Neuroscience

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Brain imaging study finds evidence of basis for caregiving impulse

March 16, 2012

 MRI brain scan

Distinct patterns of activity— which may indicate a predisposition to care for infants — appear in the brains of adults who view an image of an infant face — even when the child is not theirs, according to a study by researchers at the National Institutes of Health and in Germany, Italy, and Japan.

Seeing images of infant faces appeared to activate in the adult’s brains circuits that reflect preparation for movement and speech as well as feelings of reward.

The findings raise the possibility that studying this activity will yield insights into care giving behavior, but also in cases of child neglect or abuse.

"These adults have no children of their own. Yet images of a baby’s face triggered what we think might be a deeply embedded response to reach out and care for that child," said senior author Marc H. Bornstein, Ph.D., head of the Child and Family Research Section of the Eunice Kennedy Shriver National Institute of Child Health and Human Development, the NIH institute that collaborated on the study.

While the researchers recorded participants’ brain activity, the participants did not speak or move. Yet their brain activity was typical of patterns preceding such actions as picking up or talking to an infant, the researchers explained. The activity pattern could represent a biological impulse that governs adults’ interactions with small children.

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Combination treatment in mice shows promise for fatal neurological disorder in kids

March 15, 2012

In Batten disease, a rare but fatal neurodegenerative disorder in infants and children, proteins (shown in pink) accumulate in the brain and contribute to mental decline, paralysis and seizures. In mice with the infantile form of the disease, combination treatment with gene therapy and bone marrow transplantation reduced the buildup of proteins, dramatically increasing life span and improving motor function. Credit: Mark Sands, Ph.D

Infants with Batten disease, a rare but fatal neurological disorder, appear healthy at birth. But within a few short years, the illness takes a heavy toll, leaving children blind, speechless and paralyzed. Most die by age 5.

There are no effective treatments for the disease, which can also strike older children. And several therapeutic approaches, evaluated in mouse models and in young children, have produced disappointing results.

But now, working in mice with the infantile form of Batten disease, scientists at Washington University School of Medicine in St. Louis and Kings College London have discovered dramatic improvements in life span and motor function by treating the animals with gene therapy and bone marrow transplants.

The results are surprising, the researchers say, because the combination therapy is far more effective than either treatment alone. Gene therapy was moderately effective in the mice, and bone marrow transplants provided no benefit, but together the two treatments created a striking synergy.

The research is online in the Annals of Neurology.

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Stem Cells Hint at Potential Treatment for Huntington’s Disease
Huntington’s disease, the debilitating congenital neurological disorder that progressively robs patients of muscle coordination and cognitive ability, is a condition without effective treatment, a slow death sentence.
But if researchers can build on new research reported this week (March 15, 2012) in the journal Cell Stem Cell, a special type of brain cell forged from stem cells could help restore the muscle coordination deficits that cause the uncontrollable spasms characteristic of the disease.
“This is really something unexpected,” says Su-Chun Zhang, a University of Wisconsin-Madison neuroscientist and the senior author of the new study, which showed that locomotion could be restored in mice with a Huntington’s-like condition.
Zhang is an expert at making different types of brain cells from human embryonic or induced pluripotent stem cells. In the new study, his group focused on what are known as GABA neurons, cells whose degradation is responsible for disruption of a key neural circuit and loss of motor function in Huntington’s patients. GABA neurons, Zhang explains, produce a key neurotransmitter, a chemical that helps underpin the communication network in the brain that coordinates movement.
In the laboratory, Zhang and his colleagues at the UW-Madison Waisman Center have learned how to make large amounts of GABA neurons from human embryonic stem cells, which they sought to test in a mouse model of Huntington’s disease. The goal of the study, Zhang notes, was simply to see if the cells would safely integrate into the mouse brain. To their astonishment, the cells not only integrated but also project to the right target and effectively reestablished the broken communication network, restoring motor function.
The results of the study were surprising, Zhang explains, because GABA neurons reside in one part of the brain, the basal ganglia, which plays a key role in voluntary motor coordination. But the GABA neurons exert their influence at a distance on cells in the midbrain through the circuit fueled by the GABA neuron chemical neurotransmitter.
“This circuitry is essential for motor coordination,” Zhang says, “and it is what is broken in Huntington patients. The GABA neurons exert their influence at a distance through this circuit. Their cell targets are far away.”
That the transplanted cells could effectively reestablish the circuit was completely unexpected: “Many in the field feel that successful cell transplants would be impossible because it would require rebuilding the circuitry. But what we’ve shown is that the GABA neurons can remake the circuitry and produce the right neurotransmitter.”
The implications of the new study are important not only because they suggest it may one day be possible to use cell therapy to treat Huntington’s, but also because it suggests the adult brain may be more malleable than previously believed.
The adult brain, notes Zhang, is considered by neuroscientists to be stable, and not easily susceptible to therapies that seek to correct things like the broken circuits at the root of conditions like Huntington’s. For a therapy to work, it has to be engineered so that only cells of interest are affected. “The brain is wired in such a precise way that if a neuron projects the wrong way, it could be chaotic.”
Zhang stresses that while the new research is promising, working up from the mouse model to human patients will take much time and effort. But for a disease that now has no effective treatment, the work could become the next best hope for those with Huntington’s.
Article by Terry Devitt
Source: Neuroscience News

Stem Cells Hint at Potential Treatment for Huntington’s Disease

Huntington’s disease, the debilitating congenital neurological disorder that progressively robs patients of muscle coordination and cognitive ability, is a condition without effective treatment, a slow death sentence.

But if researchers can build on new research reported this week (March 15, 2012) in the journal Cell Stem Cell, a special type of brain cell forged from stem cells could help restore the muscle coordination deficits that cause the uncontrollable spasms characteristic of the disease.

“This is really something unexpected,” says Su-Chun Zhang, a University of Wisconsin-Madison neuroscientist and the senior author of the new study, which showed that locomotion could be restored in mice with a Huntington’s-like condition.

Zhang is an expert at making different types of brain cells from human embryonic or induced pluripotent stem cells. In the new study, his group focused on what are known as GABA neurons, cells whose degradation is responsible for disruption of a key neural circuit and loss of motor function in Huntington’s patients. GABA neurons, Zhang explains, produce a key neurotransmitter, a chemical that helps underpin the communication network in the brain that coordinates movement.

In the laboratory, Zhang and his colleagues at the UW-Madison Waisman Center have learned how to make large amounts of GABA neurons from human embryonic stem cells, which they sought to test in a mouse model of Huntington’s disease. The goal of the study, Zhang notes, was simply to see if the cells would safely integrate into the mouse brain. To their astonishment, the cells not only integrated but also project to the right target and effectively reestablished the broken communication network, restoring motor function.

The results of the study were surprising, Zhang explains, because GABA neurons reside in one part of the brain, the basal ganglia, which plays a key role in voluntary motor coordination. But the GABA neurons exert their influence at a distance on cells in the midbrain through the circuit fueled by the GABA neuron chemical neurotransmitter.

“This circuitry is essential for motor coordination,” Zhang says, “and it is what is broken in Huntington patients. The GABA neurons exert their influence at a distance through this circuit. Their cell targets are far away.”

That the transplanted cells could effectively reestablish the circuit was completely unexpected: “Many in the field feel that successful cell transplants would be impossible because it would require rebuilding the circuitry. But what we’ve shown is that the GABA neurons can remake the circuitry and produce the right neurotransmitter.”

The implications of the new study are important not only because they suggest it may one day be possible to use cell therapy to treat Huntington’s, but also because it suggests the adult brain may be more malleable than previously believed.

The adult brain, notes Zhang, is considered by neuroscientists to be stable, and not easily susceptible to therapies that seek to correct things like the broken circuits at the root of conditions like Huntington’s. For a therapy to work, it has to be engineered so that only cells of interest are affected. “The brain is wired in such a precise way that if a neuron projects the wrong way, it could be chaotic.”

Zhang stresses that while the new research is promising, working up from the mouse model to human patients will take much time and effort. But for a disease that now has no effective treatment, the work could become the next best hope for those with Huntington’s.

Article by Terry Devitt

Source: Neuroscience News

Filed under science neuroscience psychology brain disease

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A Wandering Mind Reveals Mental Processes and Priorities

ScienceDaily (Mar. 15, 2012) — Odds are, you’re not going to make it all the way through this article without thinking about something else. In fact, studies have found that our minds are wandering half the time, drifting off to thoughts unrelated to what we’re doing — did I remember to turn off the light? What should I have for dinner?

Odds are, you’re not going to make it all the way through this article without thinking about something else. In fact, studies have found that our minds are wandering half the time, drifting off to thoughts unrelated to what we’re doing — did I remember to turn off the light? What should I have for dinner? (Credit: © Yuri Arcurs / Fotolia)

A new study investigating the mental processes underlying a wandering mind reports a role for working memory, a sort of a mental workspace that allows you to juggle multiple thoughts simultaneously.

Imagine you see your neighbor upon arriving home one day and schedule a lunch date. On your way to add it to your calendar, you stop to turn off the drippy faucet, feed the cat, and add milk to your grocery list. The capacity that allows you to retain the lunch information through those unrelated tasks is working memory.

The new study, published online March 14 in the journal Psychological Science by Daniel Levinson and Richard Davidson at the University of Wisconsin-Madison and Jonathan Smallwood at the Max Planck Institute for Human Cognitive and Brain Science, reports that a person’s working memory capacity relates to the tendency of their mind to wander during a routine assignment. Lead author Levinson is a graduate student with Davidson, a professor of psychology and psychiatry, in the Center for Investigating Healthy Minds at the UW-Madison Waisman Center.

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Loss of Appetite Deciphered in Brain Cell Circuit

ScienceDaily (Mar. 14, 2012) — The meal is pushed way, untouched. Loss of appetite can be a fleeting queasiness or continue to the point of emaciation. While it’s felt in the gut, more is going on inside the head.

New findings are emerging about brain and body messaging pathways that lead to loss of appetite, and the systems in place to avoid starvation.

Today, scientists report in Nature about a brain circuit that mediates the loss of appetite in mice. The researchers also discovered potential therapeutic targets within the pathway. Their experimental results may be valuable for developing new treatments for a variety of eating disorders. These include unrelenting nausea, food aversions, and anorexia nervosa, a condition in which a person no longer wants to eat enough to maintain a normal weight.

The senior author of the paper is Dr. Richard D. Palmiter, University of Washington professor of biochemistry and an investigator with the Howard Hughes Medical Institute. His co-authors are Dr. Qi Wu, formerly of the UW and now at the Eagles Diabetes Research Center and Department of Pharmacology at Carver College of Medicine, University of Iowa, and Dr. Michael S. Clark of the UW Department of Psychiatry and Behavioral Sciences. Palmiter is known for co-developing the first transgenic mice in the 1980s with Dr. Ralph Brinster at the University of Pennsylvania. His more recent studies are of chemicals that nerve cells use to communicate with each other, their roles in mouse brain development and function, and their relation to behavior.

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'Brain Fog' of Menopause Confirmed

ScienceDaily (Mar. 14, 2012) — The difficulties that many women describe as memory problems when menopause approaches are real, according to a study published recently  in the journal Menopause, the journal of the North American Menopause Society.

The findings won’t come as a surprise to the millions of women who have had bouts of forgetfulness or who describe struggles with “brain fog” in their late 40s and 50s. But the results of the study, by scientists at the University of Rochester Medical Center and the University of Illinois at Chicago who gave women a rigorous battery of cognitive tests, validate their experiences and provide some clues to what is happening in the brain as women hit menopause.

"The most important thing to realize is that there really are some cognitive changes that occur during this phase in a woman’s life," said Miriam Weber, Ph.D., the neuropsychologist at the University of Rochester Medical Center who led the study. "If a woman approaching menopause feels she is having memory problems, no one should brush it off or attribute it to a jam-packed schedule. She can find comfort in knowing that there are new research findings that support her experience. She can view her experience as normal."

The study is one of only a handful to analyze in detail a woman’s brain function during menopause and to compare those findings to the woman’s own reports of memory or cognitive difficulties.

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REM Sleep Disorder Doubles Risk of Mild Cognitive Impairment, Parkinson’s, Study Finds

ScienceDaily (Mar. 14, 2012) — People with symptoms suggesting rapid eye movement sleep behavior disorder, or RBD, have twice the risk of developing mild cognitive impairment (MCI) or Parkinson’s disease within four years of diagnosis with the sleep problem, compared with people without the disorder, a Mayo Clinic study has found.

The researchers published their findings recently in the Annals of Neurology.

One of the hallmarks of rapid eye movement (REM) sleep is a state of paralysis. In contrast, people with rapid eye movement sleep behavior disorder, appear to act out their dreams when they are in REM sleep. Researchers used the Mayo Sleep Questionnaire to diagnose probable RBD in people who were otherwise neurologically normal. Approximately 34 percent of people diagnosed with probable RBD developed MCI or Parkinson’s disease within four years of entering the study, a rate 2.2 times greater than those with normal rapid eye movement sleep.

"Understanding that certain patients are at greater risk for MCI or Parkinson’s disease will allow for early intervention, which is vital in the case of such disorders that destroy brain cells. Although we are still searching for effective treatments, our best chance of success is to identify and treat these disorders early, before cell death," says co-author Brad Boeve, M.D., a Mayo Clinic neurologist.

Previous studies of Mayo Clinic patients have shown that an estimated 45 percent of people who suffer from RBD will develop a neurodegenerative syndrome such as mild cognitive impairment or Parkinson’s disease within five years of diagnosis.

RBD, MCI and Parkinson’s Disease

"This study is the first to quantify the risk associated with probable RBD in average people, not clinical patients, and it shows that we can predict the onset of some neurodegenerative disorders simply by asking a few critical questions," says lead author Brendon P. Boot, M.D., a behavioral neurologist. Dr. Boot was at Mayo Clinic when the study was conducted. He is now at Harvard University.

  • MCI is an intermediate stage between the expected cognitive decline of normal aging and the more pronounced decline of dementia. It involves problems with memory, language, thinking and judgment that are greater than typical age-related changes.
  • An estimated 500,000 Americans suffer from Parkinson’s disease, which is characterized by tremor or shakiness, stiffness of the limbs and trunk, slowness of movement, and impaired balance and coordination. 

Source: Science Daily

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Few Genes Control Neuronal Function

ScienceDaily (Mar. 14, 2012) — How are 100 billion cells created, each with specific duties? The human brain is evidence that nature can achieve this. Researchers at Linköping University in Sweden have now taken a step closer to solving this mystery.

The magenta-colored structures are nerve cells that use odourant receptor 47b, which senses pheromones. Expression of this receptor is controlled by the transcription factor E93. When E93 is removed, the neurons lose their ability to fulfill their task do detect pheromones, as evidenced by the deactivation of the fluorescent proteins (image to the right). The glowing, green cells, that use olfactory receptor 92a, are not affected because they are controlled by other transcription factors. (Credit: Image courtesy of Linkoeping Universitet)

"Knowledge about the mechanisms that diversify neurons and keep them diverse is necessary in order to cultivate and replace nerve cells in the future," says Mattias Alenius, Assistant Professor of Neuroscience, who has published his research breakthrough in the current issue of the journal PLoS Biology.

Alenius and his research team at the Department of Experimental and Clinical Medicine seek the answer to this pivotal question from a smaller perspective: the fruit fly’s olfactory system.

The humble fly’s olfactory system consists of 1200 olfactory neurons (humans have six million) divided into 34 groups. Each group responds to a particular set of odours, since all the neurons of the group use only one of the olfactory receptors present in the fly’s antennas. Together, the receptors provide the fly with the ability to distinguish between thousands of odours: one olfactory receptor — one neuron group, simple yet complex.

Alenius and his colleagues are the first to go through all of the fruit fly’s 753 gene regulatory genes, called transcription factors. They have identified a set of seven that, in different combinations, are required to create each of the 34 neuron groups in the antenna. A surprising finding is that most transcription factors perform two tasks simultaneously: they can activate odorant receptors’ expression; while at the same time turning off others in the same cell.

Alenius explains, “This is one of the many tricks that are useful to know for the future if you want to make and cultivate each of the many thousands of nerve cell groups that make up our brains.”

Source: Science Daily

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Evidence builds that meditation strengthens the brain, researchers say

March 14, 2012

Earlier evidence out of UCLA suggested that meditating for years thickens the brain (in a good way) and strengthens the connections between brain cells. Now a further report by UCLA researchers suggests yet another benefit.

Eileen Luders, an assistant professor at the UCLA Laboratory of Neuro Imaging, and colleagues, have found that long-term meditators have larger amounts of gyrification (“folding” of the cortex, which may allow the brain to process information faster) than people who do not meditate. Further, a direct correlation was found between the amount of gyrification and the number of meditation years, possibly providing further proof of the brain’s neuroplasticity, or ability to adapt to environmental changes.

The article appears in the online edition of the journal Frontiers in Human Neuroscience.

The cerebral cortex is the outermost layer of neural tissue. Among other functions, it plays a key role in memory, attention, thought and consciousness. Gyrification or cortical folding is the process by which the surface of the brain undergoes changes to create narrow furrows and folds called sulci and gyri. Their formation may promote and enhance neural processing. Presumably then, the more folding that occurs, the better the brain is at processing information, making decisions, forming memories and so forth.

"Rather than just comparing meditators and non-meditators, we wanted to see if there is a link between the amount of meditation practice and the extent of brain alteration," said Luders. "That is, correlating the number of years of meditation with the degree of folding."

The researchers took MRI scans of 50 meditators, 28 men and 22 women, and compared them to 50 control subjects matched for age, handedness and sex. The scans for the controls were obtained from an existing MRI database, while the meditators were recruited from various meditation venues. The meditators had practiced their craft on average for 20 years using a variety of meditation types — Samatha, Vipassana, Zen and more. The researchers applied a well-established and automated whole-brain approach to measure cortical gyrification at thousands of points across the surface of the brain.

They found pronounced group differences (heightened levels of gyrification in active meditation practitioners) across a wide swatch of the cortex, including the left precentral gyrus, the left and right anterior dorsal insula, the right fusiform gyrus and the right cuneus.

Perhaps most interesting, though, was the positive correlation between the number of meditation years and the amount of insular gyrification.

"The insula has been suggested to function as a hub for autonomic, affective and cognitive integration," said Luders. "Meditators are known to be masters in introspection and awareness as well as emotional control and self-regulation, so the findings make sense that the longer someone has meditated, the higher the degree of folding in the insula."

While Luders cautions that genetic and other environmental factors could have contributed to the effects the researchers observed, still, “The positive correlation between gyrification and the number of practice years supports the idea that meditation enhances regional gyrification.”

Provided by University of California - Los Angeles

Source: medicalxpress.com

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Aging brain gets stuck in time, researchers show

March 14, 2012 By Bill Hathaway

The aging brain loses its ability to recognize when it is time to move on to a new task, explaining why the elderly have difficulty multi-tasking, Yale University researchers report.

“The aged brain seems to get lost in transition,” said Mark Laubach, associate professor at the John B. Pierce Laboratory and the Yale School of Medicine, and senior author of a study that appears in the March 14 issue of The Journal of Neuroscience.

Laubach’s team was studying the impact of aging on working memory, the type of memory that allows you to recall that dinner is in the oven when you are talking on the phone. The researchers examined brain activity in the medial prefrontal cortex of young and older rats that is related to spatial working memory — the type of memory that allows you to recall, for example, that mashed potatoes are on the stove and the turkey is in the oven

Based on previous studies, they expected that it would be spatial memory most affected by aging. Instead, the Yale team found that the aged brain seems to lose its ability to respond to cues that indicate when it is time to move on to a new task.

This ability to transition between tasks is critical for many daily activities, such as cooking dinner or handling situations that can arise in the workplace. The brain’s failure to monitor the timing of actions leads people to forget to turn off a burner on the stove while setting the table.

The research team found that neurons in the medial prefrontal cortex of older rats reacted more slowly to signals indicating that reward was available. Conversely, these signals immediately triggered a response in younger rats.

“Neurons in older rats fired fewer spikes in response to reward-predictive cues. The animals failed to respond immediately to the cues. They seemed to be stuck in time,” Laubach said.

Researchers hope that by understanding the mechanisms of working memory, scientists might one day be able to slow or perhaps eliminate deterioration of these brain functions over a lifespan, Laubach said.

Provided by Yale University

Source: medicalxpress.com

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