Posts tagged psychology
Articles and news from the latest research reports.
This is an image of white matter pathways extracted from diffusion tensor imaging data for infants at-risk for autism. Warmer colors represent higher fractional anisotropy. Credit: Image created by Jason Wolff, Ph.D.
A new study led by the University of North Carolina at Chapel Hill found significant differences in brain development starting at age 6 months in high-risk infants who later develop autism, compared to high-risk infants who did not develop autism.
"It’s a promising finding," said Jason J. Wolff, PhD, lead author of the study and a postdoctoral fellow at UNC’s Carolina Institute for Developmental Disabilities (CIDD). "At this point, it’s a preliminary albeit great first step towards thinking about developing a biomarker for risk in advance of our current ability to diagnose autism."
The study also suggests, Wolff said, that autism does not appear suddenly in young children, but instead develops over time during infancy. This raises the possibility “that we may be able to interrupt that process with targeted intervention,” he said.
Joseph Piven, MD, director of the CIDD, is senior author of the study.
The study was published online on Friday, Feb. 17 at AJP in Advance, a section of the website of the American Journal of Psychiatry. Its results are the latest from the ongoing Infant Brain Imaging Study (IBIS) Network, which is funded by the National Institutes of Health and headquartered at UNC. Piven received an NIH Autism Centers of Excellence (ACE) program network award for the IBIS Network in 2007. ACE networks consist of researchers at many facilities in locations throughout the country, all of whom work together on a single research question.
Participants in the study were 92 infants who all have older siblings with autism and thus are considered to be at high risk for autism themselves. All had diffusion tensor imaging – which is a type of magnetic resonance imaging (MRI) – at 6 months and behavioral assessments at 24 months. Most also had additional brain imaging scans at either or both 12 and 24 months.
At 24 months, 28 infants (30 percent) met criteria for autism spectrum disorders while 64 infants (70 percent) did not. The two groups differed in white matter fiber tract development – pathways that connect brain regions – as measured by fractional anisotropy (FA). FA measures white matter organization and development, based on the movement of water molecules through brain tissue.
This study examined 15 separate fiber tracts, and found significant differences in FA trajectories in 12 of the 15 tracts between infants who did develop autism versus infants who did not. Infants who later developed autism had elevated FA at six months but then experienced slower change over time. By 24 months of age, infants with autism had lower FA values than infants without autism.
"This evidence, which implicates multiple fiber pathways, suggests that autism is a whole-brain phenomenon not isolated to any particular brain region," Wolff said.
Provided by University of North Carolina School of Medicine
Source: medicalxpress
Neurons change shape after gene therapy
February 16, 2012
(Medical Xpress) — Gene therapy not only helps injured brain cells to live longer and regenerate, but also changes the shape of the cells, according to researchers The University of Western Australia.
The study, published in the international science and medicine journal PLoS One, was led by Winthrop Professor Alan Harvey from UWA’s School of Anatomy, Physiology and Human Biology, and Associate Professor Jennifer Rodger, NHMRC Research Fellow in Experimental and Regenerative Neurosciences at UWA’s School of Animal Biology. The research was funded primarily by the WA Neurotrauma Research Program.
Professor Harvey said gene therapy was a relatively new strategy that attempted to help injured brain cells survive and regrow.
"Our previous work has shown that when growth-promoting genes are introduced into injured brain cells for long periods of time (up to nine months), the cells’ capacity for survival and regeneration is significantly increased," he said.
"We have now shown that these same neurons have also changed shape in response to persistent over-expression of the growth factors. Importantly, it is not just neurons containing the introduced growth-promoting gene that are affected, but neighbouring "bystander" neurons."
Professor Harvey said neural morphology was very important in determining how a cell communicated with other cells and formed the circuits that allowed the brain to function.
"Any changes in morphology are therefore likely to alter the way neurons receive and transmit information. These changes may be beneficial but could also interfere with normal brain circuits, reducing the benefits of improved survival and regeneration."
Professor Harvey said the results were significant for those involved in designing gene therapy-based protocols to treat brain and spinal cord injury and degeneration.
"These new results suggest that we may need to be careful about the types of genes we use in neurotherapy and how long we continue the therapy. While it may be beneficial for these genes to move around and cause changes in other cells, we need to be able to switch them off once the change has taken place."
Provided by University of Western Australia
Source: medicalxpress.com
Researchers Make Living Model of Brain Tumor
February 16th, 2012
Researchers have created a living 3-D model of a brain tumor and its surrounding blood vessels. In experiments, the scientists report that iron-oxide nanoparticles carrying the agent tumstatin were taken by blood vessels, meaning they should block blood vessel growth. The living-tissue model could be used to test the effectiveness of nanoparticles in fighting other diseases. Results appear in Theranostics.
Brown University scientists have created the first three-dimensional living tissue model, complete with surrounding blood vessels, to analyze the effectiveness of therapeutics to combat brain tumors. The 3-D model gives medical researchers more and better information than Petri dish tissue cultures.
The researchers created a glioma, or brain tumor, and the network of blood vessels that surrounds it. In a series of experiments, the team showed that iron-oxide nanoparticles ferrying the chemical tumstatin penetrated the blood vessels that sustain the tumor with oxygen and nutrients. The iron-oxide nanoparticles are important, because they are readily taken up by endothelial cells and can be tracked by magnetic resonance imaging.
Previous experiments have shown that tumstatin was effective at blocking endothelial cell growth in gliomas. The tests by the Brown researchers took it to another level by confirming, in a 3-D, living environment, the iron-oxide nanoparticles’ ability to reach blood vessels surrounding a glioma as well as tumstatin’s ability to penetrate endothelial cells.
“The 3-D glioma model that we have developed offers a facile process to test diffusion and penetration into a glioma that is covered by a blood vessel-like coating of endothelial cells,” said Don Ho, a graduate student in the lab of chemistry professor Shouheng Sun and the lead author of the paper in the journal Theranostics. “This assay would save time and money, while reducing tests in living organisms, to examine an agent’s 3-D characteristics such as the ability for targeting and diffusion.”
The tissue model concept comes from Jeffrey Morgan, a bioengineer at Brown and a corresponding author on the paper. Building on that work, Ho and others created an agarose hydrogel mold in which rat RG2-cell gliomas roughly 200 microns in diameter formed. The team used endothelial cells derived from cow respiratory vessels, which congregated around the tumor and created the blood vessel architecture. The advantage of a 3-D model rather than Petri-dish-type analyses is that the endothelial cells attach to the tumor, rather than being separated from the substrate. This means the researchers can study their formation and growth, as well as the action of anti-therapeutic agents, just as they would in a living organism.
“You want to see nanoparticles that diffuse through the endothelial cells, which is lost in 2-D because you just have diffusion into media,” Ho said.
Other 3-D tissue models have been “forced cell arrangements,” Ho said. The 3-D glioma model, in contrast, allowed the glioma and the endothelial cells to assemble naturally, just as they would in real life. “It more clearly mimics what would actually happen,” Ho explained.
The group then attached tumstatin, part of a naturally occurring protein found in collagen, to iron-oxide nanoparticles and dosed the mold. True to form, the nanoparticles were gobbled up by the endothelial cells. In a series of in vitro experiments, the team reported the tumstatin iron-oxide nanoparticles decreased vasculature growth 2.7 times more than under normal conditions over eight days. “The growth is pretty much flat,” Ho said. “There’s no new growth of endothelial cells.” The next step is to test the tumstatin nanoparticles’ performance in the 3-D environment.
“This model has significant potential to help in the testing and optimization of the design of therapeutic/diagnostic nanocarriers and determine their therapeutic capabilities,” the researchers write.
Source: Neuroscience News
New Molecular Map to Guide Development of New Treatments for Multiple Sclerosis and Other Diseases
February 16th, 2012
A team of scientists from The Scripps Research Institute, collaborating with members of the drug discovery company Receptos, has created the first high-resolution virtual image of cellular structures called S1P1 receptors, which are critical in controlling the onset and progression of multiple sclerosis and other diseases.
This new molecular map is already pointing researchers toward promising new paths for drug discovery and aiding them in better understanding how certain existing drugs work.
Source: Neuroscience News
Inflammation In Brain Inhibited By New Class Of Potential Drugs
Article Date: 16 Feb 2012 - 1:00 PST
Scientists at Emory University School of Medicine have identified a new group of compounds that may protect brain cells from inflammation linked to seizures and neurodegenerative diseases.
The compounds block signals from EP2, one of the four receptors for prostaglandin E2, which is a hormone involved in processes such as fever, childbirth, digestion and blood pressure regulation. Chemicals that could selectively block EP2 were not previously available. In animals, the EP2 blockers could markedly reduce the injury to the brain induced after a prolonged seizure, the researchers showed.
The results were published online this week in the Proceedings of the National Academy of Sciences Early Edition.
“EP2 is involved in many disease processes where inflammation is showing up in the nervous system, such as epilepsy, stroke and neurodegenerative diseases,” says senior author Ray Dingledine, PhD, chairman of Emory’s Department of Pharmacology. “Anywhere that inflammation is playing a role via EP2, this class of compounds could be useful. Outside the brain, EP2 blockers could find uses in other diseases with a prominent inflammatory component such as cancer and inflammatory bowel disease.”
Prostaglandins are the targets for non-steroid anti-inflammatory drugs (NSAIDs) such as aspirin and ibuprofen. NSAIDSs inhibit enzymes known as cyclooxygenases, the starting point for generating prostaglandins in the body. Previous research indicates that drugs that inhibit cyclooxygenases can have harmful side effects. For example, sustained use of aspirin can weaken the stomach lining, coming from prostaglandins’ role in the stomach. Even drugs designed to inhibit only cyclooxygenases involved in pain and inflammation, such as Vioxx, have displayed cardiovascular side effects.
Dingledine’s team’s strategy was to bypass cyclooxygenase enzymes and go downstream, focusing on one set of molecules that relay signals from prostaglandins. Working with Yuhong Du in the Emory Chemical Biology Discovery Center, postdoctoral fellows Jianxiong Jiang, Thota Ganesh and colleagues sorted through a library of 262,000 compounds to find those that could block signals from the EP2 prostaglandin receptor but not related receptors. One of the compounds could prevent damage to neurons in mice after “status epilepticus,” a prolonged drug-induced seizure used to model the neurodegeneration linked to epilepsy. The team found that a family of related compounds had similar protective effects.
Dingledine says that the compounds could become valuable tools for exploring new ways to treat neurological diseases. However, given the many physiological processes prostaglandins regulate, more tests are needed, he says. Prostaglandin E2 is itself a drug used to induce labor in pregnant women, and female mice engineered to lack the EP2 receptor are infertile, so the compounds would need to be tested for effects on reproductive organs, for example.
View drug information on Vioxx.
Source: Medical News Today
Drinking Alcohol Shrinks Critical Brain Regions in Genetically Vulnerable Mice
ScienceDaily (Feb. 15, 2012) — Brain scans of two strains of mice imbibing significant quantities of alcohol reveal serious shrinkage in some brain regions — but only in mice lacking a particular type of receptor for dopamine, the brain’s “reward” chemical. The study, conducted at the U.S. Department of Energy’s Brookhaven National Laboratory and published in the May 2012 issue of Alcoholism: Clinical and Experimental Research, now online, provides new evidence that these dopamine receptors, known as DRD2, may play a protective role against alcohol-induced brain damage.
"This study clearly demonstrates the interplay of genetic and environmental factors in determining the damaging effects of alcohol on the brain, and builds upon our previous findings suggesting a protective role of dopamine D2 receptors against alcohol’s addictive effects," said study author Foteini Delis, a neuroanatomist with the Behavioral Neuropharmacology and Neuroimaging Lab at Brookhaven, which is funded through the National Institute on Alcohol Abuse and Alcoholism (NIAAA). Coauthor and Brookhaven/NIAA neuroscientist Peter Thanos stated that, "These studies should help us better understand the role of genetic variability in alcoholism and alcohol-induced brain damage in people, and point the way to more effective prevention and treatment strategies."
The current study specifically explored how alcohol consumption affects brain volume — overall and region-by-region — in normal mice and a strain of mice that lack the gene for dopamine D2 receptors. Half of each group drank plain water while the other half drank a 20 percent ethanol solution for six months. Then scientists performed magnetic resonance imaging (MRI) scans on all the mice and compared the scans of those drinking alcohol with those from the water drinkers in each group.
The scans showed that chronic alcohol drinking induced significant overall brain atrophy and specific shrinkage of the cerebral cortex and thalamus in the mice that lacked dopamine D2 receptors, but not in mice with normal receptor levels. Mice in both groups drank the same amount of alcohol.
"This pattern of brain damage mimics a unique aspect of brain pathology observed in human alcoholics, so this research extends the validity of using these mice as a model for studying human alcoholism," Thanos said.
In humans, these brain regions are critically important for processing speech, sensory information, and motor signals, and for forming long-term memories. So this research helps explain why alcohol damage can be so widespread and detrimental.
"The fact that only mice that lacked dopamine D2 receptors experienced brain damage in this study suggests that DRD2 may be protective against brain atrophy from chronic alcohol exposure," Thanos said. "Conversely, the findings imply that lower-than-normal levels of DRD2 may make individuals more vulnerable to the damaging effects of alcohol."
That would in effect deal people with low DRD2 levels a double whammy of alcohol vulnerability: Previous studies conducted by Thanos and collaborators suggest that individuals with low DRD2 levels may be more susceptible to alcohol’s addictive effects.
"The increased addictive liability and the potentially devastating increased susceptibility to alcohol toxicity resulting from low DRD2 levels make it clear that the dopamine system is an important target for further research in the search for better understanding and treatment of alcoholism," Thanos said.
Source: Science Daily
The brain’s caudate nucleus and frontal cortex are less active in people who drink more
Alcohol abuse and dependence are common problems in the United States due to a number of factors, two of which may be social drinking by college students and young adults, and risk taking that may lead to heavier drinking later in life. A study of the neural underpinnings of risk-taking in young, non-dependent social drinkers has found that the caudate nucleus and frontal cortex regions of the brain show less activation in people who drink more heavily.
Segmented synapses Synaptic structures in mice engineered to lack the protein biglycan (bottom row) appear discontinuous compared to the synaptic structures in normal mice (top).
(Credit: Fallon Lab/Brown University)
Turmeric-Based Drug Effective On Alzheimer Flies
ScienceDaily (Feb. 14, 2012) — Curcumin, a substance extracted from turmeric, prolongs life and enhances activity of fruit flies with a nervous disorder similar to Alzheimers, according to new research. The study conducted at Linköping University, indicates that it is the initial stages of fibril formation and fragments of the amyloid fibrils that are most toxic to neurons.
Above left are the survival curves for “Alzheimer flies” treated (dashed line) and those not treated with curcumin. The flies that were administered curcumin lived longer and were more active. The scientists identified an accelerated formation of amyloid plaque in the treated flies, which seemed to protect the nerve cells. On the right we see microscopic images of neurons (blue) and plaque (green) in the fruit fly’s brain. The study strengthens the hypothesis that a curcumin-based drug can contribute to toxic fibrils being encapsulated (bottom left of the figure). (Credit: Per Hammarström, Ina Caesar)
Ina Caesar, as the lead author, has published the results of the study in the journal PLoS ONE.
For several years curcumin has been studied as a possible drug candidate to combat Alzheimer’s disease, which is characterized by the accumulation of sticky amyloid-beta and Tau protein fibres. Linköping researchers wanted to investigate how the substance affected transgenic fruit flies (Drosophila melanogaster), which developed evident Alzheimer’s symptoms. The fruit fly is increasingly used as a model for neurodegenerative diseases.
Five groups of diseased flies with different genetic manipulations were administered curcumin. They lived up to 75 % longer and maintained their mobility longer than the sick flies that did not receive the substance.
However, the scientists saw no decrease of amyloid in the brain or eyes. Curcumin did not dissolve the amyloid plaque; on the contrary it accelerated the formation of fibres by reducing the amount of their precursor forms, known as oligomers.
"The results confirm our belief that it is the oligomers that are most harmful to the nerve cells," says Professor Per Hammarstrom, who led the study.
"We now see that small molecules in an animal model can influence the amyloid form. To our knowledge the encapsulation of oligomers is a new and exciting treatment strategy," he said.
Several theories have been established about how oligomers can instigate the disease process. According to one hypothesis, they become trapped at synapses, inhibiting nerve impulse signals. Others claim that they cause cell death by puncturing the cell membrane.
Curcumin is extracted from the root of herbaceous plant turmeric and has been used as medicine for thousands of years. More recently, it has been tested against pain, thrombosis and cancer.
Source: Science Daily
People Forage for Memories in the Same Way Birds Forage for Berries
February 14th, 2012
Humans move between ‘patches’ in their memory using the same strategy as bees flitting between flowers for pollen or birds searching among bushes for berries.
Researchers at the University of Warwick and Indiana University have identified parallels between animals looking for food in the wild and humans searching for items within their memory – suggesting that people with the best ‘memory foraging’ strategies are better at recalling items.
Scientists asked people to name as many animals as they could in three minutes and then compared the results with a classic model of optimal foraging in the real world, the marginal value theorem, which predicts how long animals will stay in one patch before jumping to another.
Dr Thomas Hills, associate professor in the psychology department at the University of Warwick, said: “A bird’s food tends to be clumped together in a specific patch – for example on a bush laden with berries.
“But when the berries on a bush are depleted to the point where the bird’s energy is best focused on another more fruitful bush, it will move on.
“This kind of behaviour is predicted by the marginal value theorem, for a wide variety of animals.
“Because of the way human attention has evolved, we wondered if humans might use the same strategies to forage in memory. It turns out, they do.
“When faced with a memory task, we focus on specific clusters of information and jump between them like a bird between bushes. For example, when hunting for animals in memory, most people start with a patch of household pets—like dog, cat and hamster.
“But then as this patch becomes depleted, they look elsewhere. They might then alight on another semantically distinct ‘patch’, for example predatory animals such as lion, tiger and jaguar.”
The study shows that people who either stay too long or not long enough in one ‘patch’ did not recall as many animals as those who better judged the best time to switch between patches.
In other words, people who most closely adhered to the marginal value theorem produced more items.
The study Optimal Foraging in Semantic Memory, published in Psychological Review, asked 141 undergraduates (46 men and 95 women) at Indiana University to name as many animals as they could in three minutes.
They then analysed the responses using a categorisation scheme and also a semantic space model, called BEAGLE, which identifies clusters in the memory landscape based on the way words are related to one another in natural language.
Source: Neuroscience News