Posts tagged neuroscience
Articles and news from the latest research reports.
Recovery of brain volumes with abstinence may vary for different brain regions
Chronic alcohol abuse can severely damage the nervous system, particularly cognitive functions, cerebral metabolism, and brain morphology. Building upon previous findings that alcoholics can experience brain volume recovery with abstinence, this study found that recovery of cerebral gray matter (GM) can take place within the first two weeks of abstinence, but may vary between brain regions.
Results will be published in the January 2013 issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.
"Shrinkage of brain matter, and an accompanying increase of cerebrospinal fluid, which acts as a cushion or buffer for the brain, are well-known degradations caused by alcohol abuse," explained Gabriele Ende, professor of medical physics in the Department of Neuroimaging at the Central Institute of Mental Health. "This volume loss has previously been associated with neuropsychological deficits such as memory loss, concentration deficits, and increased impulsivity."
"Several processes likely account for changes in brain tissue volume observed through bouts of drinking and abstinence over the course of alcoholism," added Natalie May Zahr, a research scientist in the Department of Psychiatry and Behavioral Sciences at Stanford University School of Medicine. "One process likely reflects true, irreversible neuronal cell death, while another process likely reflects shrinkage, a mechanism that would allow for volume changes in both negative and positive directions, and could account for brain volume recovery with abstinence."
"Gray matter (GM) and white matter (WM) are the main components of the brain that can be distinguished with magnetic resonance imaging (MRI)," explained Ende. "GM consists of neuronal cell bodies, neuropil, glial cells, and capillaries. WM mostly contains myelinated axon tracts."
"Myelin forms an insulating sheath around axons that increases the speed at which they are able to conduct electrical activity," added Zahr. "Because myelin is composed primarily of fat, it gives white matter its color. Cerebrospinal fluid (CSF) is a clear fluid that surrounds and thereby cushions the brain in the skull. Conventional brain structural MRI produces images of protons, with contributions primarily from water and some from fat. Tissue contrast is possible because of the fundamental differences in water content in the primary tissues of the brain: WM consists of about 70 percent water, GM 80 percent, and CSF 99 percent."
(Source: eurekalert.org)
UM Researchers Create Device to Help Stutterers
Drawing on one another’s expertise, a trio of University of Mississippi faculty members from different areas of campus has created a patent-pending device that could change the lives of people who stutter.
Paul Goggans, an electrical engineering professor, developed the prosthetic device, about the size of a cell phone, with Greg Snyder, associate professor of communications sciences and disorders, and Dwight Waddell, associate professor of health, exercise science and recreation management. The friends began working on the device after Snyder, himself a lifelong stutterer, demonstrated how he could speak much more fluently simply by feeling his throat while he and Waddell chatted over coffee.
“By feeling my throat vibrate when I speak, I get tactile speech feedback, which significantly reduces my stuttering,” Snyder said. “Dwight immediately understood my application of speech feedback and neural circuitry, and he then approached Paul, who agreed to make the device development a senior-level design project in his class.”
Since that time, the team has been focused on supporting and empowering the stuttering community by fighting social stigma and challenging the normal remedies associated with stuttering.
“Our device is portable, battery-powered and easy to use,” said Goggans, professor of electrical engineering and lead partner in the instrument’s design and fabrication. “These are important attributes because other behavioral treatments for stuttering are more intense; they require too much concentration and are exhausting.”A prototype of the device was presented Tuesday (Oct. 16) as a “Hot Topic” at the 2012 Society of Neuroscience conference in New Orleans. The paper is among 150 selected from thousands of submissions.
Robot Suit HAL
“Robot Suit HAL" is a cyborg-type robot that can supplement, expand or improve physical capability.
When a person attempts to move, nerve signals are sent from the brain to the muscles via motoneurons, moving the musculoskeletal system as a consequence. At this moment, very weak biosignals can be detected on the surface of the skin. “HAL” catches these signals through a sensor attached on the skin of the wearer. Based on the signals obtained, the power unit is controlled to move the joint in unison with the wearer’s muscle movement, enabling HAL to support the wearer’s daily activities. This is what we call a ‘voluntary control system’ that provides movement interpreting the wearer’s intention from the biosignals in advance of the actual movement. Not only a ‘voluntary control system’ “HAL” has, but also a ‘robotic autonomous control system’ that provides human-like movement based on a robotic system which integrally work together with the ‘autonomous control system’. “HAL” is the world’s first cyborg-type robot controlled by this unique Hybrid System.
"HAL" is expected to be applied in various fields such as rehabilitation support and physical training support in medical field, ADL support for disabled people, heavy labour support at factories, and rescue support at disaster sites, as well as in the entertainment field.
(Source: cyberdyne.jp)
A little science goes a long way: Engaging kids improves math, language scores
A Washington State University researcher has found that engaging elementary school students in science for as little as 10 hours a year can lead to improved test scores in math and language arts.
Samantha Gizerian, a clinical assistant professor in WSU’s Department of Veterinary and Comparative Anatomy, Pharmacology and Physiology, saw improved test scores among fourth-grade students in South Los Angeles after students from the Charles R. Drew University of Medicine and Science gave 10 one-hour presentations on science.
"A lot of students say things like, ‘I didn’t know science was fun,’” says Gizerian, who helped with the classes while on the Drew faculty. "And because they think it’s fun, all of a sudden it’s not work anymore. It’s not homework. It’s not something extra that they have to do.”
Decreased Gene Activity Is Likely Involved in Childhood Risk for Anxiety and Depression
Decreased activity of a group of genes may explain why in young children the “fear center” of the anxious brain can’t learn to distinguish real threats from the imaginary, according to a new University of Wisconsin study.
The study, published this week in the Proceedings of the National Academy of Sciences (PNAS), lays out evidence that young primates with highly anxious temperaments have decreased activity of specific genes within the amygdala, the brain’s fear center.
The authors hypothesize that this may result in over activity of the brain circuit that leads to higher risk for developing disabling anxiety and depression.
This may be particularly important since the genes involved play a major role in forming the brain connections needed for learning about fears. While all children have fears and anxieties, the authors suggest that children with low levels of activity of these genes develop anxious dispositions because they fail to learn to cope by overcoming their early childhood fears.
“Working with my close collaborator and graduate student, Drew Fox, we focused on understanding the function of genes that promote learning and plasticity in the amygdala,” says Dr. Ned H. Kalin, chair of psychiatry at the University of Wisconsin School of Medicine and Public Health, who led the research. “We found reduced activity in key genes that could impair the ability to sculpt the brain, resulting in a failure to develop the capacity to discriminate between real and imaginary fears.”
Kalin says the study helps support the need for early intervention in children identified as excessively shy and anxious. It may also point a way to better treatments aimed at decreasing the likelihood of children developing more severe psychiatric problems. Anxiety in children is quite common and can lead to anxiety and depression in adolescence and often precedes anxiety disorders, depression and substance abuse in adults.
Most small children go through a phase when they’re frightened of many things, including monsters or new social situations, Kalin says, but their maturing brains soon learn to distinguish real threats from the imaginary. But some children do not adapt, generalize their fears to numerous situations, and may later develop serious anxiety and mood disorders. These children tend to be more sensitive to stress, produce more stress hormones and have heightened nervous-system activity.
Kalin, Fox and co-authors wondered whether some differences in the developing amygdala prevent it from learning how to regulate and adapt to anxiety. Kalin’s earlier work identified a subset of young monkeys, similar to extremely shy children, with an inherited anxious disposition. Using brain imaging, the authors showed that high levels of amygdala activity predicted trait-like anxiety in anxious young primates. Like their stable and enduring anxious dispositions, these individuals also had chronically elevated levels of amygdala activity.
“We believe that this pinpoints a critical region in the brain that determines an individual’s level of trait anxiety,’’ Kalin explains.
In examining a specific part of the amygdala, the central nucleus, the researchers analyzed gene expression, which reflects both environmental and inherited influences. Within the central nucleus of the amygdala the authors found that anxious individuals tended to have decreased expression of a gene called neurotrophic tyrosine kinase, receptor, type 3 (NTRK3). Low levels of this gene that encodes for a brain cell surface receptor may be why the amygdala of an anxious monkey or child is chronically overactive and unable to overcome anxiety and fears.
“This is the first demonstration that the early risk to develop anxiety and depression may be related to the underactivity of particular genes in the developing primate amygdala,’’ Kalin says. “These findings have provided the basis for our hypothesis that can explain the early childhood risk to develop anxiety and depression. It also suggests some creative ways to help children with extreme anxiety by developing new treatments focused on increasing the activity of specific genes involved in facilitating the brain development that underlies fear learning and coping.”
(Source: newswise.com)
Fear really resides in a different area of the brain than its inhibitory mechanisms
Do you suffer from a phobia? Maybe arachnophobia? Then you know very well that even if you do not feel uneasy when imagining a huge and hairy tarantula in the therapist’s office, you still jump out of the shower screaming upon seeing a tiny spider. Why is it so hard to get rid of a phobia?
Extinguishing the fear response does not consist of erasing the memory of the fear provoking stimuli, but creating new, competitive memory traces. It has been suspected for some time that neuronal brain circuits responsible for extinguishing fear differ from circuits involved in reoccurrence of the fear response. This assumption has finally been experimentally confirmed. Novel experiments, described in PNAS, a prestigious journal of the American National Academy of Sciences, have been conducted by scientists from the Nencki Institute of Experimental Biology of the Polish Academy of Sciences and the International Institute of Molecular and Cell Biology in Warsaw. This research team was headed by Dr Ewelina Knapska, Dr Jacek Jaworski and Prof. Leszek Kaczmarek.
“Research has been carried out using a special, genetically modified strain of rats developed in the Nencki Institute. As a result we were able to observe the connections between neurons activated in the brains of animals experiencing fear”, explains Dr Ewelina Knapska, head of the Laboratory of Emotions Neurobiology in the Nencki Institute.
Cutis Verticis Gyrata
A 21-year-old man presented with scalp changes that had begun 2 years earlier. Physical examination revealed excessive growth of the scalp, with the formation of convoluted folds and furrows in a cerebriform pattern. The patient had intellectual impairment, although he had no symptoms of neurologic or psychiatric disorders. A 4-mm punch-biopsy specimen from the scalp revealed no inflammatory or neoplastic changes. This clinical presentation was consistent with a diagnosis of cutis verticis gyrata, which is an unusual morphologic condition of the scalp characterized by ridges and furrows resembling the brain’s surface. No intervention was attempted because the patient had no associated disorders and the condition did not bother him cosmetically. At the 1-year follow-up, there were no changes in the patient’s presentation.
A glance at the brain’s circuit diagram
The human brain accomplishes its remarkable feats through the interplay of an unimaginable number of neurons that are interconnected in complex networks. A team of scientists from the Max Planck Institute for Dynamics and Self-Organization, the University of Göttingen and the Bernstein Center for Computational Neuroscience Göttingen has now developed a method for decoding neural circuit diagrams. Using measurements of total neuronal activity, they can determine the probability that two neurons are connected with each other.
From the twitching whiskers of babes: Naptime behavior shapes the brain
The whiskers of newborn rats twitch as they sleep, and that could open the door to new understandings about the intimate connections between brain and body. The discovery reinforces the notion that such involuntary movements are a vital contributor to the development of sensorimotor systems, say researchers who report their findings along with video of those whisker twitches on October 18 in Current Biology, a Cell Press publication.
"We found that even whiskers twitch during sleep—and they do so in infant rats long before they move their whiskers in the coordinated fashion known as whisking," said Mark Blumberg of The University of Iowa. "This discovery opens up new avenues for investigating how we develop critical connections between the sensors in our body and the parts of the brain that interpret and organize sensory information."
Researchers use stem cells to show connection between neural cell disruption and Parkinson’s disease
A diverse team of biologists has shown using induced pluripotent stem cells (iPSCs) that a gene mutation that causes malformations in the structure of the nuclear envelope of neural cells, is associated with Parkinson’s disease. In their paper published in the journal Nature, they describe how they found iPSC cells taken from Parkinson’s patients over time demonstrated the same cell disruption found in neural cells taken from other deceased patient’s with the disease. They also found that by introducing a compound known to disrupt the gene mutation, that they could reverse the cell malformation.
Parkinson’s disease is a degenerative disorder of the nervous system characterized by shaking, slowness of movement and difficulty walking. Over time most patients succumb to dementia and eventually die. Much research has centered on the disruption and death of dopamine-generating cells as the root cause of the disorder despite evidence that such a disruption would not result in all of the symptoms Parkinson’s patient’s exhibit. For that reason, researchers have looked to other causes.
In this new effort, the researchers looked at possible reasons for disruption to the nuclear envelope, the thin film that separates the nucleus from the cytoplasm in neural cells. Such disruptions have been associated with Parkinson’s but no definitive correlation has been found, until now.
To gain a better understanding of what might be causing such disruptions, the research team obtained samples of induced iPSCs from Parkinson’s patients and allowed them to grow in an external environment. They noted that the same disruptions occurred as the iPSCs grew into neural cells, suggesting a genetic cause. Prior research had indicated that a mutation of the LRRK2 gene was connected to Parkinson’s disease but no clear indication of the mechanism involved had been found. Testing the cells derived from the iPSCs showed the same mutation, implicating it as a possible cause of the disorder. The researchers also induced the mutation in human embryo stem cells and found that they too developed the same disruption as they grew into neural cells as was found with the iPSCs.
Next the researchers generated a line of iPSCs minus the mutation and found that the cells did not develop the disruptions. They followed that up by adding a chemical compound known to disrupt the mutation to already affected cells and discovered that it prevented them from being disrupted as well.
The researchers don’t know why the mutation occurs but believe a new therapy for treating Parkinson’s patients might be on the horizon as a result of their research.
(Source: medicalxpress.com)