Posts tagged neuroscience

ScienceDaily (May 22, 2012) — When brain cells start oozing too much of the amyloid protein that is the hallmark of Alzheimer’s disease, the astrocytes that normally nourish and protect them deliver a suicide package instead, researchers report.

Drs. Michael Dinkins (from left), Guanghu Wang and Erhard Bieberich. (Credit: Image courtesy of Georgia Health Sciences University)

Amyloid is excreted by all neurons, but rates increase with aging and dramatically accelerate in Alzheimer’s. Astrocytes, which deliver blood, oxygen and nutrients to neurons in addition to hauling off some of their garbage, get activated and inflamed by excessive amyloid.

Now researchers have shown another way astrocytes respond is by packaging the lipid ceramide with the protein PAR-4, which independently can do damage but together are a more “deadly duo,” said Dr. Erhard Bieberich, biochemist at the Medical College of Georgia at Georgia Health Sciences University.

"If the neuron makes something toxic and dumps it at your door, what would you do?" said Bieberich, corresponding author of the study published in the Journal of Biological Chemistry. “You would probably do something to defend yourself.”

The researchers hypothesize that this lipid-coated package ultimately kills them both, which could help explain the brain-cell death and shrinkage that occurs in Alzheimer’s. “If the astrocytes die, the neurons die,” Bieberich said, noting studies suggest that excess amyloid alone does not kill brain cells. “There must be a secondary process toxifying the amyloid; otherwise the neuron would self-intoxicate before it made a big plaque,” he said. “The neuron would die first.”

One of many avenues for future pursuit include whether a ceramide antibody could be a viable Alzheimer’s treatment. In the researchers’ studies of brain cells of humans with Alzheimer’s as well as an animal model of the disease, antibodies to ceramide and Par-4 prevented astrocytes’ amyloid-induced death.

Ceramide and Par-4 get packaged in lipid-coated vesicles called exosomes; all cells secrete thousands of these vesicles but scientists are only beginning to understand their normal function. When exosomes become deadly, they are called apoxosomes.

Ceramide and Par-4 are typically not in a vesicle, rather in two distinct parts of a cell. Ceramide appears to take the lead in bringing the two together when confronted with amyloid. Bieberich and colleagues at the University of Georgia reported in 2003 that the deadly duo helps eliminate duplicate brain cells that occur early in brain development when their survival could result in a malformed brain. They suspected then that the duo might also have a role in Alzheimer’s.

Risk factors for Alzheimer’s include aging, family history and genetics, according to the Alzheimer’s Association. Increasing evidence suggests that Alzheimer’s also shares many of the same risk factors for cardiovascular disease, such as high cholesterol, high blood pressure and inactivity.

Source: Science Daily

May 22, 2012

(Medical Xpress) — Researchers at the Institut Pasteur and the CNRS have recently identified in mice the role played by neo-neurons formed in the adult brain. By using selective stimulation the researchers were able to show that these neo-neurons increase the ability to learn and memorize difficult cognitive tasks. This newly discovered characteristic of neo-neurons to assimilate complex information could open up new avenues in the treatment of some neurodegenerative diseases. This publication is available online on the Nature Neuroscience journal’s website.

Section of a mouse brain observed using a fluorescence microscope. The green filaments represent neo-neurons in an organized network. Credit: Institut Pasteur

The discovery that new neurons could be formed in the adult brain created quite a stir in 2003 by debunking the age-old belief that a person is born with a set number of neurons and that any loss of neurons is irreversible. This discovery was all the more incredible considering that the function of these new neurons remained undetermined. That is, until today.

Using mice models the team working under Pierre-Marie Lledo, head of the Laboratory for Perception and Memory (Institut Pasteur/CNRS) recently revealed the role of these neo-neurons formed in the adult brain with respect to learning and memory. With the help of an experimental approach using optogenetics, developed by this very same team and published in December 2010, the researchers were able to show that when stimulated by a brief flash of light these neo-neurons facilitate both learning and the memorization of complex tasks. This resulted in mice models that were able to memorize information given during the learning activity more quickly and remember exercises even 50 days after experimentation had ended. The study also shows that neo-neurons generated just after birth hold no added advantages as relates to either learning or memory. In this respect it is only the neurons produced by the adult brain that have any considerable significance.

“This study shows that the activity of just a few neurons produced in the adult brain can still have considerable effects on cognitive processes and behavior. Moreover, this work helps to illustrate how the brain assimilates new stimulations seeing as normally electrical activity (which we mimic using flashes of light) is produced within the brain’s attention centers”, explains the study’s director Pierre-Marie Lledo.

Beyond simply discovering the functional contribution of these neo-neurons, the study has also reaffirmed the clear link between “mood” (defined here by a specific pattern of stimulation) and cerebral activity. It has been shown that curiosity, attentiveness and pleasure all promote the formation of neo-neurons and consequently the acquisition of new cognitive abilities. Conversely, a state of depression is detrimental to the production of new neurons and triggers a vicious cycle which prolongs this state of despondency. These results, and the optogenetics technologies that enabled this study, may prove very useful for devising therapeutic protocols which aim to counter the development of neurologic or psychiatric diseases.

Provided by CNRS

Source: medicalxpress.com

May 22, 2012

University of Georgia researchers have developed a map of the human brain that shows great promise as a new guide to the inner workings of the body’s most complex and critical organ.

With this map, researchers hope to create a next-generation brain atlas that will be an alternative option to the atlas created by German anatomist Korbinian Brodmann more than 100 years ago, which is still commonly used in clinical and research settings.

Tianming Liu, assistant professor of computer science in the UGA Franklin College of Arts and Sciences, and his students Dajiang Zhu and Kaiming Li identified 358 landmarks throughout the brain related to memory, vision, language, arousal regulation and many other fundamental bodily operations. Their findings were published in the April issue of Cerebral Cortex.

The landmarks were discovered using diffusion tensor imaging, a sophisticated neuroimaging technique that allows scientists to visualize nerve fiber connections throughout the brain. Unlike many other neuroimaging studies, their map does not focus only on one section of the brain but rather the whole cerebral cortex.

"Previously, researchers would examine at most three or four small brain networks," Liu said. "We want to examine the whole brain connection, and this is the so-called connectome."

The new map provides a clearer picture of how different areas of the brain are physically connected and how these connections relate to basic brain function. Liu and his team examined hundreds of healthy young adults to establish the landmarks, which they call dense individualized and common connectivity-based cortical landmarks, or DICCCOL.

After extensive testing and comparison, the team determined that these nodes are present in every normal brain, meaning they can be used as a basis of comparison for those with damaged brain tissue or altered brain function.

"DICCCOL is very similar to a GPS system," Zhu said, "only it’s a GPS map of the human brain."

Now, thanks in part to a five-year, $1.6 million grant from the National Institutes of Health, Liu and collaborators Xiaoping Hu and Claire Coles at Emory University are preparing to test their brain map by comparing healthy brains with those of children whose brains were damaged by exposure to cocaine while in the womb.

Prenatal cocaine exposure, or PCE, can cause serious damage to brain networks. Because of this, analysis of the damage provides Liu and his team with an excellent opportunity to evaluate the usefulness of their map.

After comparing the PCE brains to those of healthy individuals, they hope to determine the segments of the brain responsible for physical or mental disabilities observed in children exposed to cocaine.

"The PCE brain is disrupted in a systematic way; the whole brain is wrongly wired," Liu said. "We want to test our map in one of the worst cases, and then we will know if it will work in other cases."

Once the robustness of their map is established, Liu and his team hope that it may prove useful in the evaluation of many other brain disorders, such as Alzheimer’s disease, Parkinson’s disease or stroke.

"This really is a fundamental technology," Liu said. "When we establish these DICCCOLS, we can very easily extend this project to other populations, to other brain diseases."

More information: Liu’s team published their DICCCOL data sets, which includes the source code and diffusion tensor images, at http://dicccol.cs.uga.edu so other researchers may use the findings in their own experiments.

The article, “DICCCOL: Dense Individualized and Common Connectivity-Based Cortical Landmarks,” is available at http://cercor.oxfordjournals.org/content/early/2012/04/05/cercor.bhs072.short

Provided by University of Georgia

Source: medicalxpress.com

ScienceDaily (May 21, 2012) — Seventy-two percent of teenagers participating in a study experienced reduced hearing ability following exposure to a pop rock performance by a popular female singer.

Seventy-two percent of teenagers participating in a study experienced reduced hearing ability following exposure to a pop rock performance by a popular female singer. (Credit: © DWP / Fotolia)

M. Jennifer Derebery, MD, House Clinic physician, along with the House Research Institute tested teens’ hearing before and after a concert and presented the study findings at the American Otologic Society meeting on April 21, 2012. The study has been accepted for publication in an upcoming issue of Otology & Neurotology.

The hearing loss that may be experienced after a pop rock concert is not generally believed to be permanent. It is called a temporary threshold shift and usually disappears within 16-48 hours, after which a person’s hearing returns to previous levels.

“Teenagers need to understand a single exposure to loud noise either from a concert or personal listening device can lead to hearing loss,” said M. Jennifer Derebery, MD, lead author and physician at the House Clinic. “With multiple exposures to noise over 85 decibels, the tiny hair cells may stop functioning and the hearing loss may be permanent.”

In the study, twenty-nine teenagers were given free tickets to a rock concert. To ensure a similar level of noise exposure for the teens, there were two blocks of seats within close range of each other. The seats were located in front of the stage at the far end of the venue approximately 15-18 rows up from the floor.

Parental consent was obtained for all of the underage study participants. The importance of using hearing protection was explained to the teenagers. Researchers then offered hearing protection to the subjects and encouraged them to use the foam ear plugs. However, only three teenagers chose to do so.

Three adult researchers sat with the teenagers. Using a calibrated sound pressure meter, 1,645 measurements of sound decibel (dBA) levels were recorded during the 26 songs played during the three hour concert. The sound levels ranged from 82-110 dBA, with an average of 98.5 dBA. The mean level was greater than 100 dBA for 10 of the 26 songs.

The decibel levels experienced at the concert exceeded what is allowable in the workplace, according to Occupational Safety and Health Administration (OSHA). OSHA safe listening guidelines set time limits for exposures to sound levels of 85 dB and greater in the workplace. The volumes recorded during the concert would have violated OSHA standards in less than 30 minutes. In fact, one third of the teen listeners showed a temporary threshold shift that would not be acceptable in adult workplace environments.

Following the concert, the majority of the study participants also were found to have a significant reduction in the Distortion Product Otoacoustic Emissions (OAE) test. This test checks the function of the tiny outer hair cells in the inner ear that are believed to be the most vulnerable to damage from prolonged noise exposure, and are crucial to normal hearing, the ability to hear soft (or low level sounds), and the ability to understand speech, especially in noisy environments. With exposure to loud noise, the outer hair cells show a reduction in their ability to function, which may later recover. However, it is known that with repeated exposure to loud noise, the tiny hair cells may become permanently damaged. Recent animal research suggests that a single exposure to loud noise may result in permanent damage to the hearing nerve connections themselves that are necessary to hear sound.

Following the concert, 53.6 percent of the teens said they did not think they were hearing as well after the concert. Twenty-five percent reported they were experiencing tinnitus or ringing in their ears, which they did not have before the concert.

Researchers are especially concerned, because in the most recent government survey on health in the United States National Health and Nutrition Examination Survey (NHANES) 2005-2006, 20% of adolescents were found to have at least slight hearing loss, a 31% increase from a similar survey done from 1988-1994.

The findings of the study clearly indicate more research is necessary to determine if the guidelines for noise exposure need to be revised for teenagers. More research is also needed to determine if teenager’s ears are more sensitive to noise than adults.

“It also means we definitely need to be doing more to ensure the sound levels at concerts are not so loud as to cause hearing loss and neurological damage in teenagers, as well as adults,” said Derebery. “Only 3 of our 29 teens chose to use ear protection, even when it was given to them and they were encouraged to do so. We have to assume this is typical behavior for most teen listeners, so we have the responsibility to get the sound levels down to safer levels.”

Researchers recommend teenagers and young adults take an active role in protecting their hearing by utilizing a variety of sound meter ‘apps’ available for smart phones. The sound meters will give a rough estimate of the noise level allowing someone to take the necessary steps to protect their hearing such as wearing ear plugs at a concert.

In addition, Derebery and the study co-authors would like to see concert promoters and the musicians themselves take steps to lower sound levels as well as encourage young concert goers to use hearing protection.

Source: Science Daily

ScienceDaily (May 21, 2012) — Turns out it’s not bad being top dog, or in this case, top baboon.

Wounded baboon. (Credit: Image courtesy of University of Notre Dame)

A new study by University of Notre Dame biologist Beth Archie and colleagues from Princeton and Duke Universities finds that high-ranking male baboons recover more quickly from injuries and are less likely to become ill than other males.

Archie, Jeanne Altmann of Princeton and Susan Alberts of Duke examined health records from the Amboseli Baboon Research Project in Kenya. They found that high rank is associated with faster wound healing. The finding is somewhat surprising, given that top-ranked males also experience high stress, which should suppress immune responses. They also found that social status is a better predictor of wound healing than age.

"In humans and animals, it has always been a big debate whether the stress of being on top is better or worse than the stress of being on the bottom," said Archie, lead researcher on the study. "Our results suggest that, while animals in both positions experience stress, several factors that go along with high rank might serve to protect males from the negative effects of stress."

"The power of this study is in identifying the biological mechanisms that may confer health benefits to high-ranking members of society," said George Gilchrist, program director in the National Science Foundation (NSF)’s Division of Biology, which funded the research. "We know that humans have such benefits, but it took meticulous long-term research on baboon society to tease out the specific mechanisms. The question remains of causation: Is one a society leader because of stronger immune function or vice versa?"

The researchers examined 27 years of data on naturally occurring illness and injuries in wild male baboons, which is a notably large data set. Although research of health and disease in animals in laboratory settings has been quite extensive, this study is one of most comprehensive ever conducted on animals in a natural setting.

The research team investigated how differences in age, physical condition, stress, reproductive effort and testosterone levels contribute to status-related differences in immune functions. Previous research found that high testosterone levels and intense reproductive efforts can suppress immune function and are highest among high-ranking males.

However, Archie and her colleagues found that high-ranking males were less likely to become ill and recovered faster from injuries and illnesses than low-ranking males. The authors suggest that chronic stress, old age and poor physical condition associated with low rank may suppress immune function in low-ranking males.

"The complex interplay among social context, physiology and immune system-mediated health costs and benefits illustrates the power of interdisciplinary research," said Carolyn Ehardt, NSF program director for biological anthropology, which co-funded the research. "This research begins to tease apart the trade-offs in both high and low status in primates, including ourselves, which may lead to understanding the effects of social status on death and disease — not inconsequential for society as a whole."

Source: Science Daily

ScienceDaily (May 21, 2012) — Johns Hopkins scientists have discovered a protein that appears to play an important regulatory role in deciding whether stem cells differentiate into the cells that make up the brain, as well as countless other tissues. This finding, published in the April Developmental Cell, could eventually shed light on developmental disorders as well as a variety of conditions that involve the generation of new neurons into adulthood, including depression, stroke, and posttraumatic stress disorder.

Researchers have long known that a small group of proteins called Notch plays a pivotal role in helping the immature cells present in embryos to develop into the variety of cells present throughout the body, including those that make up the brain, blood, kidneys and muscles.

"Notch signaling is involved in almost all aspects of tissue development," explains study leader Valina Dawson, Ph.D., a professor in the departments of Neurology, Neuroscience, and Physiology and co-director of the Stem Cell and Neuroregeneration Programs at the Institute for Cell Engineering at the Johns Hopkins University School of Medicine.

However, she says, even for researchers who have been studying Notch for decades, how this small group of proteins manages the development of such a diverse array of tissues and organs in the body remains unknown. It’s a pivotal mystery to solve, Dawson adds, since problems in Notch signaling seem to be involved in various cancers, Alzheimer’s disease, juvenile stroke and many other health problems.

In their new study, Dawson and her colleagues shed light on one way Notch proteins might be regulated, through a protein they recently discovered in the lab. This protein seemed to be involved in development, but at first, the researchers didn’t know its function.

To determine what purpose this protein serves in cells, Dawson, postdoctoral fellow Zhikai Chi, M.D., Ph.D., and their colleagues started by trying to determine what other proteins it’s able to bind to. By adding the mystery protein to cell cultures that expressed a variety of other proteins, they determined that the unknown protein altered cellular activity in those expressing Notch.

Since Notch is involved intimately in determining the fate of brain precursor cells, driving neural stem cells to proliferate and determining whether they become neurons or supporting cells known as glia, the researchers next examined how this mystery protein affected brain development in mouse embryos. They found that by increasing expression of the unknown protein, more neurons developed in certain parts of the developing brain, including the intermediate zone and cortical plate. In contrast, decreasing expression led to fewer neurons. Taken together, Dawson says, these experiments provided even more evidence that their unknown protein was somehow influencing Notch.

To determine exactly how the mystery protein was affecting Notch, the researchers examined the effect of the protein on neural stem cells in the process of differentiating into mature cell types. Increasing the amount of the unknown protein swayed development as if Notch wasn’t working. Since the unknown protein appeared to prevent Notch from acting on cells, the researchers named it Botch for “blocks Notch.”

With Botch’s role now clear, the researchers turned next to the mechanism behind how this protein exerts its influence. A series of experiments suggests that Botch interacts with Notch in the Golgi body, a cellular organelle involved in modifying proteins. For Notch to act in development, an immature version of this protein needs to be cleaved in order for the protein to be rearranged. Botch appears to prevent this pivotal modification from taking place, reducing the amount of mature Notch available to do its job.

Because Botch appears to play such an important role in regulating Notch, Dawson says, it could be involved in a number of diseases in which the generation of new neurons is misregulated. She and her colleagues are already performing some preliminary experiments to determine whether Botch expression might vary from the norm in diseases such as depression, which has been linked to a decrease in neurogenesis in the brain’s hippocampus. Eventually, researchers might be able to develop drugs that act on Botch to restart stalled neurogenesis, potentially treating depression and other diseases in which a lack of neurogenesis is thought to play a role.

"There are potentially some very large neurological problems that could be addressed through changing Botch activity," Dawson says.

Source: Science Daily

May 21, 2012

New nerve cells formed in a select part of the brain could hold considerable sway over how much you eat and consequently weigh, new animal research by Johns Hopkins scientists suggests in a study published in the May issue of Nature Neuroscience.

The idea that the brain is still forming new nerve cells, or neurons, into adulthood has become well-established over the past several decades, says study leader Seth Blackshaw, Ph.D., an associate professor in the Solomon H. Snyder Department of Neuroscience at the Johns Hopkins University School of Medicine. However, he adds, researchers had previously thought that this process, called neurogenesis, only occurs in two brain areas: the hippocampus, involved in memory, and the olfactory bulb, involved in smell.

More recent research suggests that a third area, the hypothalamus — associated with a variety of bodily functions, including sleep, body temperature, hunger and thirst — also produces new neurons. However, the precise source of this neurogenesis and the function of these newborn neurons remained a mystery.

To answer these questions, Blackshaw and his colleagues used mice as a model system. The researchers started by investigating whether any particular part of the hypothalamus had a high level of cell growth, suggesting that neurogenesis was occurring. They injected the animals with a compound called bromodeoxyuridine (BrdU), which selectively incorporates itself into newly replicating DNA of dividing cells, where it’s readily detectable. Within a few days, the researchers found high levels of BrdU in an area of the hypothalamus called the median eminence, which lies on the base of the brain’s fluid-filled third ventricle.

Further tests showed that these rapidly proliferating cells were tanycytes, a good candidate for producing new neurons since they have many characteristics in common with cells involved in neurogenesis during early development. To confirm that tanycytes were indeed producing new neurons and not other types of cells, Blackshaw and his colleagues selectively bred mice that produced a fluorescent protein only in their tanycytes. Within a few weeks, they found neurons that also fluoresced, proof that these cells came from tanycyte progenitors.

With the source of hypothalamic neurogenesis settled, the researchers turned to the question of function. Knowing that many previous studies have suggested that animals raised on a high-fat diet are at significantly greater risk of obesity and metabolic syndrome as adults, Blackshaw’s team wondered whether hypothalamic neurogenesis might play a role in this phenomenon.

The researchers fed mice a diet of high-fat chow starting at weaning and looked for evidence of neurogenesis at several different time points. While very young animals showed no difference compared with mice fed normal chow, neurogenesis quadrupled in adults that had consistently eaten the high-fat chow since weaning. These animals gained more weight and had higher fat mass than animals raised on normal chow.

When Blackshaw and his colleagues killed off new neurons in the high-fat eaters by irradiating just their median eminences with precise X-ray beams, the mice gained significantly less weight and fat than animals who had eaten the same diet and were considerably more active, suggesting that these new neurons play a critical role in regulating weight, fat storage and energy expenditure.

"People typically think growing new neurons in the brain is a good thing — but it’s really just another way for the brain to modify behavior," Blackshaw explains. He adds that hypothalamic neurogenesis is probably a mechanism that evolved to help wild animals survive and helped our ancestors do the same in the past. Wild animals that encounter a rich and abundant food source would be well-served to eat as much as possible, since such a resource is typically scarce in nature.

Being exposed to such a resource during youth, and consequently encouraging the growth of neurons that would promote more food intake and energy storage in the future, would be advantageous. However, Blackshaw explains, for lab animals as well as people in developed countries, who have nearly unlimited access to abundant food, such neurogenesis isn’t necessarily beneficial — it could encourage excessive weight gain and fat storage when they’re not necessary.

If the team’s work is confirmed in future studies, he adds, researchers might eventually use these findings as a basis to treat obesity by inhibiting hypothalamic neurogenesis, either by irradiating the median eminence or developing drugs that inhibit this process.

Provided by Johns Hopkins University School of Medicine

Source: medicalxpress.com

May 21, 2012

A substance in human mesenchymal stem cells that promotes growth appears to spur restoration of nerves and their function in rodent models of multiple sclerosis (MS), researchers at Case Western Reserve University School of Medicine have found.

Their study appeared in the online version of Nature Neuroscience on Sunday, May 20.

In animals injected with hepatocyte growth factor, inflammation declined and neural cells grew. Perhaps most important, the myelin sheath, which protects nerves and their ability to gather and send information, regrew, covering lesions caused by the disease.

"The importance of this work is we think we’ve identified the driver of the recovery," said Robert H. Miller, professor of neurosciences at the School of Medicine and vice president for research at Case Western Reserve University.

Miller, neurosciences instructor Lianhua Bai and biology professor Arnold I. Caplan, designed the study. They worked with Project Manager Anne DeChant, and research assistants Jordan Hecker, Janet Kranso and Anita Zaremba, from the School of Medicine; and Donald P. Lennon, a research assistant from the university’s Skeletal Research Center.

In MS, the immune system attacks myelin, risking injury to exposed nerves’ intricate wiring. When damaged, nerve signals can be interrupted, causing loss of balance and coordination, cognitive ability and other functions. Over time, intermittent losses may become permanent.

Miller and Caplan reported in 2009 that when they injected human mesenchymal stem cells into rodent models of MS, the animals recovered from the damage wrought by the disease. Based on their work, a clinical trial is underway in which MS patients are injected with their own stem cells.

In this study, the researchers first wanted to test whether the presence of stem cells or something cells produce promotes recovery. They injected mice with the medium in which mesenchymal stem cells, culled from bone marrow, grew.

All 11 animals, which have a version of MS, showed a rapid reduction in functional deficits.

Analysis showed that the disease remained on course unless the molecules injected were of a certain size; that is, the molecular weight ranged between 50 and 100 kiloDaltons.

Research by others and results of their own work indicated hepatocyte growth factor, which is secreted by mesenchymal stem cells, was a likely instigator.

The scientists injected animals with 50 or 100 nanograms of the growth factor every other day for five days. The level of signaling molecules that promote inflammation decreased while the level of signaling molecules that counter inflammation increased. Neural cells grew and nerves laid bare by MS were rewrapped with myelin. The 100-nanogram injections appeared to provide slightly better recovery.

To test the system further, researchers tied up cell-surface receptors, in this case cMet receptors that are known to work with the growth factor.

When they jammed the receptors with a function-blocking cMet antibody, neither the mesenchymal stem cell medium nor the hepatocyte growth factor injections had any effect on the disease. In another test, injections of an anti-hepatocyte growth factor also blocked recovery.

The researchers will continue their studies, to determine if they can screen mesenchymal stem cells for those that produce the higher amounts of hepatocyte growth factor needed for effective treatment. That could lead to a more precise cell therapy.

"Could we now take away the mesenchymal stem cells and treat only with hepatocyte growth factor?” Miller asked. “We’ve shown we can do that in an animal but it’s not clear if we can do that in a patient.”

They also plan to test whether other factors may be used to stimulate the cMet receptors and induce recovery.

Provided by Case Western Reserve University

Source: medicalxpress.com

May 21, 2012

Max Planck scientists discover brain cells in monkeys that may be linked to self-awareness and empathy in humans.

The anterior insular cortex is a small brain region that plays a crucial role in human self-awareness and in related neuropsychiatric disorders. A unique cell type – the von Economo neuron (VEN) – is located there. For a long time, the VEN was assumed to be unique to humans, great apes, whales and elephants. Henry Evrard, neuroanatomist at the Max Planck Institute for Biological Cybernetics in Tübingen, Germany, now discovered that the VEN occurs also in the insula of macaque monkeys. The morphology, size and distribution of the monkey VEN suggest that it is at least a primal anatomical homolog of the human VEN. This finding offers new and much-needed opportunities to examine in detail the connections and functions of a cell and brain region that could have a key role in human self-awareness and in mental disorders including autism and specific forms of dementia.

The insular cortex, or simply insula, is a hidden cortical region folded and tucked away deep in the brain – an island within the cortex. Within the last decade, the insula has emerged from darkness as having a key role in diverse functions usually linked to our internal bodily states, to our emotions, to our self-awareness, and to our social interactions. The very anterior part of the insula in particular is where humans consciously sense subjective emotions, such as love, hate, resentment, self-confidence or embarrassment. In relation to these feelings, the anterior insula is involved in various psychopathologies. Damage of the insula leads to apathy, and to the inability to tell what feelings we or our conversational partner experience. These inabilities and alteration of the insula are also encountered in autism and other highly detrimental neuropsychiatric disorders including the behavioural variant of frontotemporal dementia (bvFTD).

The von Economo neuron (VEN) occurs almost exclusively in the anterior insula and anterior cingulate cortex. Until recently it was believed that the VEN is only present in humans, great apes and some large-brained mammals with complex social behaviour such as whales and elephants. In contrast to the typical neighbouring pyramidal neuron that is present in all mammals and all brain regions, the VEN has a peculiar spindle shape and is about three times as large. Their numeral density is selectively altered in autism and bvFTD. Henry Evrard and his team, at the Max Planck Institute for Biological Cybernetics in Tübingen now discovered VENs in the anterior insula in macaque monkeys. His present work provides compelling evidence that monkeys possess at least a primitive form of the human VEN although they do not have the ability to recognize themselves in a mirror, a behavioural hallmark of self-awareness.

"This means, other than previously believed, that highly concentrated VEN populations are not an exclusivity of hominids, but also occurs in other primate species", explains Henry Evrard. "The VEN phylogeny needs to be reexamined. Most importantly, the very much-needed analysis of the connections and physiology of these specific neurons is now possible.” Knowing the functions of the VEN and its connections to other regions of the brain in monkeys could give us clues on the evolution of the anatomical substrate of self-awareness in humans and may help us in better understanding serious neuropsychiatric disabilities including autism, or even addictions such as to drugs or smoking.

Provided by Max Planck Society

Source: medicalxpress.com

May 21, 2012

(Medical Xpress) — People with a curious condition that causes them to apply make-up on only one side of their face, or ignore food on half of their plate, are playing a new role in understanding stroke recovery.

Researchers from the Queensland Brain Institute (QBI) at The University of Queensland have found the condition, a subset of the stroke called ‘unilateral spatial neglect’, tend to have the worst recovery outcomes in regaining lost functioning in their bodies, leading them to believe attention may have an important impact on recovering successfully.

Unilateral spatial neglect is typically caused by strokes on the right hand side of the brain and manifests in patients ignoring the left side of their body.

People with the condition may ignore food on the left hand side of their plate or, if asked to draw a clock, squash all 12 numbers into the right side of the clock face, leaving the other side blank.

They may also fail to shave, or to put make-up on the left side of their faces and. In severe cases, they behave as though the left side of their world does not exist.

“We know that brain plasticity plays a critical role in recovering from stroke,” says Professor Jason Mattingley, who holds the Foundation Chair in Cognitive Neuroscience at The University of Queensland.

“The fact that people with spatial neglect tend to have poorer recovery of motor function suggested to us that attention may be important for guiding plasticity following stroke.”

Current research being undertaken by the Mattingley laboratory is exploring this link.

“What we’re trying to do is explore what effect attention has on brain plasticity, and how attention might be used in neurorehabilitation” says Professor Mattingley.

Volunteers first undergo a magnetic resonance imaging (MRI) scan, which provides researchers with a three-dimensional picture of the brain.

“In terms of their structure, brains are like fingerprints – no two are exactly the same, even though superficially they seem very similar,” Professor Mattingley explains.

The MRI scan allows researchers to guide a transcranial magnetic stimulation (TMS) coil into position upon a volunteer’s scalp.

The device induces a small electrical current in the underlying brain tissue, causing it to become more active.

The researchers specifically target a part of the motor cortex that controls the thumb muscle in the left hand.

“It’s well established that the more often neurons activate at the same time, the more likely they are to communicate efficiently in the future. This is how the brain learns,” says Professor Mattingley.

“We’re exploiting that general principle in this research.”

Dr Marc Kamke, Research Fellow at QBI explains: “By adjusting the type of brain stimulation delivered we can artificially induce short-term changes that resemble naturally-occurring plasticity.”

But what the researchers have found is that the effects of stimulation upon a brain’s plasticity are dependent on attention.

“When we ask people to undertake a visual task that is irrelevant to the brain stimulation, but that demands a great deal of their attention, we observe a reduction in plasticity,” Dr Marc Kamke explains.

“When the task does not require much attention, however, the brain’s plastic response is apparent.”

“These results show that attention plays an important role in guiding brain plasticity,” says Professor Mattingley.

He adds, “while practical applications remain several steps away, this knowledge may ultimately help us develop more effective strategies for physical therapy after stroke.”

The results of the research, which was funded by the National Health and Medical Research Council of Australia, are published this week in The Journal of Neuroscience.

Provided by University of Queensland 

Source: medicalxpress.com