaques.

Second person dies from 'brain-eating amoeba': confirmed

The child who died of brain abscess in Ho Chi Minh City was actually killed by “brain- eating amoeba” (Naegleria fowleri).

This was confirmed by Tran Thanh Duong, Deputy head of the Preventive Medicine Agency under the Ministry of Health, on September 19. He said the tested samples proved positive for amoeba Naegleria fowleri.

The MoH has asked HCM City to send a detailed report on the case.

Earlier on July 30, , the Ho Chi Minh City Hospital for Tropical Diseases received a 25-year-old patient from Phu Yen, who was the first identified victim of Naegleria fowleri.

So far, Vietnam has had two people killed by brain eating amoeba. However, Duong said, this is a single case, not epidemics.

Primary amoebic meningoencephalitis is a fatal disease but it is rare and can be avoidable.

 

According to experts, the amoeba lives predominately in the warm bodies of freshwater such as lakes and rivers in tropical and subtropical climates. It grows best at a temperature of 46 degrees Celsius, but it has also been found to survive at higher temperatures of 50-56 degrees Celsius. It invades the brain through the nostrils.

To avoid the disease, the Preventive Medicine Agency warns people not to bathe and swim in high-risk areas.

If they swim at swimming-pools, ponds, lakes and streams, they should minimize water from getting into their noses. After bathing or swimming, they should clean their noses by nasal antiseptic, it says.

If they have some symptoms like a headache, fever, nausea, or vomiting, they should immediate go to clinics for prompt diagnosis and treatment.

Meow meow: The party drug that fries your brain

Nightclub Meow meow is causing significant memory loss.

IT'S cheap, it's easy to find, and it's more addictive than cocaine. But experts warn meow meow (or Drone, among other names) is no party drug - it's literally frying your brain.

Meow meow, Drone and MCAT are street names for mephedrone, a synthetic psychoactive drug that is also found in so-called "Bath Salts".

It's been on the party scene for a number of years in Australia and it's estimated that tens of thousands of revellers dabble in the off-white power.

It's said to produce a similar but more powerful high than either ecstasy or cocaine and is dangerously addictive. Yet the dangers of this relatively new and unknown drug are only just beginning to surface.

Researchers from the University of Sydney have found compelling evidence that mephedrone can give users significant memory loss, the long-term effects of which aren't yet fully understood.

Craig Motbey, the leader of the controlled testing on rats, says meow meow is similar to amphetamine and huge numbers of people have been taking it for years.

"It exploded so fast and so wide," he told news.com.au.

"[But] we know virtually nothing about the drug. Now there's a big push to find out if it's doing damage.
"It might be something that causes subtle damage that builds up, but we don't realise anything's wrong until a couple of years later when we have tens of thousands of fried brains."

Disturbing research
Mr Motbey's research confirms the fears of anti-drug campaigners. You mightn't be able to convince people to ditch recreational drugs, but they might take notice if they realise the damage it's causing.

What sounded the alarm was a simple memory test called the Novel Object Recognition Test. It works like this: A rat, given a dose of the drug, spends time in a fixed area with two identical objects (let's call them A and A). The rat is taken away, then brought back later to spend time with one object the same (A) and one entirely new object (B). A rat with a normal, healthy memory would only ever spend time investigating object B.

"Rats are naturally curious critters," Mr Motbey said. "If you put a new object in front of them, they'll spend all their time checking out the new thing.

"If they spend equal time with both things (one new and one old), then that's a clear sign of memory damage – which confirmed earlier theories about mephedrone."

Mr Motbey refers to an earlier uncontrolled study in the UK, where mephedrone users were brought in a month apart and given standard cognitive tests. The results showed some evidence of memory impairment.
"When you take the drug you get a massive wave of euphoria from serotonin, which then goes away," Mr Motbey added.

"Then there's a persistent dopamine hook that motivates people to re-dope. Mephedrone is extremely addictive. So people are getting this short-term high, the major thing driving people to take the drug, but then they're re-dosing regularly to get that initial hit back."

‘As bad as any drug'
The latest research figures show mephedrone usage in Australia is down two percentage points from 2011 in 2010. But it's still a significant problem.

Steve Patton, the acting commander of the NSW Drug Squad, said there haven't been many seizures of mephedrone but that certainly didn't mean the drug was free from risks.

"People shouldn't be taking it. It's a drug that's just as bad other drugs," he told news.com.au
"It doesn't surprise me that it does have ill-effects for people's health."

Louise, a young woman from Bondi Beach who'd dabbled with other party drugs before, says she regularly took meow meow around two to three years ago. Why?

"It was a lot stronger than pills or other drugs with a bigger high and it was cheaper," she told news.com.au.
"You can sniff it or you can eat it. It used to be about $100 per gram, which compared to coke is much cheaper.

"It gives you more of a buzz than cocaine. It's more like taking a pill, and in terms of the effects it was slightly different."

Breaking bad
Louise says it's not as readily available these days and admits, although she didn't experience major side effects, she's noticed lapses in her memory.

"How significant the effects of the memory damage, we just don't know. The research hasn't been done," Mr Motbey adds.

"We don't know what's causing the memory damage. We looked at the brains - and they were exactly the same. It's a subtle change, it's not immediately obvious."

"Hopefully we can get the word out to users that this is not a harmless, innocuous drug, it can do damage to you."

If meow meow is shut down then another, potentially more dangerous drug will inevitably pop up in its place. A drug we know nothing about.

"Modern chemistry has become so flexible you can make virtually anything," Mr Motbey added.
"A new drug comes out, the authorities ban it, and crack down on the supply. Then another drug comes out, the authorities ban it, crack down on the supply.

"It only takes moving a carbon atom from one place to another to change a drug from harmless and fun to absolutely lethal. It's just a matter of time before the drug-taking community hits on something incredibly dangerous."

Baby who suffered massive stroke after 'ticking time bomb' blood clot burst in brain makes miracle recovery

     * Jacob was born with a group of malformed blood vessels in his brain, which burst when he
        was two weeks old 
     * Parents could only watch and wait as surgeons battled to save him. They were told he might 
        never walk 
     * Doctors told family Jacob had a healthy brain in February this year 

No stopping him: Jacob Edwards took his first steps just after his first birthday 

Jacob Edwards took his first steps just after his first birthdayA baby who suffered a massive stroke after a 'ticking time bomb' of malformed blood vessels burst in his brain, has made a miraculous recovery.

Jacob Edwards fell ill when he was just two weeks old. He was rushed to hospital where surgeons had to perform a risky operation to remove a blood clot from his brain to reduce the pressure.

However, they were unable to remove all of it because it was too deep in Jacob’s brain. His parents Hayley Leon and Lee Edwards, from Coventry, were warned it could burst again and their son may be left with with brain damage.

But doctors were left stunned when a brain scan showed the Arteriovenous malformation - or AVM - had vanished. Now Jacob, 15 months, has beat the odds by learning to walk and talk - something his parents feared he may never do.

Hayley, 30, said: 'It’s amazing. We’re so proud of him. Not a day goes by when I don’t think about what happened. It could have been so different. We were very close to losing him. Jacob seemed healthy when he was born in July last year.

 But when he was two weeks old, he woke up screaming and vomiting. The couple, who also have two older sons, Callum, 11, and five-year-old Jack, immediately took him to University Hospital, Coventry, where doctors thought he had gastroenteritis. Hayley said: 'Jacob was getting worse by the hour.

He was slipping in and out of consciousness. Lee noticed his left eye was lifeless. He asked the doctors to check it and that’s when they knew something was seriously wrong. They did a CT scan and told us they had found a bleed on his brain.

Lee and I didn’t know what to say. It’s not something that happens to you. It happens to other people. We were in total shock.' Jacob was placed on a life support machine before being rushed to Birmingham Children’s Hospital for more specialist care.

Full time mother Hayley said: 'A special ambulance came to pick him up. We weren’t allowed to go with him because there wasn’t enough room. 'It was horrible leaving him. I just wanted to be with him and to make him better. 'When we got there, they took him for an MRI scan. We were taken into a side room and the surgeon came to see us. After his operation: Surgeons didn't manage to remove all of the AVM, but the rest disappeared by itself After his operation: Surgeons didn't manage to remove all of the AVM, but the rest disappeared by itself

Jacob's brain before the operation: The malformed area can be seen bottom rightWe had to sign a consent form for emergency surgery. It said the main risk was death but without surgery, he would die. My heart was breaking as the word death was mentioned a lot. Lee likes to keep his emotions to himself but he was the most upset.
He kept saying: ‘he can’t leave us yet.’ He was really panicking. But it was out of our hands so we just had to trust the surgeon.

Doctors explained to the couple they still didn’t know what had caused the bleed but that they needed to remove it and reduce the pressure in his brain immediately to stop any further damage.

 Amazingly, Jacob survived the six-hour operation but he remained in a critical condition in intensive care. Jacob's brain before the operation: The malformed area can be seen bottom right Hayley said: 'A nurse brought us to see him. It was horrible. It didn’t look like him. His head was really swollen and so were his eyes.

He had a tube coming out of his head to drain all the fluid from his brain. He had so many wires coming out of him I was scared to touch him.

(Pictured is Jacob in hospital)A scan showed the operation had been a success but surgeons were unable to remove all of the AVM. Three days later, Jacob was taken off his life support machine to see if he could breathe on his own. To everyone’s amazement, he took his first breaths unaided and was later moved to the high dependency unit, where he continued to make progress.

Due to the stroke, Jacob suffered weakness on his left side so severe he couldn’t even hold his head up and he needed intensive physiotherapy. After two weeks in hospital, doctors were so pleased with Jacob’s progress, he was discharged.

Hayley said: 'I was so scared to bring him home as at this time he still had the AVM inside his brain and there was a very high chance of it bleeding again. I didn’t sleep and didn’t leave the house for weeks. We had to go back and forth to hospital for scans, which was awful as he had to be put to sleep.

They had to check his brain for any damage. In February this year, Jacob had an angiogram, where a special dye is used to take pictures of blood flow to the brain.
Jacob with mum Hayley and dad Lee

Hayley said: 'The doctor came to see us and said it had gone. He told us Jacob had a healthy brain. He was gob-smacked and so were we. But he was still having difficulty lifting his head and he couldn’t crawl. At his development check, we were told he probably had cerebral palsy and he may not walk. We didn’t know what the future held for our brave boy.'

But three days after his first birthday, Jacob took his first steps Now there is no stopping him and he continues to amaze his parents and doctors.

Hayley said: 'He’s going from strength to strength and is reaching all his milestones. He’s so determined. I can’t thank the staff at both hospitals enough for saving my baby’s life. They are my heroes.'

Jacob Jacob’s neurosurgeon, Mr Desiderio Rodrigues, from Birmimgham Children’s Hospital said: 'Jacob was in a very poor state in coma when he was presented to the hospital and had to be intubated and ventilated prior to transfer.
Neurosurgeon Mr Desiderio Rodrigues, from Birmimgham Childrens Hospital, who performed life-saving surgery on Jacob
The scan showed a large blood clot in the back of his brain. It was obstructing the flow of the cerebro spinal fluid, which travels from the brain to the spine. I performed an operation to relieve the pressure and then remove the clot from the back of the brain. 'I spoke to the parents prior to the operation and told them it was a high risk operation.

The child could even bleed profusely and die during surgery, as the emergency scan had not identified the cause for the bleed. 'There was no choice but as a life saving measure to take the risk and operate. 'During surgery I found a leash of abnormal blood vessels which were the cause of the clot. 'I only removed part of it and follow up MRI scans have showed whatever was left has now gone.

The angiogram has confirmed that Jacob has no residual AVM.

'We are very pleased with his progress.'