Posts tagged neuroscience

June 15, 2012

Researchers from the Peninsula College of Medicine and Dentistry, University of Exeter, in collaboration with colleagues from Rutgers University, Newark and University College London, have furthered understanding of the mechanism by which the cells that insulate the nerve cells in the peripheral nervous system, Schwann cells, protect and repair damage caused by trauma and disease.

The findings of the study, published on-line by the Journal of Neuroscience and supported by the Wellcome Trust, are exciting in that they point to future therapies for the repair and improvement of damage to the peripheral nervous system.

The peripheral nervous system is the part of the nervous system outside the brain and the spinal cord. It regulates almost every aspect of our bodily function, carrying sensory information that allows us to feel the sun on our face and motor information, that allows us to move. It also controls the functions of all the organs of the body.

Damage can occur through trauma: it can occur in diabetic neuropathy (suffered by almost half of those with diabetes) and patients with common inherited conditions such as Charcot-Marie-Tooth (CMT) disease. There can be a wide range of symptoms, from loss of sensation in the hands and feet to problems with digestion, blood pressure regulation, sexual function and bladder control.

Schwann cells provide the insulation, or myelin sheath, for the nerve cells that carry electrical impulses to and from the spinal cord. Schwann cells, because of their plasticity, are able to revert back to an immature ‘repair’ cell to repair damage to the peripheral nervous system. The level of repair is remarkably good but incomplete repair, perhaps after the severance of a nerve, may lead to long-term loss of function and pain.

The ability of Schwann cells to demyelinate can make them susceptible to the disease process seen in conditions such as CMT. CMT affects one in 2500people, so is a comparatively common inherited disease of the nervous system. Mutations in the many different genes in CMT can cause cycles of repair and re-insulation (re-myelination) which lead to long-term damage and the death of both Schwann and nerve cells. There is currently no therapy for CMT and patients experience increased sensory and motor problems which may lead to permanent disability.

The research team believes that its work to understand the ability of Schwann cells to revert back to an immature state and stimulate repair will lead to therapies to improve damage from severe trauma and break the cycle of damage caused by CMT. They also believe that there may also be potential to improve repair in cases of diabetic neuropathy.

They have identified a DNA binding protein, cJun, as a key player in the plasticity that allows a Schwann cell to revert back to the active repair state. cJun may be activated by a number of pathways that convey signals from the surface of the Schwann cell to the nucleus. One such pathway, the p38 Mitogen Activated Protein Kinase Pathway, appears to play a vital role: it is activated after PNS damage and may promote the process of repair; conversely it may be abnormally activated in demyelinating diseases such as CMT.

Professor David Parkinson, Associate Professor in Neuroscience, Peninsula College of Medicine and Dentistry, University of Exeter, said: “The findings of our research are exciting because we have pinpointed and are understanding the mechanism by which our bodies can repair damage to the peripheral nervous system. With further investigation, this could well lead to therapies to repair nerve damage from trauma and mitigate the damage which relates to common illnesses, such as CMT.”

Provided by The Peninsula College of Medicine and Dentistry

Source: medicalxpress.com

June 15, 2012

Whether or not a neuron transmits an electrical impulse is a function of many factors. European research is using a heady mixture of techniques – molecular, microscopy and electrophysiological – to identify the necessary input for nerve transmission in the cortex.

Credit: Thinkstock

In the central nervous system (CNS), a nerve cell or neuron has a ‘forest’ of elaborate dendritic trees arising from the cell body. These literally receive many thousands of synapses (junctions that allow transmission of a signal) at positions around the tree. These inputs then are able to generate an impulse, or ‘spike’, known as an action potential at the initial part of the axon.

Previous research has confirmed that an activated synapse will generate an electric signal as a result of neurotransmitters released from pre-synaptic axons. Electrical recordings from the neocortex have confirmed that, in line with the cable theory prediction, that modulation of potential at the dendrite is highly distance-dependent from the cell body or soma.

The ‘Information processing in distal dendrites of neocortical layer 5 pyramidal neurons’ (Channelrhodopsin) project aimed to shed more light on how more distal sites in the ‘tree’ influence the action potential of the post-synaptic neuron. Furthermore, they investigated exactly how dendritic spikes can be generated, another issue about which there is little information so far.

Recent research has highlighted the importance of activation of N-methyl-D-aspartate (NMDA) receptors to bring about the production of a signal that will proceed to the soma and then result in a spike. There is also indirect evidence that interneurons targeting dendrites can control level of dendrite excitability.

Channelrhodopsin scientists simultaneously recorded the pre- and post-synaptic electrical recordings of identified interneurons and a special type of neuron, pyramidal cells that are primary excitation units in the mammalian cortex.

The project team first characterised the different types of inhibitory neuron deep in the cortex in layer 5 at apical tuft dendrites. The researchers then showed that a special type of inhibitory interneuron in the outer layer of the neocortex can suppress dendritic spiking in layer 5.

Project results show that a superficial inhibitory neuron can impact information processing in a specific pyramidal neuron. The research will have massive implications for neuroscience and help to unravel the integrative operations of CNS neurons.

Provided by CORDIS

Source: medicalxpress.com

ScienceDaily (June 14, 2012) — Rockville, Md. — Scientists have found new evidence that people spot a face in the crowd more quickly when teeth are visible — whether smiling or grimacing — than a face with a particular facial expression. The new findings, published in the Journal of Vision, counters the long held “face-in -the-crowd” effect that suggests only angry looking faces are detected more readily in a crowd.

Examples of stimuli — closed mouth and open mouth with visible teeth — presented in the experiment. (Credit: ARVO)

"The research concerned with the face-in-the-crowd effect essentially deals with the question of how we detect social signals of friendly or unfriendly intent in the human face," said author Gernot Horstmann, PhD, of the Center for Interdisciplinary Research and Department of Psychology at Bielefeld University, Germany. "Our results indicate that, contrary to previous assertions, detection of smiles or frowns is relatively slow in crowds of neutral faces, whereas toothy grins and snarls are quite easily detected."

In two studies, the researchers asked subjects to search for a happy or an angry face within a crowd of neutral faces, and measured the search speed. While the search was relatively slow when emotion was signaled with a closed mouth face, the speed search doubled when emotion was signaled with an open mouth and visible teeth. This was the case for both happy and angry faces, and happy faces were found even somewhat faster than angry faces.

Horstmann and his colleagues conducted these experiments as a result of discrepancies in previous studies that investigated visual search for emotional faces. According to the research team, the inconsistent results with respect to which of the two expressions are found faster — the happy face or the angry face — suggested that the emotional expression category could not be the only important factor determining the face-in- the-crowd effect.

The scientists believe this new study may explain the discrepancies. “This will probably inspire researchers to clarify whether emotion and, in particular, threat plays an additional, unique role in face detection,” said Horstmann.

Source: Science Daily

ScienceDaily (June 14, 2012) — An international team of researchers’ study of the spatial patterns of the spread of obesity suggests America’s bulging waistlines may have more to do with collective behavior than genetics or individual choices. The team, led by City College of New York physicist Hernán Makse, found correlations between the epidemic’s geography and food marketing and distribution patterns.

Supermarket. Physicists found correlations between the obesity epidemic’s geography and food marketing and distribution patterns. (Credit: © flashpics / Fotolia)

"We found there is a relationship between the prevalence of obesity and the growth of the supermarket economy," Professor Makse said. "While we can’t claim causality because we don’t know whether obesity is driven by market forces or vice versa, the obesity epidemic can’t be solved by focus on individual behavior."

The teams findings, published online this week in Scientific Reports, come as a policymakers are starting to address the role of environmental factors in obesity. For example, in New York Mayor Michael Bloomberg wants to limit serving sizes of soda sweetened with sugar to 16 ounces as a way to combat obesity.

The World Health Organization considers obesity a global epidemic similar to cancer or diabetes. It is a non-communicable disease for which no prevention strategy has been able to contain the spread.

Because obesity is related to increased calorie intake and physical inactivity, prevention has focused on changing individuals’ behaviors. However, prevalence of non-communicable diseases shows spatial clustering, and the spread of obesity has shown “high susceptibility to social pressure and global economic drivers.”

Professor Makse and his colleagues hypothesized that these earlier findings suggest collective behavior plays a more significant role in the spread of the epidemic than individual factors such as genetics and lifestyle choices. To study collective behavior’s role, they implemented a statistical clustering analysis based on the physics on the critical phenomena.

Using county-level microdata provided by the U.S. Centers for Disease Control Behavior Risk Factor Surveillance Systems for 2004 through 2008, they investigated spatial correlations for specific years. Over that time span, the pattern of the spreading of the epidemic, which has Greene County, Ala., as its epicenter, has shown that two clusters spanning distances of 1,000 kilometers have emerged; one along the Appalachian Mountains, the second in the lower Mississippi River valley.

The spatial map of obesity prevalence in the United States shows that neighboring areas tend to have similar percentages of their populations considered obese, i.e. have a body mass index greater than or equal to 30. Such areas are considered obesity clusters, and their spread can be seen in the maps from 2004 to 2008.

To assess the properties of these spatial arrangements, the researchers calculated an equal-time, two-point correlation function that measured the influence of a set of characteristics in one county on another county at a given distance. The characteristics studied were population density, prevalence of adult obesity and diabetes, cancer mortality rates and economic activity.

The researchers said the form of the correlations in obesity were reminiscent of those in physical systems at a critical point of second-order phase transition. Such systems are uncorrelated and characterized by short-range vanishing fluctuations when they are not at a critical stage.

However, at critical points long-range correlations appear, and these may signal the emergence of strong critical fluctuations in the spreading of obesity and diabetes. Consequently, they concluded the clustering patterns found in obesity were the result of “collective behavior, which may not merely be the consequence of fluctuations in individual habits.”

Professor Makse and his colleagues believe the correlations of fluctuations in the prevalence of obesity may be linked to demographic and economic variables. To test this hypothesis, they compared the spatial characteristics of industries associated with food production and sales, e.g. supermarkets, food and beverage stores, restaurants and bars, to other sectors of the economy.

Their analysis of spatial fluctuations in food economic activity gave rise to the same anomalous values as obesity and diabetes. Areas with above-average concentrations of food-related businesses had high-than-normal prevalence of obesity and diabetes.

In future studies, Professor Makse plans to apply physics concepts to measure the spread of cancer and diabetes. “The basic idea is that if a non-communicable disease is spreading like a virus, then environmental factors have to be at work,” he said. “If only genetics determined obesity, we wouldn’t have seen the correlations.”

Source: Science Daily

ScienceDaily (June 14, 2012) — The first U.S. population prevalence study of mutations in the gene that causes fragile X syndrome, the most common inherited form of intellectual disability, suggests the mutation in the gene — and its associated health risks — may be more common than previously believed.

Writing this month (June 2012) in the American Journal of Medical Genetics, a team of Wisconsin researchers reports that the cascade of genetic amino acid repeats, which accumulate over generations and culminate in the mutation of a single gene causing fragile X, is occurring with more frequency among Americans than previously believed. The study also shows that as the genetic basis for the condition is passed from generation to generation and amplified, risks to neurological and reproductive health emerge in many carriers.

"The premutation of this condition is much more prevalent than we previously thought and there are some clinical risks associated with that," explains Marsha Mailick Seltzer, director of the University of Wisconsin-Madison Waisman Center, who led the new study.

Fragile X is caused by the unexplained runaway expansion of a set of amino acid repeats in a single X chromosome gene known as FMR1. When fully mutated, the gene fails to express and produce a protein that’s required for healthy brain development. The syndrome, which is more common in boys, results in a spectrum of intellectual disability.

However, before the gene fully mutates, carriers of the faulty gene exhibit a smaller number of elevated repeats, which expand as the gene is passed from generation to generation. Normal FMR1 genes exhibit anywhere from five to 40 repeats. Carriers with a premutation may have anywhere from 55 to 200. Those with between 45 and 54 repeats are characterized as falling into a “gray zone.” Carriers of gray zone expansions often pass the mutation on to their children who themselves are at greater risk of having the premutation, and in subsequent generations the risk of a full mutation causing fragile X syndrome is high.

The goal of the new study was to calculate the prevalence in a U.S. population of the premutation and the gray zone. The research was based on data from the Wisconsin Longitudinal Study (WLS), also known as the “Happy Days study,” which for more than 50 years has tracked the careers, family life, health and education of more than 10,000 graduates of Wisconsin’s high school class of 1957.

Using genetic samples from 6,747 WLS participants, the team led by Seltzer, an expert on developmental disability and family life, found that 1 in 151 females and 1 in 468 males carry the fragile X premutation while 1 in 35 females and 1 of every 42 males fall into the gray zone.

"The prevalence is high, the second highest reported in the world literature," says Seltzer, noting that the incidence of fragile X varies by population and is higher in some places such as Israel, and lower in others like Asia.

The expansion of the FMR1 gene is known to vary across ethnic groups. The sample in the WLS study is primarily white and of northern European descent.

People with the premutation are more likely to have a child with disability; to have neurological symptoms such as numbness, dizziness and faintness; and, for women, to experience early menopause. Although these symptoms have been recognized previously in clinical studies, the WLS data represent an unbiased sample and supports those observations.

"This study confirms that there are health risks associated with the premutation," says Seltzer. "People with the premutation have a higher probability of neurological and reproductive problems. There is a significant public health burden."

Source: Science Daily

ScienceDaily (June 14, 2012) — No effective treatments are currently available for the prevention or cure of Alzheimer’s disease (AD), the most frequent form of dementia in the elderly. The most recognized risk factors, advancing age and having the apolipoprotein E Ɛ4 gene, cannot be modified or treated. Increasingly, scientists are looking toward other risk factors to identify preventive and therapeutic strategies. Much attention recently has focused on the metabolic syndrome (MetS), with a strong and growing body of research suggesting that metabolic disorders and obesity may play a role in the development of dementia.

A new supplement to the Journal of Alzheimer’s Disease provides a state-of-the-art assessment of research into the link between metabolic syndrome and cognitive disorders. The supplement is guest edited by Vincenza Frisardi, of the Department of Neurological and Psychiatric Sciences, University of Bari, and the Geriatric Unit and Gerontology-Geriatrics Research Laboratory, IRCCS, Foggia, Italy, and Bruno P. Imbimbo, Research and Development Department, Chiesi Farmaceutici, Parma, Italy.

The prevalence of MetS and obesity has increased over the past several decades. MetS is a cluster of vascular and metabolic risk factors including obesity, hypertension, an abnormal cholesterol profile, and impaired blood glucose regulation. “Although molecular mechanisms underlying the relationship between MetS and neurological disorders are not fully understood, it is becoming increasingly clear that cellular and biochemical alterations observed in MetS may represent a pathological bridge between MetS and various neurological disorders,” explains Dr. Frisardi.

Type 2 diabetes (T2D) has been linked with cognitive impairment in a number of studies. The risk for developing both T2D and AD increases proportionately with age, and evidence shows that individuals with T2D have a nearly twofold higher risk of AD than nondiabetic individuals.

Paula I. Moreira, Faculty of Medicine and Center for Neuroscience and Cell Biology, University of Coimbra, Portugal, outlines some of the likely mechanisms. Both AD and T2D present similar abnormalities in the mitochondria, which play a pivotal role in cellular processes that impair their ability to regulate oxidation in the cell. Human amylin, a peptide that forms deposits in the pancreatic cells of T2D patients, shares several properties with amyloid-ß plaques in the Alzheimer’s brain. Insulin resistance is another feature shared by both disorders. Impairment of insulin signalling is directly involved in the development of tau tangles and amyloid ß (Aß) plaques. “Understanding the key mechanisms underlying this deleterious interaction may provide opportunities for the design of effective therapeutic strategies,” Dr. Moreira notes.

In another article, author, José A. Luchsinger of the Division of General Medicine, Department of Medicine, Columbia University College of Physicians and Surgeons, New York, notes that while there seems to be little dispute that T2D can cause cerebrovascular disease and vascular cognitive impairment, whether T2D can cause late onset AD remains to be determined. “Although the idea is highly speculative, the association between T2D and cognitive impairment may not be causal. Several lines of evidence provide some support to the idea that late onset Alzheimer’s disease could cause T2D, or that both could share causal pathways,” he notes. He reviews epidemiological, imaging, and pathological studies and clinical trials to provide insight. “Given the epidemic of T2D in the world, it’s important to determine whether the association between T2D and cognitive impairment, particularly late onset AD, is causal and if so, what are the mechanisms underlying it.”

Dr. Frisardi notes that most efforts by the pharmaceutical industry have been directed against the production and accumulation of amyloid-ß. “Unfortunately, these efforts have not produced effective therapies yet, since the exact mechanisms of AD are largely unknown. Given that the onset of AD most likely results from the interaction of genetic and environmental factors, the research agenda should consider new platforms of study, going beyond the monolithic outlook of AD, by synthesizing epidemiological, experimental, and biological data under a unique pathophysiological model as a point of reference for further advances in the field.”

Source: Science Daily

June 14, 2012

Visual and auditory stimuli that elicit high levels of engagement and emotional response can be linked to reliable patterns of brain activity, a team of researchers from The City College of New York and Columbia University reports. Their findings could lead to new ways for producers of films, television programs and commercials to predict what kinds of scenes their audiences will respond to.

"Peak correlations of neural activity across viewings can occur in remarkable correspondence with arousing moments of the film,” the researchers said in an article published in the journal Frontiers in Human Neuroscience. “Moreover, a significant reduction in neural correlation occurs upon a second viewing of the film or when the narrative is disrupted by presenting its scenes scrambled in time.”

The researchers used EEG (electroencephalography), which measures electrical activity across the scalp, to collect data on brainwaves of 20 human subjects, who were shown scenes from three films with repeat viewings. Two films, Alfred Hitchcock’s “Bang! You’re Dead” and Sergio Leone’s “The Good, the Bad and the Ugly,” contained moments of high drama expected to trigger responses. The third, an amateur film of people walking on a college campus, was used as a control.

"We found moments of high correlation (between brainwave activity during separate viewings) and moments when this did not occur," said Dr. Lucas C. Parra, Herbert G. Kayser Professor of Biomedical Engineering in CCNY’s Grove School of Engineering, and a corresponding author. "By looking at patterns of oscillation we could tell at which moments a person was particularly engaged. Additionally, we could see whether the correlation occurred across subjects and repeated viewings."

[Video: Reading the Brain during Film Viewing]
Video of EEG readings during scenes from “Bang, You’re Dead”

Measurements along the EEG alpha activity scale show the degree of attentiveness in a person, he explained. When the oscillations are strong, a person is relaxed, i.e. not engaged. When a person is very attentive, alpha activity is low.

Peaks in engagement were correlated to three kinds of scenes, said Dr. Jasek Dmochowski, a post-doctoral fellow in the Grove School and a corresponding author. They included moments with powerful visual cues, such as a close-up on the gun in “Bang! You’re Dead,” scenes with ominous music in which the visual component was not significant, and meaningful scene changes.

The researchers found significantly less neural correlation on participants’ second viewings and when scenes were scrambled and shown out of sequence. “Following a narrative is complex and involves a lot of distributed processing. When a person doesn’t have a sense of the narrative there is much less correlation (across views of the same or another subject),” Dr. Dmochowski said.

Having demonstrated the correlations between intense stimuli and brainwave reliability, the research team now wants to locate where in the brain the response occurs, Professor Parra said. He wants to deploy a combination of EEG and magnetic resonance imaging to “get the best of both worlds:” the fine temporal resolution of EEG and the detailed imagery of MRI.

The team sees several potential applications for the ability to quantify levels of engagement, including neuro-marketing, quantitative assessment of entertainment, measuring the impact of narrative discourse and the study of attention deficit disorders. “Advertisers would love to know where and when an ad is engaging,” he noted.

"The potential to measure engagement is huge since this provides an objective way to collect data," added Dr. Dmochowski, who currently is investigating whether there is a correlation between social media usage and brain activity in young people while watching “The Walking Dead,” a drama series on the American Movie Classics cable network.

"We are mining Twitter to measure the depth of watching," he continued. "We think there will be many correlations between scenes that elicit social media responses and neural signatures, and we can look at both positive and negative responses."

Provided by City College of New York

Source: medicalxpress.com

ScienceDaily (June 13, 2012) — Ever wonder why Jimi Hendrix’s rendition of “The Star-Spangled Banner” moved so many people in 1969 or why the music in the shower scene of “Psycho” still sends chills down your spine?

Jimi Hendrix (Credit: Public domain image, courtesy of UCLA)

A UCLA-based team of researchers has isolated some of the ways in which distorted and jarring music is so evocative, and they believe that the mechanisms are closely related to distress calls in animals.

They report their findings in the latest issue of the peer-reviewed scientific journal Biology Letters, which publishes online June 12.

"Music that shares aural characteristics with the vocalizations of distressed animals captures human attention and is uniquely arousing," said Daniel Blumstein, one of the study’s authors and chair of the UCLA Department of Ecology and Evolutionary Biology.

Read more …

ScienceDaily (June 13, 2012) — Children who are skilled in understanding how shapes fit together to make recognizable objects also have an advantage when it comes to learning the number line and solving math problems, research at the University of Chicago shows.

The work is further evidence of the value of providing young children with early opportunities in spatial learning, which contributes to their ability to mentally manipulate objects and understand spatial relationships, which are important in a wide range of tasks, including reading maps and graphs and understanding diagrams showing how to put things together. Those skills also have been shown to be important in Science Technology, Engineering and Math (STEM) fields.

Scholars at UChicago have shown, for instance, that working with puzzles and learning to identify shapes are connected to improved spatial understanding and better achievement, particularly in geometry. A new paper, however, is the first to connect robust spatial learning with better comprehension of other aspects of mathematics, such as arithmetic.

"We found that children’s spatial skills at the beginning of first and second grades predicted improvements in linear number line knowledge over the course of the school year," said Elizabeth Gunderson, a UChicago postdoctoral scholar who is lead author of the paper, "The Relation Between Spatial Skill and Early Number Knowledge: The Role of the Linear Number Line," published in the current issue of the journal Development Psychology.

In addition to finding the importance of spatial learning to improving understanding of the number line, the team also showed that better understanding of the number line boosted mathematics performance on a calculation task.

Read more …

ScienceDaily (June 13, 2012) — Wake up, America, and lose some weight — it’s keeping you tired and prone to accidents. Three studies being presented June 13 at sleep 2012 conclude that obesity and depression are the two main culprits making us excessively sleepy while awake.

Researchers at Penn State examined a random population sample of 1,741 adults and determined that obesity and emotional stress are the main causes of the current “epidemic” of sleepiness and fatigue plaguing the country. Insufficient sleep and obstructive sleep apnea also play a role; both have been linked to high blood pressure, heart disease, stroke, depression, diabetes, obesity and accidents.

"The ‘epidemic’ of sleepiness parallels an ‘epidemic’ of obesity and psychosocial stress," said Alexandros Vgontzas, MD, the principal investigator for the three studies. "Weight loss, depression and sleep disorders should be our priorities in terms of preventing the medical complications and public safety hazards associated with this excessive sleepiness."

In the Penn State cohort study, 222 adults reporting excessive daytime sleepiness (EDS) were followed up 7½ years later. For those whose EDS persisted, weight gain was the strongest predicting factor. “In fact, our results showed that in individuals who lost weight, excessive sleepiness improved,” Vgontzas said.

Adults from that same cohort who developed EDS within the 7½-year span also were studied. The results show for the first time that depression and obesity are the strongest risk factors for new-onset excessive sleepiness. The third study, of a group of 103 research volunteers, determined once again that depression and obesity were the best predictors for EDS.

"The primary finding connecting our three studies are that depression and obesity are the main risk factors for both new-onset and persistent excessive sleepiness," Vgontzas said.

In the Penn State cohort study, the rate of new-onset excessive sleepiness was 8 percent, and the rate of persistent daytime sleepiness was 38 percent. Like insufficient sleep and obstructive sleep apnea, EDS also is associated with significant health risks and on-the-job accidents.

Source: Science Daily