Bird flu leaves tracks in brain

Virus might create vulnerability to neurological disorders, research in mice suggests

After surviving a bout of virulent bird flu, mice’s brains show short-term reductions of a key brain chemical and long-lasting signs of infection, a new study finds. The research suggests this type of flu might leave people more vulnerable to brain disorders such as Parkinson’s disease.
While most people think of influenza as a disorder of the body, certain kinds of flu also infect the brain. Recent studies have found that the bird flu virus known as H5N1, which kills about half the people it infects, can set up shop in the brain. But exactly what happens next has been a mystery.
In the new study, scientists at St. Jude Children’s Research Hospital in Memphis, Tenn., examined the brains of mice that had survived an initial H5N1 infection. As in people, the virus kills about half of mice affected.
“The first goal with H5N1 was to characterize the neurological effects,” says study coauthor Richard Smeyne.
After being infected with H5N1 isolated from a Vietnamese boy who died from the flu, some mice initially got very sick, but then seemed to recover completely after about 21 days. Yet the story wasn’t so simple in the brain, the team reports in the Feb. 1 Journal of Neuroscience.
Nerve cells that make one of the brain’s key messengers — the neurotransmitter dopamine, which helps regulate movement — shut down production about 10 days after infection. These nerve cells, which are the same cells that degenerate in people with Parkinson’s disease, “basically take a time out,” Smeyne says. “All efforts are to survive.”
By day 60, the dopamine starts to reappear, and levels are back to normal 90 days later. Signs of inflammation in the brain remain, though.
Just three days into the infection, the brains of these mice showed evidence of a strong inflammatory response, and this response appeared to linger over time. Proteins that accompany inflammation, and cells that patrol the brain looking for threats, were still present and on duty in parts of the brain 90 days after the initial infection. Scientists don’t know whether the response ever goes away. “My guess is that it’s permanent,” Smeyne says.
He notes that it’s unlikely that an influenza infection could cause neurological diseases such as Parkinson’s, but an infection might be a contributing factor, perhaps even precipitating the disease in someone already at risk.
The results are intriguing because they offer a way to understand H5N1’s consequences in the brain, says neuroimmunologist Stephanie Bissel of the University of Pittsburgh School of Medicine. Future experiments on such survivor mice could reveal whether the mice show behavioral signs of neurological impairment, she says.
The research team has evidence that H5N1 breaks into the brain by traveling along the vagus nerve from nerve cells in the gut. The virus might also enter the brain from the nose by crawling along the olfactory nerve, Smeyne says.

Study Spots Where Humor Tickles Kids' Brains

Kids may not giggle over the awkwardness on "The Office," and adults usually aren't all that tickled by Elmo. But new research shows that the same brain regions are active when both children and grown ups find something funny.
Researchers at Stanford University have shown that the brain's network for appreciating humor develops in childhood. They studied 15 children ages 6 to 12, showing them clips from "America's Funniest Home Videos," like people stumbling while skiing or running, animals doing tricks or a kid being catapulted off of an inflatable couch. (To be sure the videos would be funny to kids and not just scientists, the researchers first had children of the same ages rate videos as funny or not.)
While the kids were watching the videos, researchers were monitoring their brain activity using technology called functional magnetic resonance imaging.
The results, published today in the Journal of Neuroscience, showed that funny videos turned on kids' brains in two key areas – the temporo-occipito-parietal junction, or TOPJ, an area located just above the ear, and the midbrain, an area deep inside the brain near the bottom of the skull. The fact that these areas were more active during funny videos and not just positive ones shows that these areas are distinctly part of the brain's humor network.

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Dr. Allan Reiss, one of the study's authors, has researched how humor lights up adult brains, and he said the same areas that lit up when kids were laughing were also active when adults found something funny. One of the brain regions tickled by humor, the TOPJ, helps humans perceive and appreciate the unexpected things in life. Reiss said that could be one reason why humor is often cited as a major stress reliever.
"A lot of humor is setting up a joke or something funny and then giving the punch line, often going in an unexpected direction," Reiss said. "One of the reasons why a good sense of humor might serve as a means of stress reduction is that many times stress comes from incongruities in our daily lives."
The other brain region that lit up when kids viewed the funny videos, the midbrain, is the area of the brain that helps humans process rewarding feelings, which could explain why just the right joke can be a quick way to improve a bad day. The younger children in the study showed more activity in this rewarding area of the brain.
"That may well be because of the type of stimuli that we used," Reiss said. "The younger children probably found those videos funnier."
The study is the first to look at how kids' brains detect and appreciate humor. Dr. Rebecca Schrag, a child psychologist at the Healthy Steps Program at Montefiore Medical Center in Bronx, N.Y., said the fact that the brain is hard-wired for humor gives humans an important tool for coping with life.
"Humor isn't just a casual thing you do at a dinner party. It has been shown to be a factor that can contribute to resilience," she said. "Being able to see the humor in stressful situations, to see the upside of things, to be able to laugh at yourself or things that are difficult has been shown to contribute to positive development."
Reiss said he hopes to learn more about how children develop senses of humor, and how that impacts their experiences in life.
"Humor is a ubiquitous part of our social lives. Clearly, children who have well-developed senses of humor and can use them appropriately often are quite successful," Reiss said.

Scientists shift on brain speech center

An analysis of the brain imaging coordinates in those studies pointed to the new location for Wernicke’s area, offering new insight for patients suffering from brain damage or stroke. 

WASHINGTON: The part of the brain used for speech processing is in a different location than originally believed, according to a US study Monday that researchers said will require a rewrite of medical texts.
Wernicke’s area, named after the German neurologist who proposed it in the late 1800s, was long believed to be at the back of the brain’s cerebral cortex, behind the auditory cortex which receives sounds.
But a review by scientists at Georgetown University Medical Center of more than 100 imaging studies has shown it is actually three centimeters closer to the front of the brain, and is in front of the auditory cortex, not behind.
“Textbooks will now have to be rewritten,” said neuroscience professor Josef Rauschecker, lead author of the study which appears in the Proceedings of the National Academy of Sciences.
“We gave old theories that have long hung a knockout punch.”Rauschecker and colleagues based their research on 115 previous peer-reviewed studies that investigated speech perception and used brain imaging scans — either MRI (functional magnetic resonance imaging) or PET (positron emission tomography).
An analysis of the brain imaging coordinates in those studies pointed to the new location for Wernicke’s area, offering new insight for patients suffering from brain damage or stroke.
“If a patient can’t speak, or understand speech, we now have a good clue as to where damage has occurred,” said Rauschecker.
It also adds an intriguing wrinkle to the origins of language in humans and primates, who have also been shown to process audible speech in the same region of the brain.
“This finding suggests the architecture and processing between the two species is more similar than many people thought.” Lead author Iain DeWitt, a PhD candidate in Georgetown’s Interdisciplinary Program in Neuroscience, said the study confirms what others have found since brain imaging began in earnest in the 1990s, though some debate has persisted.
“The majority of imagers, however, were reluctant to overturn a century of prior understanding on account of what was then a relatively new methodology,”he said.
“The point of our paper is to force a reconciliation between the data and theory.”

Zoologger: The only males with more brain than females

Zoologger is our weekly column highlighting extraordinary animals – and occasionally other organisms – from around the world

Species: an isolated population of Gasterosteus aculeatus
Habitat: Lake Mývatn, Iceland

In one of philosophy's greatest facepalm moments, the normally quite intelligent Arthur Schopenhauer wrote that "women are defective in the powers of reasoning and deliberation". If you find it hard to believe that a well-educated and original thinker could hold such a view, his essay Of Women leaves no doubt about it. Oddly enough, he never married.

However, Schopenhauer might have had a point, if only he had been a three-spined stickleback living in Lake Mývatn in Iceland. In this one population, the males have brains much larger than those of the females. They are the only species known where there is such a big disparity between the two sexes' brains.

What's surprising is that there aren't more animals like this. Species differ enormously in brain size, after all, and males and females often have different lifestyles that make different demands on their brains. Why do these few fish buck the trend?

Sticklers

Most three-spined sticklebacks live in the sea and only visit fresh water to breed, but others – like the Mývatn population – spend all their lives in fresh water. Behavioural scientists have studied them for decades because of their elaborate mating rituals.

At the start of the breeding season, the males' skin turns a bright orange-red, and their eyes go blue-green. Each male defends a patch of territory, where he builds a nest from debris like pebbles and vegetation. The males glue their building materials together with stuff called spiggin, which they make in their kidneys.

Once the nest is completed, the male installs himself in front of it and performs a zigzag dance to attract a female. When one approaches, the male leads her to the nest, and she takes a close look. If the nest is good, and the male a suitably bright red, she goes inside and lays her eggs, which the male promptly fertilises.

That done, the female clears off and leaves the male in sole charge of the eggs. They tend to get fungal infections, so he minimises the risk by waving his fins to keep water moving through the nest, and if any eggs become infected he picks them out.

Size isn't everything

Wondering if the male's complex lifestyles were reflected in their brains, Alexander Kotrschal of Uppsala University in Sweden and colleagues dissected 58 males and 61 females, and weighed their brains. On average, both sexes were 4.5 centimetres long, but the males had brains weighing 24.2 milligrams, whereas the females' weighed just 19.7 mg.

Kotrschal emphasises that the size of an animal's brain isn't everything. "It's generally assumed that larger is better," he says, because having more neurons for a given body mass should allow the brain to process more information. However, there could also be unseen differences in the numbers of connections between neurons. "The connectivity is also extremely important."

He hasn't put the males and females through intelligence tests to see whether the size difference actually translates into ability. "It's hard to infer cognitive abilities just from brain size," he says.

Nevertheless, he points out that species with larger brains in proportion to body size, like humans, do in general seem to be more intelligent than those with smaller ones. So it's possible that the male sticklebacks really are smarter than their females.

Why would that be? It could be that the males have a more challenging lifestyle: they have to build nests, perform courtship dances and then care for the eggs. The females don't help with any of this – but they do have to assess the males' dancing and nest-building, which takes quite some powers of discernment.

It could also be that the females devote a lot of energy to making eggs, leaving little to run a large brain. The female's gonads can make up 40 per cent of her body mass, and so consume lots of nutrients.

There's a precedent for that sort of effect. Similar trade-offs are seen in male bats, some of which have shrunk their brains to get bigger testes. One can only imagine what Schopenhauer would have made of that.

Human brain cells created using stem cells

Dolly the Sheep.

It's been sixteen years since Edinburgh scientists cloned a sheep and named it Dolly, but their sophomore effort appears even better: they've gone back to the studio and created some new brain tissue. Human brain tissue, that is.
By using stem cells from people suffering from schizophrenia, bipolar disorder and other mental illnesses, the scientists at the Centre for Regenerative Medicine were able to make brain cells to study the neurons, thus the neurological conditions.

Said director Professor Charles ffrench-Constant, "We can take a skin sample, make stem cells from it and then direct these stem cells to grow into brain cells. Essentially, we are turning a person's skin cells into brain. We are making cells that were previously inaccessible. And we could do that in future for the liver, the heart and other organs on which it is very difficult to carry out biopsies."

With the cells grown outside the body, scientists can study them in greater detail than ever before, hopefully unlocking previously unknown things about these conditions.

"We are making different types of brain cells out of skin samples from people with schizophrenia and bipolar depression," he said. "Once we have assembled these, we look at standard psychological medicines, such as lithium, to see how they affect these cells in the laboratory. After that, we can start to screen new medicines. Our lines of brain cells would become testing platforms for new drugs. We should be able to start that work in a couple of years."

Scientists also hope to work on multiple sclerosis, Parkinson's disease and motor neuron disease.
This is yet another usage of stem cells, which are being used in myriad amazing ways. In some ways, stem cells are the most awesome (in its original meaning) thing happening in a world that is changing at a rate too rapid to describe.
We just can't wait to see what happens next.

Sleep apnea may up risk of silent strokes, small lesions in brain

Washington, Feb 2 (ANI): People with severe sleep apnea may have an increased risk of silent strokes and small lesions in the brain, researchers have revealed.
The researchers found that ninety-one percent (51 of 56) of the patients who had a stroke had sleep apnea and were more likely to have silent strokes and white matter lesions that increased risk of disability at hospital discharge.
Having more than five sleep apnea episodes per night was associated with silent strokes.
More than one-third of patients with white matter lesions had severe sleep apnea and more than 50 percent of silent stroke patients had sleep apnea.
“We found a surprisingly high frequency of sleep apnea in patients with stroke that underlines its clinical relevance as a stroke risk factor,” said Jessica Kepplinger, M.D., the study’s lead researcher and stroke fellow in the Dresden University Stroke Center’s Department of Neurology at the University of Technology in Dresden, Germany.
“Sleep apnea is widely unrecognized and still neglected. Patients who had severe sleep apnea were more likely to have silent strokes and the severity of sleep apnea increased the risk of being disabled at hospital discharge,” she stated.
Even though men were more likely to have silent infarcts, correlations between sleep apnea and silent infarcts remained the same after adjustment for such gender differences.
Researchers suggested that sleep apnea should be treated the same as other vascular risk factors such as high blood pressure.
“Demographic characteristics in our study are comparable to western European populations, but our findings may not be entirely generalizable to other populations with diverse ethnicities such as in the U.S.,” Kepplinger said.
The researchers plan more studies on sleep apnea, particularly in high-risk patients with silent strokes and white matter lesions, to determine the impact of non-invasive ventilation and on short-term clinical outcome, researchers said.

Decaffeinated coffee curbs memory decline

Decaffeinated coffee curbs memory decline

Decaffeinated coffee may help improve brain energy metabolism associated with type 2 diabetes, researchers suggest.

This brain dysfunction is a known risk factor for dementia and other neurodegenerative disorders like Alzheimer's disease.

A research group led by Giulio Maria Pasinetti, MD, PhD, Professor of Neurology, and Psychiatry, at Mount Sinai School of Medicine, explored whether dietary supplementation with a standardized decaffeinated coffee preparation prior to diabetes onset might improve insulin resistance and glucose utilization in mice with diet-induced type 2 diabetes.

The researchers administered the supplement for five months, and evaluated the brain's genetic response in the mice. They found that the brain was able to more effectively metabolize glucose and use it for cellular energy in the brain.

Glucose utilization in the brain is reduced in people with type 2 diabetes, which can often result in neurocognitive problems.

"Impaired energy metabolism in the brain is known to be tightly correlated with cognitive decline during aging and in subjects at high risk for developing neurodegenerative disorders," said Dr. Pasinetti.

"This is the first evidence showing the potential benefits of decaffeinated coffee preparations for both preventing and treating cognitive decline caused by type 2 diabetes, aging, and/or neurodegenerative disorders," Dr. Pasinetti. Added.

Coffee intake is not recommended for everybody due to the fact that it is associated with cardiovascular health risks such as elevated blood cholesterol and blood pressure, both of which lead to an increased risk for heart disease, stroke, and premature death. These negative effects have primarily been attributed to the high caffeine content of coffee.

Nonetheless, these novel findings are evidence that some of the non-caffeine components in coffee provide health benefits in mice.

Dr. Pasinetti hopes to explore the preventive role of decaffeinated coffee delivered as a dietary supplement in humans.

"In light of recent evidence suggesting that cognitive impairment associated with Alzheimer's disease and other age-related neurodegenerative disorders may be traced back to neuropathological conditions initiated several decades before disease onset, developing preventive treatments for such disorders is critical," he said.

Stay at work for brain health

OFF TO WORK WE GO: Today's active 70-year-olds have brain scans that look up to 15 years younger than those of their parents' generation
Whether it's sudoku or brain training games, there are plenty of options claiming to sharpen our brains as we get older.
But psychiatrist Ian Hickie, Executive Director of the University of Sydney's Brain and Mind Research Institute, has a better idea - keep working.
"Work is your own personal cognitive training program because it keeps you challenged and engaged," he says.
"Through the whole of the lifespan if you compare people who are employed with those who are unemployed, their mental and physical health is better.
"Although problems with physical health can be the reason that health takes you out of the workplace - it's also true that those who get back to work after an illness improve their health."
Hickie believes there's something health-preserving about work - probably a mix of factors, including new experiences that help drive the growth of brain cells, as well as interaction with other people.
"But it could also be that the routine that keeps you going to bed and getting up at the same time each day helps regulate our sleep wake cycles, and this is important for our physical and mental health," he points out. "On the other hand, when people are not working they often tend to sleep more - and eat more."
The really good news for anyone nudging retirement age is that, despite all the gloom about dementia, the brains of many modern 65 to 70 year olds are in pretty good shape compared to those of previous generations - and, says Hickie, often too young to be retired.
"Today's physically active 70-year-olds who don't smoke have scans showing brains that look 10 to 15 years younger than those of their parents' generation at the same age - more of whom were smokers. We should never retire simply because of age - the best professors at this university are over 70 years of age," he says, adding that the retirement age of 65 is out of date, an anachronism from the 19th century when life expectancy was shorter and people were often worn out by tougher working conditions.
"You find that around the world the age of retirement is going up," says Hickie who, at the 2008 National Public Health Reform Summit, was quoted as saying that raising the retirement age from 65 to 72 would help reduce mental illness.
Still, that doesn't mean you have to keep doing the same job until you drop - most of us will have to change our job in some way. But his advice is not to just quit altogether.
It's a similar message from another brain expert, Dr Michael Valenzuela, Senior Research Fellow at the School of Psychiatry at the University of NSW.
We're trained to plan our retirement from a financial perspective, but we should also be paying just as much attention to planning our retirement from a healthy brain perspective, he writes in his latest book, Maintain your Brain (ABC Books).
"We need to replace the social, physical and cognitive activity that was an inherent part of our jobs - and which normally fills up 50 per cent of our waking lives - with new activities that also have a social, physical and cognitive component," he says.
Continuing to work, even if only part time, can be one option, although his list of other activities that tick all three boxes includes getting involved in a community garden (as opposed to solitary gardening), dancing (it's mentally demanding) and orienteering.
"I think many people will either decide to keep on working or to keep on learning," says Valenzuela, pointing to the Tasmanian Healthy Brain Project, a world first study at the University of Tasmania to find out if taking up further education at an older age can buffer our brains against dementia.
Research already suggests that a tertiary education early in life seems to help protect against cognitive decline - could picking up textbooks in our 50s, 60s and 70s do the same?

Montreal's brain bank gets hefty donation

Dr. Naguib Mechawar handles a human brain. (Feb. 1, 2012)  

3,000 brains are kept at the Douglas Mental Health Institute (Feb. 1, 2012)  

The Douglas Institute 

MONTREAL — Every day in a Montreal laboratory scientists reach into freezers, make a careful selection, and pull a human brain out of cold storage.
What may be gruesome to the average person is routine for the researchers at the Douglas Mental Health Institute, where thousands of brains are kept on ice, waiting to become the subject of research into mental illness and neurological disorders.
That research is overseen by Dr. Naguib Mechawar. who is passionate about finding cures for mental illness.
"At the Douglas in the past 30 years there have been many breakthroughs that have been made because of brain donations," said Dr. Mechawar.

Three decades of research
The Brain Bank was created in 1980 and has close to 3,000 brains in storage, all donated by people with an interest in battling mental illness.
Researchers have used the brains to help discover a gene linked to Alzheimer's Disease, and do cutting edge work on depression and suicide prevention.
"Some samples we've had since the early '80s when the brain bank was created," said Dr. Mechawar.
Comparing healthy brains to diseased ones is painstaking work, and getting people to donate their brains isn't easy either, but that is exactly what Manon-Lucie Sirois has agreed to do after her death.
Two of her aunts had Alzheimer's so taking a few minutes to sign a consent form was an easy choice.
"It's the highway for the researcher to find maybe a solution," said Sirois.
The president of the Douglas Mental Health Institute says when someone donates their brain it comes with their medical history, which is precious information for researchers looking to identify the one in five Canadians at risk of mental illness.
"When you go to the doctor today you use markers in your blood to identify if you're at risk of heart disease and then you're given a course of medication. We'd like to do the same for mental illness," said Jane Lalonde.

Bell Canada donating $2 million
Mental health research receives a small portion of federal funding compared with other illnesses.
That's one reason that CTV's parent company, Bell Canada, is donating $2 million to the Douglas Mental Health Institute.
The funding will go toward a research fellowship, upgrading technology, and improving laboratories and storage facilities.
Improved technology to make unlocking the secrets of the human brain a little easier.

Mexican ‘brain bank’ furthers Alzheimer’s research

MEXICO CITY – Mexican scientists are making inroads in Alzheimer’s research thanks to the creation of one of the primary “brain banks” in Latin America.

The brain bank, housed in a laboratory of the National Polytechnic Institute’s Center for Investigation and Advanced Studies (CINVESTAV), has given scientists here an opportunity contribute more fully to international research into Alzheimer’s and dementia.
A CINVESTAV team led by Dr. Raul Mena y Dr. José Luna-Muñoz has been studying the early stages of certain protein changes in neurons – with the goal of providing evidence of the changes, first, and, second, to eventually provide the basis for developing drugs that could stop insidious changes at the cellular level that lead to Alzheimer’s.
Mexico’s brain bank supplies the physical matter for research that is otherwise largely unavailable in Latin America. To study the inner working of brain cells, scientists need to study a brain that has been retrieved between two and six hours postmortem, otherwise proteins begin to break down and the research does not retain the same integrity, according to Dr. José Luna-Muñoz, CINVESTAV professor and researcher.
The concept of a brain bank in Mexico – or Latin America for that matter – was taboo until recently. The cultural belief that a body should be buried in tact prevented many families from considering donating the brain.
“That ideology has been changing,” said Luna-Muñoz. “People want to prove and know why their family members have died, whether it was Alzheimer’s or dementia. It’s been a cultural shift.”
Eighteen brains have been donated since a scientist named Dr. Raul Mena founded the bank in 1992. Previously, Mexican scientists had to request brain fragments from France, England, Canada or the United States in order to perform research. Now Mexico sends fragments abroad to labs in need, including recently to Chile.
The brain bank is also furthering research into the factors that may be environmental or specific to Mexicans. Right now the scientists are looking at the early stages of “tau” protein processing in Alzheimer’s disease. Among their contributions, the scientists have determined a morphological model and the underlying molecular mechanism involved in early stages of the abnormal processing of the tau protein. They have also suggested that the “neurofibrillary tangle formation,” as that abnormal processing of the tau protein is known, may be a protective mechanism of the neuron to prolong cell life.
“Between 5 percent and 10 percent (of Alzheimer’s cases) are associated with a genetic factor,” said Luna-Muñoz. “The rest are know as sporadic Alzheimer’s and the cause is unknown. Is there some environment that could be favoring the expression of this disease?”
That’s what the CINVESTAV researchers (and their counterparts around the world) are working to find out.
The image, taken from an Alzheimer’s affected brain, characterizes the initial stage of degeneration in the neuron known as the “pre-tangle” stage. Photo taken with a confocal microscope by Dr. José Luna-Muñoz.

Man survives piece of wood stuck in brain

Mumbai:  When 22-year-old Vinod Pal was wheeled into KEM hospital's emergency unit on Monday afternoon, he was not a sight for sore eyes. Nurses, ward boys, patients and even doctors did a double take at the sight of a bloody piece of wood jutting out of his skull.

Inspections revealed that the wooden piece had pierced Pal's head, entering the brain matter and compressing it.

On Monday afternoon, Pal -- a carpenter -- was working on the eighth floor of an under-construction building in Badlapur. He was trying to separate a cluster of bamboo sticks, when a thick piece of wood used to support the bamboos hit Pal's head, penetrating it.

A native of Uttar Pradesh, Pal's search for employment had brought him to the shores of Mumbai just six months ago. After the accident, he was put in an auto by his co-workers and taken to a local hospital.

"The doctors at the hospital took a CT scan and informed us that the splinter had entered his brain, and advised that we take him to KEM hospital. We did not suspect that it was such a serious matter. He seemed fine on his way to the hospital," said Govind Pal, who witnessed the accident.

By Monday evening, Vinod was conveyed to KEM hospital, where doctors immediately took him to the Operation Theatre, after evaluating the nature of his injuries.

"The big splinter had fractured his skull, piercing the dura mater covering the brain, and entering the brain substance, which can expose him to extensive infection, apart from the risk of paralysis. It could have been fatal if it had gone in any deeper," said Dr A K Gvalani, head of the surgery department of KEM hospital, adding that a team of neurosurgeons had operated on Pal.

Recollecting the incident, Pal said, "I was working as I do on any other day, when suddenly the piece of wood flew into the air and hit my head. Till the surgery was performed on me, I didn't know that the wooden piece had penetrated my brain. I am thankful to God and the doctors who saved me."

"A lot of wooden dust had spread in the brain matter, all of which was removed during the surgery to avoid further infection. We removed the wooden piece which had fractured the skull, and elevated the depression caused in the brain by it," said Ragvendra Ramdasi, resident doctor from the Neurosurgery department.

Meanwhile, Dr Nimisha Kantharia, lecturer of Surgery, said, "The patient had complained of right side weakness, and we have already put him on antibiotics to control infection, if any. We were all shocked to see the patient with this kind of injury. He is fortunate to have escaped death."

At present, Pal is admitted under Dr Sameer Rege, unit head of the Surgery department.

Read more at: http://www.ndtv.com/article/cities/man-survives-piece-of-wood-stuck-in-brain-172672&cp

Changes to Neurons Hamper the Aging Brain

The good news is that most people in the developed world are living longer; the not-so-good news is that the brain often does not stay sharp in our older age.
Currently, experts do not fully understood why the brain’s cognitive functions such as memory and speech decline as we age. This despite the realization that cognitive decline can be detected before an individual reaches age 50.
Neuroscientists Andy Randall, Ph.D. and Jon Brown, Ph.D. from the University of Bristol have identified a novel cellular mechanism that causes changes to the activity of neurons — an action which may contribute to cognitive decline during normal healthy aging.
The brain largely uses electrical signals to encode and convey information. Modifications to this electrical activity are likely to cause age-dependent changes to cognitive abilities.
The researchers examined the brain’s electrical activity by making recordings of electrical signals in single cells of the hippocampus, a structure with a crucial role in cognitive function. By doing this, they were able to assess “neuronal excitability” – the ease with which a neuron can produce brief, but very large, electrical signals called action potentials.
An action potential occurs in practically all nerve cells and is essential for transmission of a signal or communication within all the circuits of the nervous system.
Action potentials are triggered near the neuron’s cell body and once produced, travel rapidly through the massively branching structure of the nerve cell, along the way activating the synapses the nerve cell makes with the numerous other nerve cells to which it is connected.
Researchers discovered the hippocampal neurons within an aged brain have trouble generating action potentials.
Furthermore, they demonstrated that this relative reluctance to produce action potential arises from changes to the activation properties of membrane proteins called sodium channels. The sodium channels influence the rapid initiation of the action potential by allowing a flow of sodium ions into neurons.
Randall, a professor in applied neurophysiology, said: “Much of our work is about understanding dysfunctional electrical signaling in the diseased brain, in particular Alzheimer’s disease.
“We began to question, however, why even the healthy brain can slow down once you reach my age. Previous investigations elsewhere have described age-related changes in processes that are triggered by action potentials, but our findings are significant because they show that generating the action potential in the first place is harder work in aged brain cells.
“Also by identifying sodium channels as the likely culprit for this reluctance to produce action potentials, our work even points to ways in which we might be able modify age-related changes to neuronal excitability, and by inference cognitive ability.”

Scientists decode how the brain hears words

Brains of healthy adults showing low (L) and high (R) levels of beta-amyloid protein (AFP/UNIVERSITY OF TEXAS AT DALLAS)

WASHINGTON — US scientists said Wednesday they have found a way to decode how the brain hears words, in what researchers described as a major step toward one day helping people communicate after paralysis or stroke.
By placing electrodes on the brains of research subjects and then having them listen to conversations, scientists were able to analyze the sound frequencies registered and figure out which words they were hearing.
"We were focused on how the brain processes the sounds of speech," researcher Brian Pasley of the Helen Wills Neuroscience Institute at the University of California Berkeley told AFP.
"Most of the information in speech is between one to 8,000 hertz. Essentially the brain analyzes those different sound frequencies in somewhat separate locations."
By tracking how and where the brain registered sounds in the temporal lobe -- the center of the auditory system -- scientists were able to map out the words and then recreate them as heard by the brain.
"When a particular brain site is being activated, we know that roughly corresponds to some sound frequency that the patient is actually listening to," Pasley said.
"So we could map that out to an extent that would allow us to use that brain activity to resynthesize the sound from the frequencies we were guessing."
One word the researchers mapped was "structure." The high-frequency "s" sound showed up as a certain pattern in the brain, while the lower harmonics of the "u" sound appeared as a different pattern.
"There is to some extent a correspondence between these features of sound and the brain activity that they cause," and putting together the physical registry in the brain helped rebuild the words, Pasley explained.
The work builds on previous research in ferrets, in which scientists read to the animals and recorded their brain activity.
They were able to decode which words the creatures heard even though the ferrets themselves didn't understand the words.
The next step for researchers is to figure out just how similar the process of hearing sounds may be to the process of imagining words and sounds.
That information could one day help scientists determine what people want to say when they cannot physically speak.
Some previous research has suggested there may be similarities, but much more work needs to be done, Pasley said.
"This is huge for patients who have damage to their speech mechanisms because of a stroke or Lou Gehrig's disease and can't speak," co-author Robert Knight, a UC Berkeley professor of psychology and neuroscience, said in a statement.
"If you could eventually reconstruct imagined conversations from brain activity, thousands of people could benefit."
Participating researchers came from the University of Maryland, UC Berkeley and Johns Hopkins University in Baltimore, Maryland.

AstraZeneca Streamlining Brain R&D Activities, Closing Sites

LONDON (Dow Jones)--AstraZeneca PLC (AZN) said Thursday its need to cut costs had driven the difficult decision to carry out further restructuring -- a move which will see the drug maker reduce its financial exposure to research into disorders of the brain.
"While the patient need for better medicines in neuroscience is huge and the science is promising, advances in treatments have proved elusive for the pharmaceutical industry in recent years, despite significant investment," the company said, adding: "AstraZeneca believes that it will have the best chance of success in future by combining the company's internal expertise with innovative external science."
The move, part of the company's latest restructuring to rein in costs and shrink operations, is aimed at making "a simpler and more innovative R&D organization with a lower and more flexible cost base. Excess capacity in certain R&D functions will be reduced, matching resources to AstraZeneca's more focused R&D portfolio."
As a result, AstraZeneca will create a new "virtual" neuroscience Innovative Medicines unit made up of a small team of around 40 to 50 AstraZeneca scientists conducting discovery and development externally, through a network of some of the most innovative partners in academia and industry globally.
The team will be based in major neuroscience hubs - Boston, Massachusetts and Cambridge, England - and work closely with innovative partners such as the Karolinska Institute in Stockholm, Sweden.
Drug companies have always had difficulty making money from neuroscience, because researching the brain is a riskier enterprise, with lower successful hit rates and higher risks of failure than some other therapeutic areas.
AstraZeneca's head of R&D Martin Mackay said: "We've made an active choice to stay in neuroscience though we will work very differently to share cost, risk and reward with partners in this especially challenging but important field of medical research. The creation of a virtual neuroscience iMed will make us more agile scientifically and financially - we will be able to collaborate flexibly with the best scientific expertise, wherever it exists in the world."
Implementation of the plan will lead to a significant reduction in employee numbers and the end of R&D activity at two sites that are focused on neuroscience: Soedertaelje in Sweden and Montreal in Canada.
As the location of the company's largest manufacturing site, and the base of the commercial business covering the Scandinavian markets, Soedertälje remains an important part of the AstraZeneca network. The company's Montreal facility will close.
AstraZeneca said the latest restructuring in R&D will lead to the loss of around 2,200 positions globally.
The U.K.'s second-biggest drug maker said its latest phase of cost cutting would see the loss of around 7,300 jobs throughout the company and deliver a further $1.6 billion in annual savings by the end of 2014.
At 0935 GMT, AstraZeneca shares were down 3.4% or 105.5 pence at 2984p in a broadly lower London market.

Path Is Found for the Spread of Alzheimer’s

From left, Li Liu, Scott A. Small and Karen Duff examining a mouse brain. Dr. Small and Dr. Duff used mice to study Alzheimer's. 

Alzheimer’s disease seems to spread like an infection from brain cell to brain cell, two new studies in mice have found. But instead of viruses or bacteria, what is being spread is a distorted protein known as tau. 

The surprising finding answers a longstanding question and has immediate implications for developing treatments, researchers said. And they suspect that other degenerative brain diseases like Parkinson’s may spread in a similar way.

Alzheimer’s researchers have long known that dying, tau-filled cells first emerge in a small area of the brain where memories are made and stored. The disease then slowly moves outward to larger areas that involve remembering and reasoning.

But for more than a quarter-century, researchers have been unable to decide between two explanations. One is that the spread may mean that the disease is transmitted from neuron to neuron, perhaps along the paths that nerve cells use to communicate with one another. Or it could simply mean that some brain areas are more resilient than others and resist the disease longer.

The new studies provide an answer. And they indicate it may be possible to bring Alzheimer’s disease to an abrupt halt early on by preventing cell-to-cell transmission, perhaps with an antibody that blocks tau.

The studies, done independently by researchers at Columbia and Harvard, involved genetically engineered mice that could make abnormal human tau proteins, predominantly in the entorhinal (pronounced en-toh-RYE-nal) cortex, a sliver of tissue behind the ears, toward the middle of the brain, where cells first start dying in Alzheimer’s disease. As expected, tau showed up there. And, as also expected, entorhinal cortex cells in the mice started dying, filled with tangled, spaghettilike strands of tau.

Over the next two years, the cell death and destruction spread outward to other cells along the same network. Since those other cells could not make human tau, the only way they could get the protein was by transmission from nerve cell to nerve cell.

And that, said Dr. Samuel E. Gandy, associate director of the Alzheimer’s Disease Research Center at Mount Sinai School of Medicine in New York, was “very unexpected, very intriguing.”

Although the studies were in mice, researchers say they expect that the same phenomenon occurs in humans because the mice had a human tau gene and the progressive wave of cell death matched what they see in people with Alzheimer’s disease.

One study, by Karen Duff and Dr. Scott A. Small and their colleagues at the Taub Institute for Research on Alzheimer’s Disease and the Aging Brain at Columbia University Medical Center, was published on Wednesday in the journal PLoS One. The other, by Dr. Bradley T. Hyman, director of the Alzheimer’s Disease Research Center at Massachusetts General Hospital, and his colleagues, is to be published in the journal Neuron.

Both groups of researchers were inspired by the many observations over the years that Alzheimer’s starts in the entorhinal cortex and spreads.

But, said Dr. Small, “what do we mean by ‘spreads?’ ”

Researchers knew that something set off Alzheimer’s disease. The most likely candidate is a protein known as beta amyloid, which accumulates in the brain of Alzheimer’s patients, forming hard, barnaclelike plaques. But beta amyloid is very different from tau. It is secreted and clumps outside cells. Although researchers have looked, they have never seen evidence that amyloid spreads from cell to cell in a network.

Still, amyloid creates what amounts to a bad neighborhood in memory regions of the brain. Then tau comes in — some researchers call it “the executioner” — piling up inside cells and killing them. If some cells take longer than others to succumb to the bad neighborhood, that would explain the spread of the disease in the brain, and there would be no need to blame something odd, like the spread of tau from cell to cell.

Studies in humans, though, could not determine whether that hypothesis was correct. They involved autopsy and brain imaging studies and were “indirect and inconclusive,” Dr. Small said.

Looking at the brains of people who have died of the disease, Dr. Duff said, is like looking at a wrecked car and trying to figure out the accident’s cause. Faulty brakes? Broken struts?

The question of which hypothesis was correct — tau spreading cell to cell, or a bad neighborhood in the brain and cells with different vulnerabilities to it — remained unanswerable. Dr. Hyman said he tried for 25 years to find a good way to address it. One of his ideas was to find a patient or two who had had a stroke or other injury that severed the entorhinal cortex from the rest of the brain. If the patient developed Alzheimer’s in the entorhinal cortex — and it remained contained there — he would have evidence that the disease spread like an infection. But he never found such patients.

The solution came when researchers were able to develop genetically engineered mice that expressed abnormal human tau, but only in their entorhinal cortexes. Those mice offered the cleanest way to get an answer, said John Hardy, an Alzheimer’s researcher at University College London who was not involved in either of the new studies.

There is another advantage, too, Dr. Hyman said. The mice give him a tool to test ways to block tau’s spread — and that, he added, “is one of the things we’re excited about.”

But if tau spreads from neuron to neuron, Dr. Hardy said, it may be necessary to block both beta amyloid production, which seems to get the disease going, and the spread of tau, which continues it, to bring Alzheimer’s to a halt.

He and others are also asking if other degenerative diseases spread through the brain because proteins pass from nerve cell to nerve cell.

Dr. Hardy thought he saw provocative human evidence that it might be happening in Parkinson’s disease. Two Parkinson’s patients being treated by a colleague had fetal brain cells implanted to replace dead and dying neurons. When the patients died, years later, autopsies showed they still had the fetal cells, but they had balls of a Parkinson’s disease protein, synuclein, inside. The most obvious way that could happen, the researchers reasoned, was if the toxic protein had spread from the patient’s diseased cells to the healthy fetal cells. But they could not rule out the bad-neighborhood hypothesis.

Now, Dr. Hardy said, with the mouse studies, the issue of a bad neighborhood is settled. The answer in Alzheimer’s disease, he said, “is that isn’t possible.”

“That is what is different between these papers and all the others,” Dr. Hardy said. “It isn’t a bad neighborhood. It is contagion from one neuron to another.”

Could brain size determine whether you are good at maintaining friendships?

Being popular is linked to an ability to 'mind-read'

Researchers are suggesting that there is a link between the number of friends you have and the size of the region of the brain – known as the orbital prefrontal cortex – that is found just above the eyes.

A new study, published today in the journal Proceedings of the Royal Society B, shows that this brain region is bigger in people who have a larger number of friendships.
The research was carried out as part of the British Academy Centenary ‘Lucy to Language’ project, led by Professor Robin Dunbar of the University of Oxford in a collaboration with Dr Penny Lewis at The University of Manchester, Dr Joanne Powell and Dr Marta Garcia-Finana at Liverpool University, and Professor Neil Roberts at Edinburgh University.
The study suggests that we need to employ a set of cognitive skills to maintain a number of friends (and the keyword is ‘friends’ as opposed to just the total number of people we know). These skills are described by social scientists as ‘mentalising’ or ‘mind-reading’– a capacity to understand what another person is thinking, which is crucial to our ability to handle our complex social world, including the ability to hold conversations with one another. This study, for the first time, suggests that our competency in these skills is determined by the size of key regions of our brains (in particular, the frontal lobe).
Professor Dunbar, from the Institute of Cognitive and Evolutionary Anthropology, explained: “’Mentalising’ is where one individual is able to follow a natural hierarchy involving other individuals’ mind states. For example, in the play ‘Othello’, Shakespeare manages to keep track of five separate mental states: he intended that his audience believes that Iago wants Othello to suppose that Desdemona loves Cassio [the italics signify the different mind states]. Being able to maintain five separate individuals’ mental states is the natural upper limit for most adults.”
The researchers took anatomical MR images of the brains of 40 volunteers at the Magnetic Resonance and Image Analysis Research Centre at the University of Liverpool to measure the size of the prefrontal cortex, the part of the brain used in high-level thinking. Participants were asked to make a list of everyone they had had social, as opposed to professional, contact with over the previous seven days. They also took a test to determine their competency in mentalising.

Professor Dunbar said: “We found that individuals who had more friends did better on mentalising tasks and had more neural volume in the orbital frontal cortex, the part of the forebrain immediately above the eyes. Understanding this link between an individual’s brain size and the number of friends they have helps us understand the mechanisms that have led to humans developing bigger brains than other primate species. The frontal lobes of the brain, in particular, have enlarged dramatically in humans over the last half million years.”
Dr Penny Lewis, from the School of Psychological Sciences at The University of Manchester, said: “Both the number of friends people had and their ability to think about other people’s feelings predicted the size of this same small brain area. This not only suggests that we’ve found a region which is critical for sociality, it also shows that the link between brain anatomy and social success is much more direct than previously believed.”
Dr Joanne Powell, from the Department of Psychology, University of Liverpool, said: “Perhaps the most important finding of our study is that we have been able to show that the relationship between brain size and social network size is mediated by mentalising skills. What this tells us is that the size of your brain determines your social skills, and it is these that allow you to have many friends.”
Dr Lewis added: “This research is particularly important because it provides the strongest support to date for the social brain hypothesis – that is, the idea that human brains evolved to accommodate the social demands of living in a big group. Cross-species comparisons between various monkey brains have already supported this, but our work is some of the first to show that people with larger social groups actually have more neural matter in this particular bit of cortex. It looks as though size really does matter when it comes to social success.”

Positive reinforcement may boost kids' brains

ST. LOUIS — If your child forgets his lunch or struggles with school work, a little more loving might turn things around.
Supportive mothers who practice positive reinforcement seem to help their kids’ brains grow, according to new research from Washington University.
Brain scans show that school-age children of nurturing mothers have a 10 percent larger hippocampus — the region of the brain that plays a role in memory, learning and stress response — compared to the brains of children whose mothers were deemed less supportive.
The take-home message for working and stay-at-home parents is to praise children more than you scold them, the researchers said.
“Parents might feel guilty because they’re working, and we work a lot as well,” said Dr. Kelly Botteron, a professor of child psychiatry and co-author of the study. “But when you’re home in the evening and you’re trying to rush through homework and trying to get dinner ready, if you remember to say a couple nice, really positive things … I think a lot of parents could do that and it’s a practical thing that has very little risk to it.”
It’s long been known that orphans and other neglected children who are placed in loving homes can improve their behavior and health. And while a link between nurturing mothers and their offspring’s brain growth has been established in rats, the study is the first to show the same anatomical process in humans.
As part of their ongoing research on childhood depression, staff members watched how two groups of 92 children ages 3 to 5 interacted with their caregivers (usually mothers) during a stressful task. One group of children had symptoms of depression and the others were assigned to a control group.
For the task, the mothers were told to fill out a questionnaire. The child was given a wrapped present but told not to open it right away. The eight-minute “waiting task,” as it’s known, has previously been used by researchers as a reliable indicator of parental nurturing skills. The task is thought to simulate situations at home, such as a parent distracted by cooking dinner while the child needs to focus on homework.
Researchers who reviewed the taped interactions rated the mothers’ responses to their children’s behavior. Mothers received points each time they praised the child’s patience or offered encouragement to not open the gift.
The researchers acknowledged they’re not getting a complete picture of family life, especially if Mom was having a bad day. But they are confident that the results of the MRI brain scans on the kids, performed four years after the “waiting task,” indicate that children who have more supportive mothers also have bigger brains.
Children with less supportive mothers had a hippocampus volume that was 9.2 percent smaller than the children of more nurturing mothers. In children with depression, the effects of nurturing were not as positive, and the researchers think the disease process has a greater impact on their brain development.
The researchers plan to run second and third MRI brain scans on the children, who are now pre-teens, to watch for brain development over time.
Although the study wasn’t designed to look at fathers, foster parents or grandparents, the researchers said the positive effects of nurturing can come from any caregivers, which can be reasonably stretched to include teachers.
“If you know your child is in a difficult situation, to reinforce to them that you know it’s a hard situation but they’re doing such a great job, that’s the kind of parenting we would try to encourage,” Botteron said.
The researchers were careful to point out they’re not opposed to disciplining children or giving them boundaries.
“You should be supportive and nurturing, which is not the same as spoiling, and not the same as smothering,” said the study’s lead author Dr. Joan Luby, a professor of child psychiatry.
One local mom said it was exciting to hear that something she already believes in could have an effect on her children’s intellectual, and not just emotional, development.
“For a nurturing parent it’s both beautiful and frightening because many of us who spend a lot of nights wondering whether we’re doing everything we possibly can for our children, this falls into the category of one more thing to worry about,” said Danielle Smith of O’Fallon, Mo., who has two young children and writes the blog www.extraordinarymommy.com. “It sounds like a bonus to me but I have to embrace the idea that what I’m doing is enough.