Posts tagged psychology
Articles and news from the latest research reports.
A new study from The University of Queensland shows monitoring the brain of stroke patients using Quantitative EEG (QEEG) studies could inform treatments and therefore, minimising brain damage of stroke victims.
“The main goals of this research were to evaluate key findings, identify common trends and determine what the future priorities should be, both for research and for translating this to best inform clinical management of stroke patients,” Dr Finnigan from UQ’s Centre for Clinical Research said.
The review of outcomes from hundreds of patients has highlighted that QEEG indicators are particularly informative in two ways.
“Firstly they can help predict long-term deficits caused by stroke, … In addition, they could provide immediate information on how patients are responding to treatments and guide decisions about follow-on treatments, even before stroke symptoms change,” Dr Finnigan said.
A condition believed to be a normal part of the ageing process has been found to have a negative effect on the brain function of older adults.
Leukoaraiosis, also known as small vessel ischemia, is a condition in which diseased blood vessels lead to small areas of damage in the white matter of the brain. The lesions are common in the brains of people over the age of 60, although the amount of disease varies among individuals.
"We know that aging is a risk factor for leukoaraiosis, and we suspect that high blood pressure may also play a role, … Different systems of the brain respond differently to disease, … White matter damage affects connections within the brain’s language network, which leads to an overall reduction in network activity." -Kirk M. Welker, M.D., assistant professor of radiology in the College of Medicine at Mayo Clinic in Rochester, Minn.
(Source: medicalxpress.com)
Mount Sinai Researchers Identify New Drug Target for Schizophrenia
August 13, 2012
Researchers at Mount Sinai School of Medicine may have discovered why certain drugs to treat schizophrenia are ineffective in some patients. Published online in Nature Neuroscience, the research will pave the way for a new class of drugs to help treat this devastating mental illness, which impacts one percent of the world’s population, 30 percent of whom do not respond to currently available treatments.
A team of researchers at Mount Sinai School of Medicine set out to discover what epigenetic factors, or external factors that influence gene expression, are involved in this treatment-resistance to atypical antipsychotic drugs, the standard of care for schizophrenia. They discovered that, over time, an enzyme in the brains of schizophrenic patients analyzed at autopsy begins to compensate for the prolonged chemical changes caused by antipsychotics, resulting in reduced efficacy of the drugs.
"These results are groundbreaking because they show that drug resistance may be caused by the very medications prescribed to treat schizophrenia, when administered chronically," said Javier Gonzalez-Maeso, PhD, Assistant Professor of Psychiatry and Neurology at Mount Sinai School of Medicine and lead investigator on the study.
They found that an enzyme called HDAC2 was highly expressed in the brain of mice chronically treated with antipsychotic drugs, resulting in lower expression of the receptor called mGlu2, and a recurrence of psychotic symptoms. A similar finding was observed in the postmortem brains of schizophrenic patients. The research team administered a chemical called suberoylanilide hydroxamic acid (SAHA), which inhibits the entire family of HDACs. They found that this treatment prevented the detrimental effect of the antipsychotic called clozapine on mGlu2 expression, and also improved the therapeutic effects of atypical antipsychotics in mouse models.
Previous research conducted by the team showed that chronic treatment with the antipsychotic clozapine causes repression of mGlu2 expression in the frontal cortex of mice, a brain area key to cognition and perception. The researchers hypothesized that this effect of clozapine on mGlu2 may play a crucial role in restraining the therapeutic effects of antipsychotic drugs.
"We had previously found that chronic antipsychotic drug administration causes biochemical changes in the brain that may limit the therapeutic effects of these drugs,"said Dr. Gonzalez-Maeso. "We wanted to identify the molecular mechanism responsible for this biochemical change, and explore it as a new target for new drugs that enhance the therapeutic efficacy of antipsychotic drugs."
Mitsumasa Kurita, PhD, a postdoctoral fellow at Mount Sinai and the lead author of the study, said, “We found that atypical antipsychotic drugs trigger an increase of HDAC2 in frontal cortex of individuals with schizophrenia, which then reduces the presence of mGlu2, and thereby limits the efficacy of these drugs,” said
Dr. Gonzalez-Maeso’s team is now developing compounds that specifically inhibit HDAC2 as adjunctive treatments to antipsychotics. The study was funded by the National Institutes of Health.
Source: The Mount Sinai Hospital
Dr Kristin Hillman and Professor David Bilkey have found that neurons in a specific region of the frontal cortex, called the anterior cingulate cortex, become active during decisions involving competitive effort.
The researchers have discovered that neurons in this region appear to store information on whether a course of action demands competition, what the intensity of that competition will be, and critically, whether or not the competition is ‘worth it’ to achieve an end reward.
Their study, which appears online in the journal Nature Neuroscience, is the first to examine how competitive behaviour is encoded by neurons in the brain.
Source: University of Otago
This is an abandoned and sealed science lab located in Moscow. The lab, which was operated by the Russian army, conducted sophisticated experiments studying human and animal brains.
For more photos click here
Today, neuroscientists believe that your eye doesn’t see color at all — your brain creates it and constructs it through neural processes. Different features including color, shape, location, and velocity are picked up by different regions of the brain and then integrated into a holistic perception of an object.
How Depression Shrinks the Brain
12 August 2012
Certain brain regions in people with major depression are smaller and less dense than those of their healthy counterparts. Now, researchers have traced the genetic reasons for this shrinkage.
A series of genes linked to the function of synapses, or the gaps between brain cells crucial for cell-to-cell communication, can be controlled by a single genetic “switch” that appears to be overproduced in the brains of people with depression, a new study finds.
"We show that circuits normally involved in emotion, as well as cognition, are disrupted when this single transcription factor is activated," study researcher Ronald Duman, a professor of psychiatry at Yale University, said in a statement.
Shrinking brain
Brain-imaging studies, post-mortem examinations of human brains and animal studies have all found that in depression, a part of the brain called the dorsolateral prefrontal cortex shrinks. The neurons in this region, which is responsible for complex tasks from memory and sensory integration to the planning of actions, are also smaller and less dense in depressed people compared with healthy people.
Duman and his colleagues suspected that these neuronal abnormalities would include problems with the synapses, the points where brain cells “talk” to one another. At synapses, neurons release neurotransmitters that are picked up by their neighbors, carrying signals from cell to cell at rapid speed.
The researchers conducted gene profiling on the postmortem brain tissue of both depressed and mentally healthy subjects. They found a range of genes that were significantly less active in depressed people’s dorsolateral prefrontal cortexes, particularly five related to synaptic function: synapsin 1, Rab3A, calmodulin 2, Rab4B and TUBB4.
Synaptic damage
These genes are all involved in either the chemical signaling that occurs at synapses or the cellular recycling and regeneration processes that keep the synapse-system humming. All five are regulated by a single transcription factor called GATA1, which was overproduced in depressed brains.
The researchers activated GATA1 in the brains of rats and found that the factor decreased the complexity of the long, branchlike projections, or dendrites, of brain cells. These projections are the telephone lines that carry synaptic messages, integrating all the information a cell receives.
Extra GATA1 also increased depression-like behavior in the rats. For example, when given a swimming task, rats with extra GATA1 stayed immobile in the water longer, a signal of despair, than normal-GATA1 rats, the researchers report today (Aug. 12) in the journal Nature Medicine.
The researchers believe the damage could be a result of chronic stress, and they hope the findings lead to new depression treatments.
"We hope that by enhancing synaptic connections, either with novel medications or behavioral therapy, we can develop more effective antidepressant therapies," Duman said.
Source: Live Science
Western researchers explore secret origin of déjà vu
August 10, 2012
Most people have been in a situation that suddenly feels strangely familiar, while also realizing that they have never been in that specific place before. These experiences are called ‘déjà vu’ and the phenomenon has inspired countless books, songs and movies.
What is remarkable about déjà vu, says Western University graduate student Chris Martin, is that the impression of familiarity is accompanied by a sense that the current environment or situation should in fact feel new. But how can it be that a scene or an experience evokes a sense of familiarity but at the same time a feeling that this familiarity is wrong?
Despite the curiosity and excitement about déjà vu in popular culture, these subjective experiences remain poorly understood in scientific terms. Studying déjà vu has proven difficult due to the fleeting nature of these obscure occurrences, and due to the lack of experimental procedures to elicit them in the psychological laboratory.
In an article published online by Neuropsychologia, “Déjà Vu in Unilateral Temporal-Lobe Epilepsy is Associated with Selective Familiarity Impairments on Experimental Tasks of Recognition Memory,” Martin and psychology professor Stefan Köhler were able to shed light on this fascinating phenomenon by examining a rare group of neurological patients that experience déjà vu as an early sign of advancing seizures.
Due to lasting underlying brain pathology, most patients with temporal lobe epilepsy exhibit subtle impairments in memory even at times when no seizures are present. Köhler and his team built on this link by seeking behavioural markers of déjà vu on specific memory tasks that were designed to probe feelings of familiarity. The researchers discovered a pattern of performance that clearly distinguished patients with déjà vu from those without.
Specifically, familiarity was selectively impaired only in individuals with déjà vu in their seizure profile. In an experiment that placed different types of memories in conflict, patients with déjà vu were still able to counteract inappropriate feelings of familiarity with their ability to recollect pertinent information about previous actual events.
These findings, say Köhler and Martin, open a new window towards understanding the psychological and neural mechanisms that give rise to fleeting, subjective feelings of déjà vu. Köhler says they remind us that even when lasting for just a split second, memory experiences reflect the interplay of many different, sometimes competing processes. On another level, these findings are also of clinical relevance in the surgical treatment of temporal lobe epilepsy.
Source: University of Western Ontario
Neuronal network in the cerebellum
Fluorescence microscopy image showing the cerebellar network of Purkinje neurons from a mouse. The neurons are visualised by labelling the cells with green fluorescent protein (GFP). Purkinje cells are specialised neurons found in layers within the cerebellum (at the back of the brain). In humans they are one of the longest types of neurons in the brain and are involved in transmitting motor output from the cerebellum.
The Brain Set Free
August 11th, 2012
By Laura Sanders
Lifting neural constraints could turn back time, making way for youthful flexibility
Michael Morgenstern
A baby’s brain is a thirsty sponge, slurping up words, figuring out faces and learning which foods are good and bad to eat. Information about the world flooding into a young brain begins to carve out traces, like rushing water over soft limestone. As the outside world sculpts the growing brain, important connections between nerve cells become strong rivers, while smaller unused tributaries quietly disappear.
In time, these brain connections crystallize, forming indelible patterns etched into marble. Impressionable brain systems that allowed a child to easily learn a language, for instance, go away, abandoned for the speed and strength that come with rigidity. In a fully set brain, signals fly around effortlessly, making commonplace tasks short work. A master of efficiency, the adult brain loses the exuberance of childhood.
But the adult brain need not remain in this petrified state. In a feat of neural alchemy, the brain can morph from marble back to limestone.
The potential for this metamorphosis has galvanized scientists, who now talk about a mind with the power to remake itself. In the last few years, researchers have found ways to soften the stone, recapturing some of the lost magic of a young brain.
“There’s been a very, very significant change,” says Richard Davidson of the University of Wisconsin–Madison. “I don’t think the import of that basic fact has fully expressed itself.”
Though this research is still in its early stages, studies suggest techniques that dissolve structures that pin brain cells in place, interrupt molecular stop signals and tweak the rush of nerve cell activity can restore the brain’s youthful glow. Scientists are already attempting to reverse brain rigidity, boosting what’s known as “plasticity” in people with a vision disorder once thought to be irreversible in adults.
These efforts are not an exercise in neural vanity. A malleable brain, researchers hope, can heal after a stroke, combat the decline in vision that comes with old age and perhaps even repair a severed spinal cord. An end to childhood — and the prodigal learning that comes with it — does not need to eliminate the brain’s capacity for change. “There are still windows of opportunity out there,” says neuroscientist Daphné Bavelier of the University of Rochester in New York. “It may require a little more work to open them, though.”