Posts Tagged Neuropsychology and Neurology

Good Foods Boost Moods


Good Foods Boost MoodsNew research reveals that some common foods enhance moods with a striking similarity to valproic acid, a widely used prescription mood-stabilizing drug.

“Molecules in chocolate, a variety of berries and foods containing omega-3 fatty acids have shown positive effects on mood. In turn, our studies show that some commonly used flavor components are structurally similar to valproic acid,” said Karina Martinez-Mayorga, Ph.D., leader of the research team, which presented its findings at a meeting of the American Chemical Society.

Valproic acid, which is sold under brand names such as Depakene, Depakote and Stavzor, is used to smooth out the mood swings of people with manic-depressive disorder and related conditions, she said.

“The large body of evidence that chemicals in chocolate, blueberries, raspberries, strawberries, teas and certain foods could well be mood-enhancers encourages the search for other mood modulators in food,” she added.

While people have recognized the mood-altering properties of food for years, Martinez-Mayorga’s team is looking to identify the chemical compounds that moderate mood swings, help maintain cognitive health, improve mental alertness and delay the onset of memory loss.

Her study involved the use of techniques associated with chemoinformatics ― the application of informatic methods to solve chemical problems ― to screen the chemical structures of more than 1,700 food ingredients for similarities to antidepressant drugs and other agents with reported antidepressant activity.

She noted her team plans to move from analyzing the database to actually testing the flavor/mood hypothesis experimentally. The end result may be dietary recommendations or new nutritional supplements with beneficial mood effects, she said.

“It is important to remember that just eating foods that may improve mood is not a substitute for prescribed antidepressive drugs,” Martinez-Mayorga cautioned.

She added that eating specific foods and living a healthful lifestyle can generally boost moods for people who don’t require medication.

Karina Martinez-Mayorga, Ph.D., who described research done while working at the Torrey Pines Institute for Molecular Studies, is now with the Chemistry Institute at the National Autonomous University of Mexico.

Source: The American Chemical Society

Strawberries dipped in chocolate photo by shutterstock.

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Cocoa May Slow Cognitive Impairment of Aging


Cocoa May Slow Cognitive Impairment of AgingIf there is a more pleasurable way of staving off the cognitive impairment of aging than drinking cocoa, perhaps only red wine drinkers have found it.

Flavanols are naturally occurring antioxidants found in abundance in cocoa plants. They help the body deal with free radicals that trigger negative changes in body chemistry and help prevent blood clots.

Now, a new study led by Giovambattista Desideri, M.D., study lead author and associate professor of internal medicine and public health at the University of L’Aquila in Italy, suggests ingesting cocoa flavanols daily may improve mild cognitive impairment.

Experts say that more than six percent of people aged 70 years or older develop mild cognitive impairment (MCI) annually. Moreover, MCI can progress to dementia and Alzheimer’s disease.

Researchers say flavanols may aid brain health by protecting neurons from injury, enhancing metabolism, and facilitating neuronal interaction with the molecular structures responsible for memory. They are also found in tea, grapes, red wine and apples and have been associated with a decreased risk of dementia.

Indirectly, flavanols may help by improving brain blood flow.

In the study, 90 elderly participants with mild cognitive impairment were randomized to drink daily either 990 milligrams (high), 520 mg (intermediate) or 45 mg (low) of a dairy-based cocoa flavanol drink for eight weeks.

Researchers controlled participants’ diet to eliminate other sources of flavanols from foods and beverages other than the dairy-based cocoa drink.

Cognitive function was examined by neuropsychological tests of executive function, working memory, short-term memory, long-term episodic memory, processing speed and global cognition.

Researchers found:

  • Scores significantly improved in the ability to relate visual stimuli to motor responses, working memory, task-switching and verbal memory for those drinking the high and intermediate flavanol drinks;
  • Participants drinking daily higher levels of flavanol drinks had significantly higher overall cognitive scores than those participants drinking lower-levels;
  • Insulin resistance, blood pressure and oxidative stress also decreased in those drinking high and intermediate levels of flavanols daily. Changes in insulin resistance explained about 40 percent of the composite scores for improvements in cognitive functioning.

“This study provides encouraging evidence that consuming cocoa flavanols, as a part of a calorie-controlled and nutritionally-balanced diet, could improve cognitive function,” Desideri said. However, he warns that the beneficial findings may have been influenced by a variety of factors.

“The positive effect on cognitive function may be mainly mediated (influenced) by an improvement in insulin sensitivity. It is yet unclear whether these benefits in cognition are a direct consequence of cocoa flavanols or a secondary effect of general improvements in cardiovascular function.”

Furthermore, the study population was generally in good health without known cardiovascular disease. Thus, it would not be completely representative of all mild cognitive impairment patients.

In addition, only some clinical features of mild cognitive impairment were explored in the study.

“Given the global rise in cognitive disorders, which have a true impact on an individual’s quality of life, the role of cocoa flavanols in preventing or slowing the progression of mild cognitive impairment to dementia warrants further research,” Desideri said.

“Larger studies are needed to validate the findings, figure out how long the positive effects will last and determine the levels of cocoa flavanols required for benefit.”

The research is reported in the American Heart Association’s journal Hypertension.

Source: American Heart Association

Woman drinking cocoa photo by shutterstock.

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How Drugs for Schizophrenia Sow Seeds of Resistance


How Drugs for Schizophrenia Sow Seeds of ResistanceA new study has identified why certain drugs have mixed success in treating schizophrenia; effective at first, but with chronic administration becoming less and less so.

In the study, reported online in the journal Nature Neuroscience, scientists investigated the external genetic reasons (called epigenetic factors) that cause treatment-resistance to atypical antipsychotic drugs.

Use of antipsychotic drugs is the standard of care for schizophrenia. Researchers at Mount Sinai School of Medicine report that 30 percent of individuals with schizophrenia do not respond to currently available treatments.

Researchers 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, Ph.D., lead investigator on the study.

Researchers 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.

In response, the research team administered a chemical called suberoylanilide hydroxamic acid (SAHA), which inhibits the entire family of HDACs. 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 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, Ph.D., 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 the frontal cortex of individuals with schizophrenia, which then reduces the presence of mGlu2, and thereby limits the efficacy of these drugs.”

As a result of these findings, Gonzalez-Maeso’s team is now developing compounds that specifically inhibit HDAC2 as adjunctive treatments to antipsychotics.

Source:The Mount Sinai Hospital/Mount Sinai School of Medicine

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Gene Related to Autism Behavior ID’d in Mice Study


Gene Related to Autism Behavior ID'd in Mice StudyIn a new mouse study, University of California, Davis, researchers have found that a defective gene is responsible for brain changes that lead to the disrupted social behavior that accompanies autism.

Investigators believe the discovery could lead to the development of medications to treat the condition.

Prior research had determined that the gene is defective in children with autism, but its effect on neurons in the brain was not known.

The new studies in mice show that abnormal action of just this one gene disrupted energy use in neurons. The harmful changes were coupled with antisocial and prolonged repetitive behavior — traits found in autism.

The research is published in the scientific journal PLoS ONE.

“A number of genes and environmental factors have been shown to be involved in autism, but this study points to a mechanism — how one gene defect may trigger this type of neurological behavior,” said study senior author Cecilia Giulivi, Ph.D.

“Once you understand the mechanism, that opens the way for developing drugs to treat the condition,” she said.

The defective gene appears to disrupt neurons’ use of energy, Giulivi said, the critical process that relies on the cell’s molecular energy factories called mitochondria.

In the research, a gene called pten was modififed in the mice so that neurons lacked the normal amount of pten’s protein. The scientists detected malfunctioning mitochondria in the mice as early as 4 to 6 weeks after birth.

By 20 to 29 weeks, DNA damage in the mitochondria and disruption of their function had increased dramatically.

At this time, the mice began to avoid contact with their litter mates and engage in repetitive grooming behavior. Mice without the single gene change exhibited neither the mitochondria malfunctions nor the behavioral problems.

The antisocial behavior was most pronounced in the mice at an age comparable in humans to the early teenage years – a period in which schizophrenia and other behavioral disorders become most apparent, Giulivi said.

The research showed that, when defective, pten’s protein interacts with the protein of a second gene known as p53 to dampen energy production in neurons.

The interaction causes severe stress that leads to a spike in harmful mitochondrial DNA changes and abnormal levels of energy production in the cerebellum and hippocampus — brain regions critical for social behavior and cognition.

Investigators report that pten mutations previously have been linked to Alzheimer’s disease as well as a spectrum of autism disorders.

The new research shows that when pten protein was insufficient, its interaction with p53 triggered deficiencies and defects in other proteins that also have been found in patients with learning disabilities including autism.

Source: University of California – Davis Health System

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Stress, Depression Reduce Brain Volume Thanks to Genetic ‘Switch’


Stress, Depression Reduce Brain Volume Thanks to Genetic 'Switch' Scientists have known that stress and depression can cause the brain to retract or lose volume, a condition associated with both emotional and cognitive impairment. Now, a new study discovers why this occurs.

Yale scientists have found that the deactivation of a single genetic switch can instigate a cascading loss of brain connections in humans and depression in animal models.

Researchers say the genetic switch, known as a transcription factor, represses the expression of several genes that are necessary for the formation of synaptic connections between brain cells. The loss of connections, in turn, can contribute to loss of brain mass in the prefrontal cortex, say the scientists.

“We wanted to test the idea that stress causes a loss of brain synapses in humans,” said senior author Ronald Duman, Ph.D. “We show that circuits normally involved in emotion, as well as cognition, are disrupted when this single transcription factor is activated.”

In the study, the research team analyzed tissue of depressed and non-depressed patients donated from a brain bank and looked for different patterns of gene activation.

The brains of patients who had been depressed exhibited lower levels of expression in genes that are required for the function and structure of brain synapses.

Lead author and postdoctoral researcher H.J. Kang, Ph.D., discovered that at least five of these genes could be regulated by a single transcription factor called GATA1.

When the transcription factor was activated in animal models, rodents exhibited depressive-like symptoms, suggesting GATA1 plays a role not only in the loss of connections between neurons but also in symptoms of depression.

This finding of genetic variations in GATA1 may help researchers identify people at high risk for major depression or sensitivity to stress.

“We hope that by enhancing synaptic connections, either with novel medications or behavioral therapy, we can develop more effective antidepressant therapies,” Duman said.

Source: Yale University

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Why We Can’t Live in the Moment


Why We Can't Live in the MomentThe sought-after ideal of “living in the moment” may be impossible, according to research conducted at the University of Pittsburgh, which pinpoints an area of the brain responsible for using past decisions and outcomes to guide future behavior.

The study analyzes signals associated with metacognition, which is a person’s ability to monitor and control cognition — a term described by the researchers as “thinking about thinking.”

“The brain has to keep track of decisions and the outcomes they produce,” said Marc Sommer, Ph.D., who did his research for the study as a University of Pittsburgh neuroscience faculty member and is now on the faculty at Duke University. “You need that continuity of thought. We are constantly keeping decisions in mind as we move through life, thinking about other things.”

Sommer said the researchers “guessed it was analogous to working memory,” which led them to predict that neuronal correlates of metacognition resided in the same brain areas responsible for cognition, including the frontal cortex, a part of the brain linked with personality expression, decision making, and social behavior.

The research team studied single neurons in three frontal cortical regions of the brain: The frontal eye field, associated with visual attention and eye movements; the dorsolateral prefrontal cortex, which is responsible for motor planning, organization, and regulation; and the supplementary eye field (SEF), which is involved in the planning and control of saccadic eye movements, which are the extremely fast movements of the eye that allow it to continually refocus on an object.

Study participants were asked to perform a visual decision-making task that involved random flashing lights and a dominant light on a cardboard square. They were asked to remember and pinpoint where the dominant light appeared, guessing whether they were correct. The researchers found that while neural activity correlated with decisions and guesses in all three brain areas, the metacognitive activity that linked decisions to bets resided exclusively in the SEF.

“The SEF is a complex area linked with motivational aspects of behavior,” said Sommer. “If we think we’re going to receive something good, neuronal activity tends to be high in SEF. People want good things in life, and to keep getting those good things, they have to compare what’s going on now versus the decisions made in the past.”

Sommer said he sees his research as one step in a systematic process of working toward a better understanding of consciousness. By studying metacognition, he says, he reduces the big problem of studying a “train of thought” into a simpler component: Examining how one cognitive process influences another.

“Why aren’t our thoughts independent of each other? Why don’t we just live in the moment? For a healthy person, it’s impossible to live in the moment. It’s a nice thing to say in terms of seizing the day and enjoying life, but our inner lives and experiences are much richer than that.”

The scientist said that patients with mental disorders have not been tested on these tasks, but added he is interested to see how SEF and other brain areas might be disrupted in people with these disorders.

“With schizophrenia and Alzheimer’s disease, there is a fracturing of the thought process,” he said. “It is constantly disrupted, and despite trying to keep a thought going, one is distracted very easily. Patients with these disorders have trouble sustaining a memory of past decisions to guide later behavior, suggesting a problem with metacognition.”

The study was published in the  journal Neuron.

Source: University of Pittsburgh

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Stress Changes Learning in the Brain


Stress Changes Learning in the BrainA new experiment from German scientists suggests stress invokes our brain to use different and more complex processes during learning.

In the study, cognitive psychologists Drs. Lars Schwabe and Oliver Wolf discovered that the presence or absence of stress is associated with use of different brain regions and different strategies in the learning process.

Stress appears to make the brain work harder and use a more complex approach when learning. Study findings are reported in the Journal of Neuroscience.

Researchers discovered that non-stressed individuals applied a deliberate learning strategy, while stressed subjects relied more on their gut feeling.

“These results demonstrate for the first time that stress has an influence on which of the different memory systems the brain turns on,” said Schwabe.

In the study researchers analyzed the data from 59 subjects. Two groups were assigned with one group asked to immerse one hand into ice-cold water for three minutes (while being observed by video surveillance).

As expected, this activity stressed the subjects with data collected and confirmed by hormone assays.

The other group was asked to immerse one of their hands in warm water. Then both the stressed and non-stressed individuals completed a task called weather prediction. The task involved having subjects look at playing cards with different symbols and then using the cards to predict which combinations of cards forecast rain and which sunshine.

Each combination of cards was associated with a certain probability of good or bad weather. People apply differently complex strategies in order to master the task.

During the weather prediction task, the researchers recorded the brain activity with MRI.

Researchers found that both stressed and non-stressed subjects learned to predict the weather according to the symbols. However, the way in which they learned the task varied.

Non-stressed participants focused on individual symbols and not on combinations of symbols. They consciously pursued a simple strategy.

The MRI data showed that they activated a brain region in the medial temporal lobe – the hippocampus, which is important for long-term memory.

Stressed subjects, on the other hand, applied a more complex strategy.

They made their decisions based on the combination of symbols. They did this, however, subconsciously, i.e. they were not able to formulate their strategy in words.

In this group of stress participants, brain scans showed that the so-called striatum in the mid-brain was activated — a brain region that is responsible for more unconscious learning.

“Stress interferes with conscious, purposeful learning, which is dependent upon the hippocampus,” concluded Schwabe. “So that makes the brain use other resources. In the case of stress, the striatum controls behavior — which saves the learning achievement.”

Source: Ruhr-University Bochum

Abstract of the brain with key photo by shutterstock.

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