April 19th, 2012

Study shows religious participation and spirituality processed in different cerebral regions.

Scientists have speculated that the human brain features a “God spot,” one distinct area of the brain responsible for spirituality. Now, University of Missouri researchers have completed research that indicates spirituality is a complex phenomenon, and multiple areas of the brain are responsible for the many aspects of spiritual experiences. Based on a previously published study that indicated spiritual transcendence is associated with decreased right parietal lobe functioning, MU researchers replicated their findings. In addition, the researchers determined that other aspects of spiritual functioning are related to increased activity in the frontal lobe.

“We have found a neuropsychological basis for spirituality, but it’s not isolated to one specific area of the brain,” said Brick Johnstone, professor of health psychology in the School of Health Professions. “Spirituality is a much more dynamic concept that uses many parts of the brain. Certain parts of the brain play more predominant roles, but they all work together to facilitate individuals’ spiritual experiences.”

In the most recent study, Johnstone studied 20 people with traumatic brain injuries affecting the right parietal lobe, the area of the brain situated a few inches above the right ear. He surveyed participants on characteristics of spirituality, such as how close they felt to a higher power and if they felt their lives were part of a divine plan. He found that the participants with more significant injury to their right parietal lobe showed an increased feeling of closeness to a higher power.

“Neuropsychology researchers consistently have shown that impairment on the right side of the brain decreases one’s focus on the self,” Johnstone said. “Since our research shows that people with this impairment are more spiritual, this suggests spiritual experiences are associated with a decreased focus on the self. This is consistent with many religious texts that suggest people should concentrate on the well-being of others rather than on themselves.”

Johnstone says the right side of the brain is associated with self-orientation, whereas the left side is associated with how individuals relate to others. Although Johnstone studied people with brain injury, previous studies of Buddhist meditators and Franciscan nuns with normal brain function have shown that people can learn to minimize the functioning of the right side of their brains to increase their spiritual connections during meditation and prayer.

In addition, Johnstone measured the frequency of participants’ religious practices, such as how often they attended church or listened to religious programs. He measured activity in the frontal lobe and found a correlation between increased activity in this part of the brain and increased participation in religious practices.

“This finding indicates that spiritual experiences are likely associated with different parts of the brain,” Johnstone said.

Written by Brad Fischer

Source: Neuroscience News

April 18, 2012

(Medical Xpress) — Practices like physical exercise, certain forms of psychological counseling and meditation can all change brains for the better, and these changes can be measured with the tools of modern neuroscience, according to a review article now online at Nature Neuroscience.

The study reflects a major transition in the focus of neuroscience from disease to well being, says first author Richard Davidson, professor of psychology at University of Wisconsin-Madison.

The brain is constantly changing in response to environmental factors, he says, and the article “reflects one of the first efforts to apply this conceptual framework to techniques to enhance qualities that we have not thought of as skills, like well-being. Modern neuroscience research leads to the inevitable conclusion that we can actually enhance well-being by training that induces neuroplastic changes in the brain.”

"Neuroplastic" changes affect the number, function and interconnections of cells in the brain, usually due to external factors.

Although the positive practices reviewed in the article were not designed using the tools and theories of modern neuroscience, “these are practices which cultivate new connections in the brain and enhance the function of neural networks that support aspects of pro-social behavior, including empathy, altruism, kindness,” says Davidson, who directs the Center for Investigating Healthy Minds at UW-Madison.

The review, co-written with Bruce McEwen of Rockefeller University, begins by considering how social stressors can harm the brain. The massive neglect of children in orphanages in Romania did not just have psychological impacts; it created measurable changes in their brains, Davidson says. “Such studies provide an important foundation for understanding the opposite effects of interventions designed to promote wellbeing.”

Davidson says his work has been shaped by his association with the Dalai Lama, who asked him in the 1990s, “Why can’t we use the same rigorous tools of neuroscience to investigate kindness, compassion and wellbeing?”

Davidson, who has explored the neurological benefits of meditation, says, “meditation is one of many different techniques, and not necessarily the best for all people. Cognitive therapy, developed in modern psychology, is one of most empirically validated treatments for depression and counteracting the effects of stress.”

Overall, Davidson says, the goal is “to use what we know about the brain to fine-tune interventions that will improve well-being, kindness, altruism. Perhaps we can develop more targeted, focused interventions that take advantage of the mechanisms of neuroplasticity to induce specific changes in specific brain circuits.”

Brains change all the time, Davidson emphasizes. “You cannot learn or retain information without a change in the brain. We all know implicitly that in order to develop expertise in any complex domain, to become an accomplished musician or athlete, requires practice, and that causes new connections to form in the brain. In extreme cases, specific parts of the brain enlarge or contract in response to our experience.”

Scientific documentation for the benefits of brain training may have broader social impacts, says Davidson. “If you go back to the 1950s, the majority of middle-class citizens in Western countries did not regularly engage in physical exercise. It was because of scientific research that established the importance of physical exercise in promoting health and well-being that more people now engage in regular physical exercise. I think mental exercise will be regarded in a similar way 20 years from now.

"Rather than think of the brain as a static organ, or one that just degenerates with age, it’s better understood as an organ that is constantly reshaping itself, is being continuously influenced, wittingly or not, by the forces around us," says Davidson, author of the new book "The Emotional Life of Your Brain." "We can take responsibility for our own brains. They are not pawns to external influences; we can be more pro-active in shaping the positive influences on the brain."

Provided by University of Wisconsin-Madison 

Source: medicalxpress.com

April 17, 2012

(HealthDay) — The ability to make decisions in new situations declines with age, apparently because of changes in the brain’s white matter, a new imaging study says.

The researchers asked 25 adults, aged 21 to 85, to perform a learning task involving money and also undergo MRI brain scans.

They found that age-related declines in decision-making are associated with the weakening of two specific white-matter pathways that connect an area called the medial prefrontal cortex (located in the cerebral cortex) with two other areas deeper in the brain, called the thalamus and the ventral striatum.

The medial prefrontal cortex is involved in decision-making, the ventral striatum is involved in emotional and motivational aspects of behavior, and the thalamus is a highly connected relay center.

"The evidence that this decline in decision-making is associated with white-matter integrity suggests that there may be effective ways to intervene," study first author Gregory Samanez-Larkin, a postdoctoral fellow in Vanderbilt University’s psychology department and Institute of Imaging Science in Nashville, Tenn., said in a university news release. "Several studies have shown that white-matter connections can be strengthened by specific forms of cognitive training."

The study was published April 11 in the Journal of Neuroscience. 

Source: medicalxpress.com

ScienceDaily (Apr. 17, 2012) — At a time when obesity has become epidemic in American society, Dartmouth scientists have found that functional magnetic resonance imaging (fMRI) brain scans may be able to predict weight gain. In a study published April 18, 2012, in The Journal of Neuroscience, the researchers demonstrated a connection between fMRI brain responses to appetite-driven cues and future behavior.

Raspberry cheesecake. The people whose brains responded more strongly to food cues were the people who went on to gain more weight six months later, researchers said. (Credit: © JJAVA / Fotolia)

"This is one of the first studies in brain imaging that uses the responses observed in the scanner to predict important, real-world outcomes over a long period of time," says Todd Heatherton, the Lincoln Filene Professor in Human Relations in the department of psychological and brain sciences and a coauthor on the study. "Using brain activity to predict a consequential behavior outside the scanner is pretty novel."

Using fMRI, the researchers targeted a region of the brain known as the nucleus accumbens, often referred to as the brain’s “reward center,” in a group of incoming first-year college students. While undergoing scans, the subjects viewed images of animals, environmental scenes, appetizing food items, and people. Six months later, their weight and responses to questionnaires regarding interim sexual behavior were compared with their previously recorded weight and brain scan data.

"The people whose brains responded more strongly to food cues were the people who went on to gain more weight six months later," explains Kathryn Demos, first author on the paper. Demos, who conducted the research as part of her doctoral dissertation at Dartmouth, is currently on the research faculty at the Warren Alpert Medical School of Brown University.

The correlation between strong food image brain responses and weight gain was also present for sexual images and activity. “Just as cue reactivity to food images was investigated as potential predictors of weight gain, cue reactivity to sexual images was used to predict sexual desire,” the authors report.

The paper stresses “material specificity,” noting that the participants who responded to food images gained weight but did not engage in more sexual behavior, and vice versa. The authors go on to say that none of the non-food images predicted weight gain.

Heatherton and William Kelley, associate professor of psychological and brain science and a senior author on the paper, have a longstanding interest in psychological theories of self-regulation, also called self-control or willpower.

"We seek to understand situations in which people face temptations and try to not act on them," says Kelley.

The researchers note that the first step toward controlling cravings may be an awareness of how much you are affected by specific triggers in the environment, such as the arrival of the dessert tray in a restaurant.

"You need to actively be thinking about the behavior you want to control in order to regulate it," remarks Kelley. "Self-regulation requires a lot of conscious effort."

Source: Science Daily

ScienceDaily (Apr. 17, 2012) — Last year, researchers from the Perelman School of Medicine at the University of Pennsylvania found that small amounts of a misfolded brain protein can be taken up by healthy neurons, replicating within them to cause neurodegeneration. The protein, alpha-synuclein (a-syn), is commonly found in the brain, but forms characteristic clumps called Lewy bodies, in neurons of patients with Parkinson’s disease (PD) and other neurodegenerative disorders. They found that abnormal forms of a-syn called fibrils acted as “seeds” that induced normal a-syn to misfold and form aggregates.

These images show the brainstem from a control animal (top) and an animal injected with pathologic alpha-synuclein. Brown spots are immunostaining using an antibody specifically recognizing an abnormal form of alpha-synuclein. (Credit: Kelvin C. Luk, Ph.D., Perelman School of Medicine, University of Pennsylvania.)

In earlier studies at other institutions, when fetal nerve cells were transplanted into the brains of PD patients, some of the transplanted cells developed Lewy bodies. This suggested that the corrupted form of a-syn could somehow be transmitted from diseased neurons to healthy ones.

Now, in a follow-up study published in the Journal of Experimental Medicine, the team, led by senior author Virginia M.-Y Lee, PhD, director of the Center for Neurodegenerative Disease Research and professor of Pathology and Laboratory Medicine, showed that brain tissue from a PD mouse model, as well as synthetically produced a-syn fibrils, injected into young, symptom-free PD mice led to spreading of a-syn pathology. By three months after a single injection, neurons containing abnormal a-syn clumps were detected throughout the mouse brains. The inoculated mice died between 100 to 125 days post-inoculation, out of their typical two-year life span.

"We think the spreading is via white-matter tracks through brain neural network connections," explains Lee. "This study will open new opportunities for novel Parkinson’s disease therapies."

One of the remaining questions is how, once inside a neuron, does the misfolded a-syn protein spread from cell to cell.

"It’s like a biochemical chain reaction," says first author Kelvin C. Luk, Ph.D., research associate, in the CNDR. Once inside the confines of a neuron, the misfolded a-syn recruits normally shaped a-syn protein that is present in the cell, causing them to eventually misfold. This occurs along the axons and dendrites (neuronal extensions that reach other neurons), leading to a dramatic accumulation of the abnormal protein. The misshapen a-syn then invades other neurons when they reach the synapse, the small space between neurons.

This transmission process is remarkably similar to what is seen in prions, the protein agents responsible for conditions such as transmissible spongiform encephalopathies ( mad cow disease). However, the researchers are quick to caution that there is no evidence that Parkinson’s or any related neurodegenerative diseases is either infectious or acquired.

The accumulation of misfolded proteins is a fundamental pathogenic process in neurodegenerative diseases, but the factors that trigger aggregation of a-syn are poorly understood.

The Penn team saw that misfolded a-syn propagated along major central nervous system pathways, reaching regions far beyond injection sites. What’s more, they showed for the first time that synthetically produced a-syn fibrils are sufficient to initiate a vicious cycle of Lewy body formation and transmission of the misfolded a-syn in mice.

The study demonstrates just how the Parkinson’s disease protein can spread in a patient’s brain in terms of uptake into a healthy neuron, expansion within the cell, and finally release to a neighboring neuron.

"Knowing this mechanism allows for possible immunotherapies to interrupt the chain reaction by stopping the mutant protein from spreading at the synapse," says Lee.

"Shedding light on how a-synuclein contributes to Parkinson’s disease and related Lewy body disorders is of significant interest both for understanding these diseases and developing potential treatments," said Beth-Anne Sieber, Ph.D., of the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. "This study provides evidence for the progressive, pathological spread of a-synuclein through the brain."

Source: Science Daily

April 13th, 2012
By Kay H. Brodersen 

Researchers at ETH Zurich and the University of Zurich identify a new method of unerringly detecting the presence of pathophysiological changes in the brain.

Brain model (left) depicting brain activity stimulated by speech processing (yellow). The new method allows for the mathematical modeling of interactions between regions within the brain (right). The prism represents the transition or “Generative Embedding.” Image adapted from pr image by Brodersen KH/ ETH Zurich.

The new method was developed in order to gain a mechanistic understanding of schizophrenia and other spectrum disorders, which will lead to more accurate diagnoses and more effective treatments.

When mathematical genius John Nash was diagnosed with schizophrenia, the chance for recovery was slim. Medicine in the 1960’s simply had no convincing explanations for his condition. Alarmingly, things don’t look much better nowadays: depression, addiction, schizophrenia, and other spectrum disorders remain among the toughest challenges for medicine. This is because they are caused by complicated and largely unknown interactions between genes and the environment. Different disease mechanisms may underlie similar, or even identical, symptoms. This means that the effect of any given drug may vary hugely across individuals, resulting in trial-and-error treatment. In addition, conditions whose biological basis is not well-understood may be perceived as particularly stigmatizing.

Most spectrum disorders lack a physiological definition altogether; they are simply described in terms of particular symptoms. This is problematic when these symptoms are caused by different disease mechanisms. Conversely, existing disease classifications frequently group patients with disjoint symptoms under the same label: a person with delusions and disorganized thought, for instance, can be diagnosed with schizophrenia, just as somebody else suffering from hallucinations and movement problems. Examples such as this one show that the development of more specific diagnoses and more effective treatment will require a mechanistic understanding of the pathophysiological mechanisms underlying spectrum disorders.

One step in this direction has recently been made by Kay Henning Brodersen and Klaas Enno Stephan at ETH Zurich and the University of Zurich. Within the framework of the SystemsX.ch project ‘Neurochoice’, the two researchers investigate how insights gained from mathematical models of decision making and underlying brain function can be translated into clinical applications. “Put simply, we develop ‘mathematical microscopes’ that allow us to estimate physiological or computational quantities that cannot be measured directly,” says Klaas Enno Stephan, director of the newly founded Translational Neuromodeling Unit (TNU) in Zurich. “This allows us to obtain more accurate classifications and gain deeper mechanistic insights into the underlying condition than previous attempts.”

To demonstrate the plausibility of their idea, the two scientists collaborated with a clinical team led by Alex Leff at University College London. They analysed brain activity from two groups of participants: one group of stroke patients that suffered from language impairments; and one group of healthy volunteers. While undergoing functional magnetic resonance imaging (fMRI), participants were asked to passively listen to speech. A mathematical model was then used to assess, separately within each participant, how brain regions involved in speech processing interacted. Notably, none of the brain regions included in the model had been affected by the stroke in the patients.

The researchers then asked whether it was possible to automatically detect the presence of a remote lesion from patterns of brain connectivity in the healthy part of the brain. “Using our model of brain function, we were able to diagnose patients with an accuracy of 98%,” says Brodersen, first author of the study. “This became possible by tying together dynamic causal models of neuronal dynamics with mathematical techniques from machine learning and Bayesian inference.” In contrast to subtle spectrum disorders, of course, this initial proof-of-principle study concerned a rather salient clinical condition, that is, language impairments caused by a stroke. In the future, Stephan and Brodersen therefore plan to investigate whether their approach might work equally well for those diseases where contemporary medicine is struggling, such as schizophrenia, depression, and addiction. The two researchers hope that their approach will help dissect these spectrum disorders into pathophysiologically well-defined subgroups. Identifying such subgroups would provide an important step towards more specific diagnoses and may eventually predict the most effective treatment for an individual patient.

Source: Neuroscience News

April 11, 2012

A vast majority of cells in the brain are glial, yet our understanding of how they are generated, a process called gliogenesis, has remained enigmatic. Researchers at Baylor College of Medicine have identified a novel transcripitonal cascade that controls these formative stages of gliogenesis and answered the longstanding question of how glial cells are generated from neural stem cells.

The findings appear in the current edition of Neuron.

"Most people are familiar with neurons, cells that process and transmit information in the brain. Glial cells, on the other hand, make-up about 80 percent of the cells in the brain and function by providing trophic support to neruons, participating in neurotransmission, myelin sheaths for axons, and comprise the blood brain barrier," said Dr. Benjamin Deneen, assistant professor of neuroscience at BCM. "Importantly, glia have been linked to numerous CNS pathologies, from brain tumors and spinal cord injury and several neurological disorders including, Retts Syndrome, ALS, and Multiple Sclerosis. Therefore deciphering how glial cells are generated is key to understanding brain function during health and disease."

As researchers began investigating glial development in chicks they started by going backwards – examing what steps were needed before the glial cells matured. They discovered that glial cells are specified in neural stem cells when the transcription factor NFIA is induced.

Taking another step back in the transcriptional cascade, they looked for what triggered NFIA induction.

"By comparing mouse and chick regulatory sequences we were able to perform enhancer screening in the chick to identify regulatory elements with activity that resembled NFIA induction. This method allowed us to pinpoint Sox9," said Peng Kang, postdoctoral associate in the Center for Stem Cell and Regenerative Medicine at BCM. "Subsequently, we found that Sox9 doesn’t just induce NFIA expression, it also associates with NFIA, forming a complex."

Just after the initiation of gliogenesis this complex was discovered to co-regulate a subset of genes that play important roles in mitochondria energy metabolism and glial precursor migration.

"Sox9 induces NFIA expression during glial initiation and then binds NFIA to drive lineage progression by cooperatively regulating a genetic program that controls cell migration and energy metabolism, two key processes associated with cellular differentiation," said Deneen. "We now need to ask what other proteins contribute to this process, and how does the nature of this complex evolve during astro-glial lineage progression."

Additionally, these findings may also help researchers to understand how certain brain tumors might begin to form, as these same developmental processes and proteins are found in both adult and pediatric brain tumors. A more comprehensive understanding how this regulatory cascade operates during development, could eventually lead to better treatment targets for brain tumors.

Provided by Baylor College of Medicine

Source: medicalxpress.com

April 11, 2012

No matter what novel objects we come to behold, our brains effortlessly take us from an initial “What’s that?” to “Oh, that old thing” after a few casual encounters. In research that helps shed light on the malleability of this recognition process, Brown University neuroscientists have teased apart the potentially different roles that two distinct cell types may play.

In a study published in the journal Neuron, the researchers document that this kind of learning is based in the inferior temporal cortex (ITC), a brain area buried deep in the skull. Scientists already knew the area was important for visual recognition of familiar items, but they hadn’t figured out the steps required to move from novelty to familiarity, a process they refer to as “plasticity.”

"We know little about that because of the level at which this plasticity is taking place," said senior author David Sheinberg, professor of neuroscience and a member of the Brown Institute for Brain Science. "The inner workings made up of individual neurons make it very hard to actually track what’s going on at that level."

Working with two monkeys, in whom they monitored single neuron activity using tiny microelectrodes, Sheinberg and graduate student Luke Woloszyn tracked the firing patterns of individual neurons in the ITC while monkeys viewed 125 objects they had been trained to recognize and 125 others that they had never seen before.

The scientists found that the two major classes of cells found in the brain, excitatory and inhibitory, responded differently depending on what the monkeys saw. Excitatory neurons were especially active when the monkeys saw a preferred familiar object — the familiar image, out of the 125 such images, that the cell “liked” best. Although the particular preferred familiar image varied across the sample of neurons, almost every excitatory cell had at least one familiar image to which it responded more robustly than its preferred novel image, Sheinberg said. Inhibitory neurons, meanwhile, were much more active when the monkeys saw any novel image, independent of the object’s actual identity. 

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April 11, 2012

(Medical Xpress) — An abnormally low level of a protein in certain nerve cells is linked to movement problems that characterize the deadly childhood disorder spinal muscular atrophy, new research in animals suggests.

Spinal muscular atrophy, or SMA, is caused when a child’s motor neurons – nerve cells that send signals from the spinal cord to muscles – produce insufficient amounts of what is called survival motor neuron protein, or SMN. This causes motor neurons to die, leading to muscle weakness and the inability to move.

Though previous research has established the disease’s genetic link to SMN in motor neurons, scientists haven’t yet uncovered how this lack of SMN does so much damage. Some children with the most severe form of the disease die before age 2.

A research team led by Ohio State University scientists showed in zebrafish that when SMN is missing – in cells throughout the body as well as in motor neurons specifically – levels of a protein called plastin 3 also decrease.

When the researchers added plastin 3 back to motor neurons in zebrafish that were genetically altered so they couldn’t produce SMN, the zebrafish regained most of their swimming abilities movement that had been severely limited by their reduced SMN. These findings tied the presence of plastin 3 – alone, without SMN – to the recovery of lost movement.

The recovery was not complete. Fish without SMN in their cells still eventually died, so the addition of plastin 3 alone is not a therapeutic option. But further defining this protein’s role increases understanding of how spinal muscular atrophy develops.

“What all is lost when SMN is lost? That’s something we’re still struggling with,” said Christine Beattie, associate professor of neuroscience at Ohio State and lead author of the study.

“We think part of the motor neuron defects that are seen in spinal muscular atrophy are caused by this decrease in plastin 3 we get when SMN is lowered. And when we add plastin 3 back to motor neurons we can rescue defects that are seen when SMN is decreased, suggesting that a decrease in plastin 3 is contributing to some of the disease’s characteristics.” 

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