Posts tagged science
Articles and news from the latest research reports.
Study: People Pay More Attention to the Upper Half of Field of Vision
A new study from North Carolina State University and the University of Toronto finds that people pay more attention to the upper half of their field of vision – a finding which could have ramifications for everything from traffic signs to software interface design.
“Specifically, we tested people’s ability to quickly identify a target amidst visual clutter,” says Dr. Jing Feng, an assistant professor of psychology at NC State and lead author of a paper on the work. “Basically, we wanted to see where people concentrate their attention at first glance.”
Researchers had participants fix their eyes on the center of a computer screen, and then flashed a target and distracting symbols onto the screen for 10 to 80 milliseconds. The screen was then replaced by an unconnected “mask” image to disrupt their train of thought. Participants were asked to indicate where the target had been located on the screen.
Researchers found that people were 7 percent better at finding the target when it was located in the upper half of the screen.
“It doesn’t mean people don’t pay attention to the lower field of vision, but they were demonstrably better at paying attention to the upper field,” Feng says.
“A difference of 7 percent could make a significant difference for technologies that are safety-related or that we interact with on a regular basis,” Feng says. “For example, this could make a difference in determining where to locate traffic signs to make them more noticeable to drivers, or where to place important information on a website to highlight that information for users.”
The paper, “Upper Visual Field Advantage in Localizing a Target among Distractors,” is published online in the open-access journal i-Perception. The paper was co-authored by Dr. Ian Spence of the University of Toronto. The work was supported, in part, by the Natural Sciences and Engineering Research Council of Canada.
Fast contractions and depolarizations in mitochondria revealed with multiparametric imaging
When something bad happens to otherwise healthy neurons it’s easy to blame the usual suspects—the mitochondria. In some cases the nucleus might be the one at fault, as in a de novo mutation in a critical gene or in some other runaway error process in the instruction pipeline. Other times there could be leakage into the brain of toxins, bacteria, or even overzealous patriot cells of the host. But by and large, it’s the mitochondria who bear responsibility for nearly everything the brain does and so it is they who must accept it when it fails. To better understand how these organelles function, researchers have turned to special imaging methods that let them observe multiple aspects of their behavior all at once.
In one of the most revealing studies of its kind to date, researchers in Germany were able to observe the tiny contractions that mitochondria undergo during their complex shifts through different redox states and levels of depolarization. Publishing in a recent issue of Nature Medicine they relate these effects to pH and calcium concentration in the both the mitochondria and surrounding axon, and also to the larger spiking activity of the neuron.
Low-fat diet helps fatigue in people with MS
People with multiple sclerosis who for one year followed a plant-based diet very low in saturated fat had much less MS-related fatigue at the end of that year — and significantly less fatigue than a control group of people with MS who didn’t follow the diet, according to an Oregon Health & Science University study being presented today at the American Academy of Neurology’s annual meeting in Philadelphia, Pa.
The study was the first randomized-controlled trial to examine the potential benefits of the low fat diet on the management of MS. The study found no significant differences between the two groups in brain lesions detected on MRI brain scans or on other measures of MS. But while the number of trial participants was relatively small, study leaders believe the significantly improved fatigue symptoms merited further and larger studies of the diet.
"Fatigue can be a debilitating problem for many people living with relapsing-remitting MS," said Vijayshree Yadav, M.D., an associate professor of neurology in the OHSU School of Medicine and clinical medical director of the OHSU Multiple Sclerosis Center. "So this study’s results — showing some notable improvement in fatigue for people who follow this diet — are a hopeful hint of something that could help many people with MS."
The study investigated the effects of following a diet called the McDougall Diet, devised by John McDougall, M.D. The diet is partly based on an MS-fighting diet developed in the 1940s and 1950s by the late Roy Swank, M.D., a former head of the division of neurology at OHSU. The McDougall diet, very low in saturated fat, focuses on eating starches, fruits and vegetables and does not include meat, fish or dairy products.
The study, which began in 2008, looked at the diet’s effect on the most common form of MS, called relapsing-remitting MS. About 85 percent of people with MS have relapsing-remitting MS, characterized by clearly defined attacks of worsening neurological function followed by recovery periods when symptoms improve partially or completely.
The study measured indicators of MS among a group of people who followed the McDougall Diet for 12 months and a control group that did not. The study measured a range of MS indicators and symptoms, including brain lesions on MRI brain scans of study participants, relapse rate, disabilities caused by the disease, body weight and cholesterol levels.
It found no difference between the diet group and the control group in the number of MS-caused brain lesions detected on the MRI scans. It also found no difference between the two groups in relapse rate or level of disability caused by the disease. People who followed the diet did lose significantly more weight than the control group and had significantly lower cholesterol levels. People who followed the diet also had higher scores on a questionnaire that measured their quality of life and overall mood.
The study’s sample size was relatively small. Fifty-three people completed the study, with 27 in the control group and 22 people in the diet group who complied with the diet’s restrictions.
"This study showed the low-fat diet might offer some promising help with the fatigue that often comes with MS," said Dennis Bourdette, M.D., F.A.A.N., chair of OHSU’s Department of Neurology, director of OHSU’s MS Center and a study co-author. "But further study is needed, hopefully with a larger trial where we can more closely look at how the diet might help fatigue and possibly affect other symptoms of MS."
(Source: eurekalert.org)
Researchers reveal new cause of epilepsy
A team of researchers from Sanford-Burnham and SUNY Downstate Medical Center has found that deficiencies in hyaluronan, also known as hyaluronic acid or HA, can lead to spontaneous epileptic seizures. HA is a polysaccharide molecule widely distributed throughout connective, epithelial, and neural tissues, including the brain’s extracellular space (ECS). Their findings, published on April 30 in The Journal of Neuroscience, equip scientists with key information that may lead to new therapeutic approaches to epilepsy.
The multicenter study used mice to provide the first evidence of a physiological role for HA in the maintenance of brain ECS volume. It also suggests a potential role in human epilepsy for HA and genes that are involved in hyaluraonan synthesis and degradation.
While epilepsy is one of the most common neurological disorders—affecting approximately 1 percent of the population worldwide—it is one of the least understood. It is characterized by recurrent spontaneous seizures caused by the abnormal firing of neurons. Although epilepsy treatment is available and effective for about 70 percent of cases, a substantial number of patients could benefit from a new therapeutic approach.
“Hyaluronan is widely known as a key structural component of cartilage and important for maintaining healthy cartilage. Curiously, it has been recognized that the adult brain also contains a lot of hyaluronan, but little is known about what hyaluronan does in the brain,” said Yu Yamaguchi, M.D., Ph.D., professor in our Human Genetics Program.
“This is the first study that demonstrates the important role of this unique molecule for normal functioning of the brain, and that its deficiency may be a cause of epileptic disorders. A better understanding of how hyaluronan regulates brain function could lead to new treatment approaches for epilepsy,” Yamaguchi added.
The extracellular matrix of the brain has a unique molecular composition. Earlier studies focused on the role of matrix molecules in cell adhesion and axon pathfinding during neural development. In recent years, increasing attention has been focused on the roles of these molecules in the regulation of physiological functions in the adult brain.
In this study, the investigators examined the role of HA using mutant mice deficient in each of the three hyaluronan synthase genes (Has1, Has2, Has3).
“We showed that Has-mutant mice develop spontaneous epileptic seizures, indicating that HA is functionally involved in the regulation of neuronal excitability. Our study revealed that deficiency of HA results in a reduction in the volume of the brain’s ECS, leading to spontaneous epileptiform activity in hippocampal CA1 pyramidal neurons,” said Sabina Hrabetova, M.D., Ph.D., associate professor in the Department of Cell Biology at SUNY.
“We believe that this study not only addresses one of the longstanding questions concerning the in-vivo role of matrix molecules in the brain, but also has broad appeal to epilepsy research in general,” said Katherine Perkins, Ph.D., associate professor in the Department of Physiology and Pharmacology at SUNY.
“More specifically, it should stimulate researchers in the epilepsy field because our study reveals a novel, non-synaptic mechanism of epileptogenesis. The fact that our research can lead to new anti-epileptic therapies based on the preservation of hyaluronan adds further significance for the broader biomedical community and the public,” the authors added.
Brain inflammation a recipe for chronic fatigue
Patients with chronic fatigue syndrome (CFS), also known as myalgic encephalomyelitis, experience severe and often disabling exhaustion. Other symptoms include cognitive dysfunction, pain and depression. Although brain inflammation is thought to be involved in the development of these symptoms, direct evidence of this relationship has proved elusive.
Yasuyoshi Watanabe, Yasuhito Nakatomi, Kei Mizuno and colleagues from the RIKEN Center for Life Science Technologies and other institutes in Japan have now shown using a noninvasive brain imaging technique that the neuropsychological symptoms of patients with CFS are closely associated with widespread inflammation in the brain.
Positron emission tomography (PET) is a brain imaging technique that uses radioactive tracers attached to particular cell types or molecules to noninvasively track changes in the brain in disease states. To examine the effect of CFS, the researchers used a radioactive tracer that labels activated glial cells, which tend to be associated with neuroinflammation. They performed PET imaging studies on nine CFS sufferers and ten healthy individuals to identify the extent to which brain inflammation plays a role in CFS. They found that the levels of tracer binding were much higher in multiple brain regions in the CFS patients compared with the same brain regions in the healthy participants.
The investigation also found correlations between tracer binding in various brain regions and the severity of symptoms in the CFS patients. The researchers found that inflammation in the thalamus—a region of the brain responsible for relaying motor and sensory information to and from the cerebral cortex—correlated with the severity of both cognitive impairment and pain in the CFS patients. They also identified a correlation between inflammation in the amygdala—a part of the brain linked to emotional memory—and the severity of cognitive impairment. The severity of depression in CFS patients, on the other hand, was linked to the extent of inflammation in the hippocampus, which is a part of the brain known to be associated with depression.
The findings suggest that inflammation in the brain plays a key role in CFS in humans. Drugs that fight inflammation in the brain may therefore offer promising therapies to prevent or treat CFS and its related symptoms of pain, depression and cognitive dysfunction.
“Because CFS is diagnosed based on subjective symptoms such as fatigue, pain, sleep problems and cognitive impairment,” says Mizuno, “neuroinflammation as observed by PET imaging could be helpful as a more objective biomarker for diagnosis of the disorder.”
Investigators Discover How Key Protein Enhances Memory and Learning
Case Western Reserve researchers have discovered that a protein previously implicated in disease plays such a positive role in learning and memory that it may someday contribute to cures of cognitive impairments. The findings regarding the potential virtues of fatty acid binding protein 5 (FABP5) — usually associated with cancer and psoriasis — appear in the May 2 edition of The Journal of Biological Chemistry.
“Overall, our data show that FABP5 enhances cognitive function and that FABP5 deficiency impairs learning and memory functions in the brain hippocampus region,” said senior author Noa Noy, PhD, a professor of pharmacology at the School of Medicine. “We believe if we could find a way to upregulate the expression of FABP5 in the brain, we might have a therapeutic handle on cognitive dysfunction or memory impairment in some human diseases.”
FABP5 resides in many tissues and is especially highly expressed in the brain. Noy and her Case Western Reserve School of Medicine and National Institute on Alcohol Abuse and Alcoholism colleagues particularly wanted to understand how this protein functioned in neurons. They performed imaging studies comparing the activation of a key transcription factor in the brain tissue of normal mice and in FABP5-deficient mice. (Transcription factor is a protein the controls the flow of genetic information). The investigations revealed that FABP5 performs two different functions in neurons. First, it facilitates the degradation of endocannabinoids, which are neurological modulators controlling appetite, pain sensation, mood and memory. Second, FABP5 regulates gene expression, a process that essentially gives cells their marching orders on structure, appearance and function.
“FABP5 improves learning and memory both because it delivers endocannabinoids to cellular machinery that breaks them down and because it shuttles compounds to a transcription factor that increases the expression of cognition-associated genes,” Noy said.
Even though endocannabinoids affect essential physiological processes from appetite to memory, the “cannabinoid” part of the word signifies that these natural biological compounds act similarly to drugs such as marijuana and hashish. Too much endocannabinoid can lead to impaired learning and memory.
In simple terms, FABP5 transports endocannabinoids for processing. FABP5 functions like a bus and carries the brain’s endocannabinoids and their biological products to two stations within the neuron cell. FABP5 captures endocannabinoids entering the neuron and delivers them to an enzyme that degrades them (station 1). Then, that degraded product is picked up by the same protein (FABP5) and shuttled to the cell nucleus — specifically, to a transcription factor within it (station 2). Binding of the degraded product activates the transcription factor and allows it to induce expression of multiple genes. The genes that are induced in this case tell the cells to take steps that promote learning and memory.
Noy and associates also compared memory and learning in FABP5-deficient mice and in normal ones. In one test, both sets of mice repeatedly swam in mazes that had a platform in one established location where they could climb out of the water. During subsequent swims, the wild-type mice reached the platform quickly because they had learned — and remembered — its location. Their FABP5-deficient counterparts took much longer, typically finding the platform’s location by chance.
“In addition to regulating cell growth as in skin and in cancer cells, for example, FABP5 also plays a key role in neurons of the brain,” Noy said. “FABP5 controls the biological actions of small compounds that affect memory and learning and that activate a transcription factor, which regulates neuronal function.”
(Source: casemed.case.edu)
Study explores genetics behind Alzheimer’s resiliency
Autopsies have revealed that some individuals develop the cellular changes indicative of Alzheimer’s disease without ever showing clinical symptoms in their lifetime.
Vanderbilt University Medical Center memory researchers have discovered a potential genetic variant in these asymptomatic individuals that may make brains more resilient against Alzheimer’s.
“Most Alzheimer’s research is searching for genes that predict the disease, but we’re taking a different approach. We’re looking for genes that predict who among those with Alzheimer’s pathology will actually show clinical symptoms of the disease,” said principal investigator Timothy Hohman, Ph.D., a post-doctoral research fellow in the Center for Human Genetics Research and the Vanderbilt Memory and Alzheimer’s Center.
The article, “Genetic modification of the relationship between phosphorylated tau and neurodegeneration,” was published online recently in the journal Alzheimer’s and Dementia.
The researchers used a marker of Alzheimer’s disease found in cerebrospinal fluid called phosphorylated tau. In brain cells, tau is a protein that stabilizes the highways of cellular transport in neurons. In Alzheimer’s disease tau forms “tangles” that disrupt cellular messages.
Analyzing a sample of 700 subjects from the Alzheimer’s Disease Neuroimaging Initiative, Hohman and colleagues looked for genetic variants that modify the relationship between phosphorylated tau and lateral ventricle dilation — a measure of disease progression visible with magnetic resonance imaging (MRI). One genetic mutation (rs4728029) was found to relate to both ventricle dilation and cognition and is a marker of neuroinflammation.
“This gene marker appears to be related to an inflammatory response in the presence of phosphorylated tau,” Hohman said.
“It appears that certain individuals with a genetic predisposition toward a ‘bad’ neuroinflammatory response have neurodegeneration. But those with a genetic predisposition toward no inflammatory response, or a reduced one, are able to endure the pathology without marked neurodegeneration.”
Hohman hopes to expand the study to include a larger sample and investigate gene and protein expression using data from a large autopsy study of Alzheimer’s disease.
“The work highlights the possible mechanism behind asymptomatic Alzheimer’s disease, and with that mechanism we may be able to approach intervention from a new perspective. Future interventions may be able to activate these innate response systems that protect against developing Alzheimer’s symptoms,” Hohman said.
(Source: news.vanderbilt.edu)
Out of shape? Your memory may suffer
Here’s another reason to drop that doughnut and hit the treadmill: A new study suggests aerobic fitness affects long-term memory.
Michigan State University researchers tested 75 college students during a two-day period and found those who were less fit had a harder time retaining information.
“The findings show that lower-fit individuals lose more memory across time,” said Kimberly Fenn, study co-author and assistant professor of psychology.
The study, which appears online in the research journal Cognitive, Affective & Behavioral Neuroscience, is one of the first to investigate young, supposedly healthy adults. Previous research on fitness and memory has focused largely on children, whose brains are still developing, and the elderly, whose memories are declining.
Participants studied related word pairs such as “camp” and “trail.” The next day, they were tested on the word pairs to evaluate long-term memory retention. Long-term memory is anything remembered more than about 30 seconds ago.
Aerobic fitness was gauged by oxygen consumption derived from a treadmill test and factored with the participants’ weight, percent body fat, age and sex.
The findings speak to the increasingly sedentary lifestyles found in the United States and other Western cultures. A surprising number of the college students in the study were significantly out of shape and did much worse at retaining information than those who were extremely fit, Fenn said.
Her co-authors included kinesiology researchers Matthew Pontifex and Karin Pfeiffer.
Scientists reveal circuitry of fundamental motor circuit
Scientists at the Salk Institute have discovered the developmental source for a key type of neuron that allows animals to walk, a finding that could help pave the way for new therapies for spinal cord injuries or other motor impairments related to disease.
The spinal cord contains a network of neurons that are able to operate largely in an autonomous manner, thus allowing animals to carry out simple rhythmic walking movements with minimal attention—giving us the ability, for example, to walk while talking on the phone. These circuits control properties such as stepping with each foot or pacing the tempo of walking or running.
The researchers, led by Salk professor Martyn Goulding, identified for the first time which neurons in the spinal cord were responsible for controlling a key output of this locomotion circuit, namely the ability to synchronously activate and deactivate opposing muscles to create a smooth bending motion (dubbed flexor-extensor alternation). The findings were published April 2 in Neuron.
Motor circuits in the spinal cord are assembled from six major types of interneurons—cells that interface between nerves descending from the brain and nerves that activate or inhibit muscles. Goulding and his team had previously implicated one class of interneuron, the V1 interneurons, as being a likely key component of the flexor-extensor circuitry. However when V1 interneurons were removed, the team saw that flexor-extensor activity was still intact, leading them to suspect another type of cell was also involved in coordinating this aspect of movement.
To determine what other interneurons were at play in the flexor-extensor circuit, the team looked for other cells in the spinal cord with properties that were similar to those of the V1 neurons. In doing this they began to focus on another class of neuron, whose function was not known, V2b interneurons. Using a specialized experimental setup that allows one to monitor locomotion in the spinal cord itself, the team saw a synchronous pattern of flexor and extensor activity when V2b interneurons were inactivated along with the V1 interneurons.
The team also showed that this synchronicity led to newborn mice displaying a tetanus-like reaction when the two types of interneurons were inactivated: the limbs froze in one position because they no longer had the push-pull balance of excitation and inhibition that is needed to move.
These findings further confirm the hypothesis put forward over 120 years ago by the Nobel Prize-winning neuroscientist, Charles Sherrington, that flexor-extensor alternation is essential for locomotion in all animals that have limbs. He proposed that specialized cells in the spinal cord called switching cells performed this function. After 120 years, Goulding and researchers have now uncovered the identity of these switching cells.
"Our whole motor system is built around flexor-extension; this is the cornerstone component of movement," says Goulding, holder of Salk’s Frederick W. and Joanna J. Mitchell Chair. "If you really want to understand how animals move you need to understand the contribution of these switching cells."
With a more thorough understanding of the basic science around how this flexor-extensor circuit works, scientists will be in a better position to, for example, create a system that can reactivate the spinal cord or mimic signals sent from the brain to the spinal cord.
Individual Brain Activity Predicts Tendency to Succumb to Daily Temptations
Activity in areas of the brain related to reward and self-control may offer neural markers that predict whether people are likely to resist or give in to temptations, like food, in daily life, according to research in Psychological Science, a journal of the Association for Psychological Science.
“Most people have difficulty resisting temptation at least occasionally, even if what tempts them differs,” say psychological scientists Rich Lopez and Todd Heatherton of Dartmouth College, authors on the study. “The overarching motivation of our work is to understand why some people are more likely to experience this self-regulation failure than others.”
The research findings reveal that activity in reward areas of the brain in response to pictures of appetizing food predicts whether people tend to give in to food cravings and desires in real life, whereas activity in prefrontal areas during taxing self-control tasks predicts their ability to resist tempting food.
Lopez and colleagues used functional MRI (fMRI) to explore the interplay between activity in prefrontal brain regions associated with self-control (e.g., inferior frontal gyrus) and subcortical areas involved in affect and reward (e.g., nucleus accumbens), and to see whether the interplay between these regions predicts how successful (or unsuccessful) people are in controlling their desires to eat on a daily basis.
The researchers recruited 31 female participants to take part in an initial fMRI scanning session that included two important tasks.
For the first task, the participants were presented with various images, including some of high-calorie foods, like dessert items, fast-food items, and snacks. The participants were simply asked to indicate whether each image was set indoors or outdoors — the researchers were specifically interested in measuring activity in the nucleus accumbens in response to the food-related images.
For the second task, the participants were asked to press or not press a button based on the specific cues provided with each image, a task designed to gauge self-control ability. During this task, the researchers measured activity in the inferior frontal gyrus (IFG).
The fMRI scanning session was followed by 1 week of so-called “experience sampling,” in which participants were signaled several times a day on a smartphone and asked to report their food desires and eating behaviors. Any time participants reported a food desire, they were then asked about the strength of the desire and their resistance to it. If they ultimately gave in to the craving, they were asked to say how much they had eaten.
As expected, participants who had relatively higher activity in the nucleus accumbens in response to the food images tended to experience more intense food desires. More importantly, they were also more likely to give in to their food cravings and eat the desired food.
The researchers were surprised by how robust this association was:
“Reward-related brain activity, which can be considered an implicit measure, predicted who gave in to temptations to eat, as well as who ate more, above and beyond the desire strength reported by participants in the moment,” say Lopez and Heatherton. “This could help to explain a previous finding from our lab that people who show this kind of brain activity the most are also the most likely to gain weight over six months.”
But brain activity also predicted who was more likely to be able to resist temptation: Participants who showed relatively higher IFG activity on the self-control task acted on their cravings less often.
When the researchers grouped the participants according to their IFG activity, the data revealed that participants who had high IFG activity were more successful at controlling how much they ate in particularly tempting situations than those who had low IFG activity. In fact, participants with low IFG activity were about 8.2 times more likely to give in to a food desire than those who had high IFG activity.
“Taken together, the results from the present study provide initial evidence for neural markers of everyday eating behaviors that can identify individuals who are more likely than others to give in to temptations to eat,” the researchers write.
Lopez, Heatherton, and colleagues are currently conducting studies focused on groups of people who are especially prone to self-regulation failure: chronic dieters.
They’re investigating, for example, how dieters’ brains respond to food cues after they’ve exhausted their self-control resources. The researchers hypothesize that depleting self-control may heighten reward-related brain activity, effectively “turning up the volume on temptations,” and predicting behaviors like overeating in daily life.
“Failures of self-control contribute to nearly half of all death in the United States each year,” the researchers note. “Our findings and future research may ultimately help people learn ways to resist their temptations.”