In an exercise study conducted by researchers at the Oregon Research Institute, tai chi training resulted in improved postural stability and walking ability, as well as reduced falls in the participants.

“These results are clinically significant because they suggest that Tai Chi, a low-to-moderate impact exercise, may be used as an add-on to current physical therapies, to address some of the key clinical problems in Parkinson’s disease, such as postural and gait instability,” said Fuzhong Li, Ph.D.

“Since many training features in the program are functionally oriented, the improvements in the balance and gait measures that we demonstrated highlight the potential of tai chi-based movements in rehabilitating patients with these types of problems and, consequently, easing cardinal symptoms of Parkinson’s disease and improving mobility, flexibility, balance, and range of motion.”

In the four-year project funded by the National Institute of Neurological Disorders and Stroke, researchers randomly assigned 195 patients to one of three exercise groups: tai chi, resistance training, or stretching. The patients participated in 60-minute exercise sessions twice a week for 24 weeks.

The results of the study showed that the tai chi group performed consistently better than the stretching group in how far they could lean in any direction without losing balance, as well as demonstrating better levels of directional control of the body and walking ability, such as longer stride length. tai chi participants also outperformed those in the resistance training group on the balance and stride length measures.

Finally, tai chi training was shown to significantly lower the incidence of falls compared to stretching, and was as equally effective as resistance training in reducing falls.

As Parkinson’s disease progresses, patients lose stability and have trouble walking, difficulty managing activities required of daily living, and experience frequent falls. Exercise is an important part of the management of Parkinson’s disease because physical activity has been shown to retard the deterioration of motor function and to prolong functional independence. However, research on alternative forms of exercise, such as tai chi, that could improve balance, gait, and function in patients with Parkinson’s disease is scarce, the researcher notes.

The program developed by Li consisted of six tai chi movements integrated into a routine that focused on weight-shifting, controlled-displacement of the center of gravity over the base of support, ankle sway, and front-to-back and sideways stepping. Natural breathing was integrated into the training routine.

“There are a number of practical advantages to using tai chi to improve motor dysfunction of Parkinson’s disease,” he said. “It is a low-cost activity that does not require equipment, it can be done anywhere, at any time, and the movements can be easily learned. It can also be incorporated into a rehabilitation setting as part of existing treatment. Similarly, because of its simplicity, certain aspects of this tai chi program can also be prescribed to patients as a self-care/home activity.”

Source: Oregon Research Institute

Elderly man performing tai chi photo by shutterstock.

Investigators discovered short-term stimulant treatment did not substantially increase the risk of cardiovascular events or symptoms in healthy youth.

ADHD affects 5-9 percent of youth and is frequently treated with stimulant medications, such as methylphenidate and amphetamine products. A recent safety communication from the US Food and Drug Administration advised that all patients undergoing ADHD treatment be monitored for changes in heart rate or blood pressure.

In the study, Dr. Mark Olfson and his colleagues assessed the risk of adverse cardiovascular events in children and adolescents without known heart conditions treated with stimulants for attention deficit hyperactivity disorder.

The investigation is one of the largest studies to date that focused primarily on youth while controlling for pre-existing cardiovascular risk factors.

As reported in the study, Olfson and colleagues examined claims records from a large privately insured population for associations between cardiovascular events in youth with ADHD and stimulant treatment.

In total 171,126 privately insured youth aged 6-21 years without known pre-existing heart-related risk factors were followed throughout the study.

Researchers included patients who have previously received stimulant treatment, patients currently receiving stimulant treatment, and patients who began or ceased stimulant treatments during the study period.

Olfson and colleagues assessed the various groups for incidents of severe cardiovascular events such as acute myocardial infarction, less severe cardiovascular events such as cardiac dysrhythmias, and cardiovascular symptoms such as tachycardia and palpitations.

Analysis showed that cardiovascular events and symptoms were rare in this cohort and not associated with stimulant use.

This finding helps to allay concerns of adverse events in otherwise healthy young people receiving treatment for ADHD. Olfson and colleagues said of the results, “It is reassuring that in these young people, short-term stimulant treatment did not substantially increase the risk of cardiovascular events or symptoms.”

The research is published in the Journal of the American Academy of Child and Adolescent Psychiatry.

Source: Elsevier

Child with pencil photo by shutterstock.

Since the mid-1950s, millions of children and adults have been prescribed stimulant medications to control attention deficit hyperactivity disorder (ADHD). But since the first experiment that gave an amphetamine drug to children diagnosed with behavioral problems, scientists have not known how stimulants work to control hyperactivity.

New research has identified a possible mechanism by which certain stimulants accomplish this paradoxical reduction of motor activity.

David Erlij, M.D., Ph.D., professor of physiology and pharmacology at SUNY Downstate, and fellow researchers have identified a network of nerve terminals in the rat brain where stimulation of dopamine D4 receptors depresses motor activity.

“This network is localized deep in the brain, in the basal ganglia and the thalamus,” said Erlij, “and its responses explain the reduction in motor activity caused by psychostimulants.”

The findings were published in a recent edition of the journal Neuropharmacology.

“When, in 1937, Dr. Charles Bradley administered Benzedrine to a group of children with hyperactivity and learning disorders and discovered that ’14 children responded in a spectacular fashion,’ a new era of psychopharmacology was inaugurated,” Erlij said.

“Bradley showed, for the first time, that taking a pill could successfully treat a behavioral abnormality. Eventually, this discovery led to the widespread use of psychostimulant drugs in the treatment of ADHD.”

“Despite their well established beneficial effects, it was not understood why psychostimulant drugs, which normally amplify the stimulatory responses of dopamine signals, reduce hyperactivity.

“Our results suggest that enhancing dopamine D4 transmission in the basal ganglia and the thalamus is likely part of the mechanism of the therapeutic effects of psychostimulants on ADHD.”

Erlij believes the therapeutic action of psychostimulants in ADHD occurs because the condition is caused by abnormalities of dopamine signaling in the brain. That is, when an individual has ADHD, the dopamine D4 receptor gene is abnormal.

Source: SUNY Downstate Medical Center

A new study suggests that the genetic contribution to the risk of being diagnosed with antisocial personal disorder comes not from a single gene or genetic risk factor, but from two distinct dimensions of genetic risk.

Currently, antisocial personality disorder is defined as “a pervasive pattern of disregard for, and violation of, the rights of others that begins in childhood or early adolescence and continues into adulthood.”

This definition is found in the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) of the American Psychiatric Association.

DSM-IV i provides formal diagnostic criteria for every psychiatric disorder. This process may be guided by rating scales that measure the traits and features associated with a personality disorder.

But, until now, no one has studied the dimensional structure associated with the DSM antisocial personality disorder criteria.

Dr. Kenneth Kendler of Virginia Commonwealth University and colleagues examined questionnaire and genetic data from adult twins. They found that the DSM-IV criteria do not reflect a single dimension of liability but rather are influenced by two dimensions of genetic risk reflecting aggressive-disregard and disinhibition.

“When psychiatrists, as clinicians or researchers, think about our psychiatric disorders, we tend to think of them as one thing – one kind of disorder – a reflection of one underlying dimension of liability,” said Dr. Kendler.
“This is also true of genetics researchers. We tend to want to identify and then detect ‘the’ risk genes underlying disorder X or Y.”

Kendler added, “What is most interesting about the results of this paper is that they falsify this inherent and rather deeply held assumption. Genetic risk factors for antisocial personality disorder are not one thing. Rather, the disorder, as conceptualized by DSM-IV, reflects two distinct genetic dimensions of risk.”

Experts believe the study results make sense.

“The distinction between the two sets of heritable traits contributing to antisocial personality disorder, aggressive-disregard and disinhibition, highlights the complexity of unraveling the genes contributing to this personality style. We now have some puzzle pieces, but we have a long way to go to fit these pieces together,” commented Dr. John Krystal, editor of Biological Psychiatry.

Source: Elsevier

Researchers say improvements are on the horizon as mobile dating, the latest iteration in digital dating, holds promise as it brings together potential partners face-to-face fast to see if “sparks” exist.

Although the research on mobile dating is scarce, Eli Finkel, associate professor of psychology at Northwestern and lead author of the study, is optimistic about this approach.

“GPS features on smartphone apps can tell you who is nearby and willing to be browsed,” Finkel said. “With a little bit of basic information, potential daters can get together right away for a quick face-to-face meet-up.”

Experts say that face-to-face contact is critical in finding that special someone — and, that the faster this happens, the better.

The human-to-human connection has been found to be superior to viewing online profiles. Previous research by Finkel and colleagues has shown that the ‘ideal’ preferences of daters (from viewing online profiles) were significantly altered after in-person meetings with potential partners.

The research will be published by Psychological Science in the Public Interest, a journal of the Association for Psychological Science.

Finkel believes the online dating industry has advanced from a version 1 to a version 3. His discussion on the evolution of online dating follow.

• The first generation in 1995—the launch of Match.com:

“We use the analogy that dating sites like Match.com are like supermarkets of love,” Finkel said. “You check out the wares (online profiles) and see what you like. Upon first blush, this approach seems reasonable, but there are two major problems with it: People really don’t learn much from a profile, and people get overloaded by choice.”

• The second generation in 2000—enter eHarmony:

Sites like eHarmony market themselves less as supermarkets of love than as something akin to real estate brokers of love. They use “matching algorithms” in an effort to identify which potential partners are especially compatible with a given online dater. The choice issue, Finkel observed, is somewhat solved by the algorithm approach. Only a handful of people are chosen as compatible matches.

“But there is no compelling evidence that any of these algorithms work,” he said. “Limiting the number of potential partners is only helpful if the algorithmic-selection process favors compatible partners over incompatible ones, which it fails to do. Even if the algorithms are cutting 2,000 potential partners down to five, if that process is random, is it really any better than strolling into the neighborhood bar?”

• The third generation in 2008—mobile dating:

With the advent of smartphone apps, mobile dating was launched. Mobile dating’s ability to get people face-to-face fast may make a big difference, according to the new Northwestern research.

“You have a little bit of basic information,” Finkel said. “Is this person below threshold or above threshold for a five-minute meet-up—five minutes from now? There’s no better way to figure out whether you’re compatible with somebody than talking to them over a cup of coffee or a pint of beer.”

Researchers hope their report will stimulate industry leaders to utilize available scientific methodologies to enhance online dating services.

Source: Northwestern University

Computer keyboard with love key photo by shutterstock.

The research on brain activity during competitive social interactions is described in a paper in the Proceedings of the National Academy of Sciences.

Experts say this is the first investigation to use a computational approach to analyze differing patterns of brain activity during these interactions.

“When players compete against each other in a game, they try to make a mental model of the other person’s intentions, what they’re going to do and how they’re going to play, so they can play strategically against them,” said University of Illinois postdoctoral researcher Kyle Mathewson, Ph.D. “We were interested in how this process happens in the brain.”

Previous studies have tended to consider only how one learns from the consequences of one’s own actions, called reinforcement learning, Mathewson said.

These studies have found heightened activity in the basal ganglia, a set of brain structures known to be involved in the control of muscle movements, goals and learning. Many of these structures signal via the neurotransmitter dopamine.

“That’s been pretty well studied and it’s been figured out that dopamine seems to carry the signal for learning about the outcome of our own actions,” Mathewson said.

“But how we learn from the actions of other people wasn’t very well characterized.”

Researchers call this type of learning “belief learning.”

Investigators used functional magnetic resonance imaging (fMRI) to track activity in the brains of participants while they played a competitive game, called a Patent Race, against other players.

The goal of the game was to invest more than one’s opponent in each round to win a prize (a patent worth considerably more than the amount wagered), while minimizing one’s own losses (the amount wagered in each trial was lost). The fMRI tracked activity at the moment the player learned the outcome of the trial and how much his or her opponent had wagered.

A computational model evaluated the players’ strategies and the outcomes of the trials to map the brain regions involved in each type of learning.

“Both types of learning were tracked by activity in the ventral striatum, which is part of the basal ganglia,” Mathewson said. “That’s traditionally known to be involved in reinforcement learning, so we were a little bit surprised to see that belief learning also was represented in that area.”

Belief learning also spurred activity in the rostral anterior cingulate, a structure deep in the front of the brain. This region is known to be involved in error processing, regret and “learning with a more social and emotional flavor,” Mathewson said.

The findings offer new insight into the workings of the brain as it is engaged in strategic thinking, says co-author Ming Hsu. This in turn may aid the understanding of neuropsychiatric illnesses that undermine those processes.

“There are a number of mental disorders that affect the brain circuits implicated in our study,” Hsu said.

“These include schizophrenia, depression and Parkinson’s disease. They all affect these dopaminergic regions in the frontal and striatal brain areas. So to the degree that we can better understand these ubiquitous social functions in strategic settings, it may help us understand how to characterize and, eventually, treat the social deficits that are symptoms of these diseases.”

Source: University of Illinois

Woman playing cards photo by shutterstock.

Prior research on metaphors, such as George Lakoff and Mark Johnson’s Metaphors we live by, suggests that our daily language is so full of metaphors, some of which are so familiar (like “rough day”), that they may not seem especially novel or striking. They argued that metaphor comprehension is grounded in our sensory and motor experiences.

In a new study using brain imaging, investigators discovered a region of the brain important for sensing texture through touch, the parietal operculum, is activated when someone listens to a sentence with a textural metaphor. The same region is not activated when a similar sentence expressing the meaning of the metaphor is heard.

The results were published online this week in the journal Brain & Language.

“We see that metaphors are engaging the areas of the cerebral cortex involved in sensory responses even though the metaphors are quite familiar,” said senior author Krish Sathian, M.D., Ph.D. “This result illustrates how we draw upon sensory experiences to achieve understanding of metaphorical language.”

In the study, seven college students were asked to listen to sentences containing textural metaphors as well as sentences that were matched for meaning and structure, and to press a button as soon as they understood each sentence.

Blood flow in their brains was monitored by functional magnetic resonance imaging (fMRI). On average, response to a sentence containing a metaphor took slightly longer (0.84 vs 0.63 seconds).

In a previous study, the researchers had already mapped out, for each of these individuals, which parts of the students’ brains were involved in processing actual textures by touch and sight.

This allowed the researchers to analyze the link within the brain between metaphors involving texture, and the sensory experience of texture itself.

“Interestingly, visual cortical regions were not activated by textural metaphors, which fits with other evidence for the primacy of touch in texture perception,” said research associate Simon Lacey, Ph.D., the first author of the paper.

The researchers did not find metaphor-specific differences in cortical regions well known to be involved in generating and processing language, such as Broca’s or Wernicke’s areas. However, this result doesn’t rule out a role for these regions in processing metaphors, Sathian said.

Also, other neurologists have seen that injury to various areas of the brain can interfere with patients’ understanding of metaphors.

“I don’t think that there’s only one area responsible for metaphor processing,” Sathian said. “Actually, several recent lines of research indicate that engagement with abstract concepts is distributed around the brain.”

“I think our research highlights the role of neural networks, rather than a single area of the brain, in these processes. What could be happening is that the brain is conducting an internal simulation as a way to understand the metaphor, and that’s why the regions associated with touch get involved.

“This also demonstrates how complex processes involving symbols, such as appreciating a painting or understanding a metaphor, do not depend just on evolutionarily new parts of the brain, but also on adaptations of older parts of the brain.”

Sathian’s future plans include asking whether similar relationships exist for other senses, such as vision. The researchers also plan to probe whether magnetic stimulation of the brain in regions associated with sensory experience can interfere with understanding metaphors.

Source: Emory University

In the brain cells of people with Alzheimer’s, tau proteins combine into twisted structures known as “neurofibrillary tangles.” The presence of tangles defines the condition as Alzheimer’s.

However, although the tangles confirm Alzheimer’s, their precise role in Alzheimer’s pathology has long been a point of contention among researchers.

New research on the intermediary steps between a single tau protein unit and a neurofibrillary tangle confirms the significance of tau to Alzheimer’s. Scientists now believe the conglomeration of two, three, four, or more tau proteins — known as “oligomers” — are the most toxic entities in Alzheimer’s.

“What we discovered is that there are smaller structures that form before the neurofibrillary tangles, and they are much more toxic than the big structures,” said Rakez Kayed, University of Texas Medical Branch.

“And we established that they were toxic in real human brains, which is important to developing an effective therapy.”

According to Kayed, a key antibody enabled the research team to produce a detailed portrait of tau oligomer behavior in human brain tissue. The anitbody made it possible for researchers to use a variety of analytical tools to compare samples of Alzheimer’s brains with samples of age-matched healthy brains.

“One thing that’s remarkable about this research is that before we developed this antibody, people couldn’t even see tau oligomers in the brain,” Kayed said.

“With the antibody — called T22 — we were able to thoroughly characterize them, and also study them in human brain cells.”

Among the researchers’ most striking findings: in some of the Alzheimer’s brains they examined, tau oligomer levels were as much as four times higher as those found in age-matched control brains.

Other experiments revealed specific biochemical behavior and structures taken on by oligomers, and demonstrated their presence outside neurons — in particular, on the walls of blood vessels.

Investigators believe the discovery will foster renewed studies on Alzheimer’s. “We think this is going to make a big impact scientifically, because it opens up a lot of new areas to study,” Kayed said. “It also relates to our main focus, developing a cure for Alzheimer’s. And I find that very, very exciting.”

Source: University of Texas Medical Branch at Galveston

Researchers discovered cases where large or small DNA segments change direction, are duplicated, or become completely lost. The changes were mainly discovered in older twins.

This finding may help to explain why the immune system is often impaired in older age.

Uppsala University researchers explain that during a person’s life, continuous alterations in the cells’ DNA occur. The alterations can be changes to the individual building blocks of the DNA but more common are rearrangements where large DNA segments change place or direction, or are duplicated or completely lost.

In the current study, scientists examined normal blood cells from identical (monozygotic) twins in different age groups and looked for large or smaller DNA rearrangements.

The results showed that large rearrangements were only present in the group older than 60 years.

The most common rearrangement was that a DNA region, for instance a part of a chromosome, had been lost in some of the blood cells. Certain, almost identical, rearrangements were found in several individuals and some of these could be associated with a known blood disease in which the bone marrow’s capacity to produce new blood cells is disturbed.

Rearrangements were also found in the younger age group. The changes were smaller and less complex but the researchers could also in this case show that the number of rearrangements correlated with age.

Investigators were surprised to find that as many as 3.5 percent of healthy individuals older than 60 years carry such large genetic alterations.

The discovery sets the stage for a better understanding of disease development in older age.

Scientists believe that this type of acquired genetic variation might be much more common, says Jan Dumanski, professor at the Department of Immunology, Genetics and Pathology and one of the authors of the paper.

A key to the potential association between DNA changes and alterations to our immune system is the understanding that although we possess a variety of blood cell types, only white blood cells contain DNA.

This distinction is important as researchers believe an increased number of WBC cells with DNA alterations can damage or alter the immune system.

Specifically, the genetic alterations lead to an increased growth of the cells that have acquired them; these cells will increase in number in relation to other white blood cells.

The consequence might be a reduced diversity among the white blood cells and thereby an impaired immune system.

Researchers have published the findings online in the American Journal of Human Genetics.

Source: Uppsala University

In a new study, the researchers report that a blood test analyzing the levels of nine biomarkers accurately identifies patients diagnosed with depression from control participants.

“Traditionally, diagnosis of major depression and other mental disorders has been made based on patients’ reported symptoms, but the accuracy of that process varies a great deal, often depending on the experience and resources of the clinician conducting the assessment,” said psychiatrist Dr. George Papakostas,  associate professor of psychiatry at Harvard Medical School, and lead author of the report.

“Adding an objective biological test could improve diagnostic accuracy and may also help us track individual patients’ response to treatment.”

“It can be difficult to convince patients of the need for treatment based on the sort of questionnaire now used to rank their reported symptoms,” said John Bilello, Ph.D., co-author of the study and chief scientific officer of Ridge Diagnostics, which sponsored it.

“We expect that the biological basis of this test may provide patients with insight into their depression as a treatable disease rather than a source of self-doubt and stigma.”

The test developed by Ridge Diagnostics measures the levels of nine biomarkers associated with factors such as inflammation, the development and maintenance of neurons, and the interaction between brain structures involved with stress response and other key functions, the researchers explain.

Those measurements are combined using a formula to produce a figure called the MDDScore — a number from 1 to 100 indicating the likelihood that the person has major depressive disorder.

The initial phase of the study included 36 adults who had been diagnosed with major depression at Massachusetts General Hospital, Vanderbilt University or Cambridge Health Alliance, along with 43 control participants from St. Elizabeth’s Hospital.

MDDScores for 33 of the 36 patients indicated the presence of depression, while only eight of the 43 controls had a positive test result. The average score for the patients was 85, while the average for controls was 33.

A second phase of the study included an additional 34 patients from MGH and Vanderbilt, 31 of whom had a positive MDDScore result.

Combining both groups indicated that the test could accurately diagnose major depression with a sensitivity of about 90 percent and a specificity of 80 percent, according to the researchers. These statistics are lower than existing diagnostic, non-invasive, paper-based tests that are used today to diagnose depression.

Determining the true utility of the test will require larger trials in clinical settings, Papakostas said, adding, “these results are already providing us with intriguing new hints on how powerfully factors such as inflammation — which we are learning has a major role in many serious medical issues — contribute to depression.”

Source: Massachusetts General Hospital

Blood test photo by shutterstock.

Currently, experts do not fully understood why the brain’s cognitive functions such as memory and speech decline as we age. This despite the realization that cognitive decline can be detected before an individual reaches age 50.

Neuroscientists Andy Randall, Ph.D. and Jon Brown, Ph.D. from the University of Bristol have identified a novel cellular mechanism that causes changes to the activity of neurons — an action which may contribute to cognitive decline during normal healthy aging.

The brain largely uses electrical signals to encode and convey information. Modifications to this electrical activity are likely to cause age-dependent changes to cognitive abilities.

The researchers examined the brain’s electrical activity by making recordings of electrical signals in single cells of the hippocampus, a structure with a crucial role in cognitive function. By doing this, they were able to assess “neuronal excitability” – the ease with which a neuron can produce brief, but very large, electrical signals called action potentials.

An action potential occurs in practically all nerve cells and is essential for transmission of a signal or communication within all the circuits of the nervous system.

Action potentials are triggered near the neuron’s cell body and once produced, travel rapidly through the massively branching structure of the nerve cell, along the way activating the synapses the nerve cell makes with the numerous other nerve cells to which it is connected.

Researchers discovered the hippocampal neurons within an aged brain have trouble generating action potentials.

Furthermore, they demonstrated that this relative reluctance to produce action potential arises from changes to the activation properties of membrane proteins called sodium channels. The sodium channels influence the rapid initiation of the action potential by allowing a flow of sodium ions into neurons.

Randall, a professor in applied neurophysiology, said: “Much of our work is about understanding dysfunctional electrical signaling in the diseased brain, in particular Alzheimer’s disease.

“We began to question, however, why even the healthy brain can slow down once you reach my age. Previous investigations elsewhere have described age-related changes in processes that are triggered by action potentials, but our findings are significant because they show that generating the action potential in the first place is harder work in aged brain cells.

“Also by identifying sodium channels as the likely culprit for this reluctance to produce action potentials, our work even points to ways in which we might be able modify age-related changes to neuronal excitability, and by inference cognitive ability.”

The findings are published in the journal Neurobiology of Aging.

Source: University of Bristol

Unfortunately, despite their widespread use, most of the medications are known to cause the metabolic side effects of obesity and diabetes.

Naturally this presents a significant dilemma to individuals as they weigh a choice between improving their mental health and damaging their physical health.

A new paper in the journal Molecular Psychiatry, discusses the biochemical changes triggered by the antipsychotic drugs.

The medications interfere with normal metabolism by activating a protein called SMAD3. The SMAD3 protein, in turn, is an important component of a cellular conduit termed the transforming growth factor beta (TGFbeta) pathway.

The TGFbeta pathway regulates many biological processes, including cell growth, inflammation, and insulin signaling.

In the current study, all antipsychotics that cause metabolic side effects activated SMAD3, while antipsychotics free from these side effects did not.

What’s more, SMAD3 activation by antipsychotics was completely independent from their neurological effects, raising the possibility that antipsychotics could be designed that retain beneficial therapeutic effects in the brain, but lack the negative metabolic side effects.

“We now believe that many antipsychotics cause obesity and diabetes because they trigger the TGFbeta pathway. Of all the drugs we tested, the only two that didn’t activate the pathway were the ones that are known not to cause metabolic side effects,” said Fred Levine, M.D., Ph.D., senior author of the study.

The TGFbeta pathway also plays an important role in metabolic disease in people who don’t take antipsychotic medications.

“It’s known that people who have elevated TGFbeta levels are more prone to diabetes. So having a dysregulated TGFbeta pathway — whether caused by antipsychotics or through some other mechanism — is clearly a very bad thing,” said Dr. Levine.

“The fact that antipsychotics activate this pathway should be a big concern to pharmaceutical companies. We hope this new information will lead to the development of improved drugs.”

Source: Sanford-Burnham Medical Research Institute

Researchers believe knowledge of the association could pave the way for aggressive therapies to minimize risk for stroke.

In the study, researchers found that people who died after stroke had more severe memory loss in the years before stroke compared to people who survived stroke or people who didn’t have a stroke.

“We’re most surprised that people who died after strokes had such sharp memory declines years before stroke onset,” said Qianyi Wang, the study’s lead author and a graduate student at the Harvard University School of Public Health in Boston, Mass.

Researchers examined 11,814 people age 50 years and older every two years for signs of declining memory. Study participants were stroke-free at enrollment and were followed up to 10 years.

A unique feature of this study is that participants continued in the study after surviving a stroke. Over the 10-year period, investigators documented 1,820 strokes, including 364 individuals who died after stroke but before the next memory assessment.

Average memory loss each year was compared for participants who remained stroke free. Memory loss was also assessed among participants who survived a stroke — considering their memory loss might be different before and after stroke.

The researchers used a standard word-recall list to measure memory loss. For participants whose memory loss became too severe to use the word lists, researchers interviewed spouses or other caregivers using a standardized assessment.

The average memory score each year dropped:

• 0.078 points in those who didn’t have a stroke while in the study;
• 0.137 points before stroke in those who later survived a stroke;
• 0.205 points before stroke in those who later died from stroke.

Researchers discovered the people who survived a stroke had worse average memory even before the stroke compared to similar individuals who never had a stroke during follow-up.

At the time of stroke, memory function dropped an average 0.321 points. This difference is about the same as the average memory decline associated with growing 4.1 years older among those who remained stroke-free.

Because of the large stroke-related declines, memory impairment was common among stroke survivors.

Researchers believe several factors may explain the presentation of increased memory loss before a fatal stroke.

“People who die after stroke may have worse underlying disease prior to stroke. This suggests early disease is accumulating and that something is happening to these people before they are diagnosed with clinical stroke.” said M. Maria Glymour, S.D., senior study author and an assistant professor at the Harvard School of Public Health.

“However, memory impairment is associated with increased mortality regardless of stroke. Memory impairment may therefore make patients more vulnerable to death in the wake of the stroke, for reasons that are unrelated to stroke severity. We’re not sure which is true and we can’t tell with these analyses, but we hope to examine this in the future.”

Studies are needed to determine whether the effects of stroke on memory differ for different groups of people; for example, these effects may vary depending on race, gender, geographic location and socioeconomic status.

“Even health conditions that are much more common at older ages may have roots earlier in life,” Glymour said. “Your entire life course influences your health in old age.”

Source: American Heart Association

Elderly woman photo by shutterstock.

Researchers agree that short-term memory is a complex cognitive act that entails the participation of multiple brain regions. However, whether and how different brain regions cooperate during memory has remained elusive.

German researchers have now come closer to answering this question. They discovered that oscillations between different brain regions are crucial in visually remembering things over a short period of time.

Scientists have known that brain regions in the frontal part of the brain are involved in short-term memory, while processing of visual information occurs primarily at the back of the brain.

The unknown factor is how the separated regions coordinate and integrate information to allow us to successfully remember information over a short period of time.

In a novel experiment, researchers recorded electrical activity both in a visual area and in the frontal part of the brain in monkeys.

The scientists then showed the animals identical or different images within short intervals while recording their brain activity. Afterwards, the animals had to indicate whether the second image was the same as the first one.

The scientists observed that, in each of the two brain regions, brain activity showed strong oscillations in a certain set of frequencies called the theta-band.

Importantly, these oscillations did not occur independently of each other, but synchronized their activity temporarily.

“It is as if you have two revolving doors in each of the two areas. During working memory, they get in sync, thereby allowing information to pass through them much more efficiently than if they were out of sync,” explains Stefanie Liebe, the first author of the study.

The more synchronized the activity was, the better could the animals remember the initial image. Thus, the authors were able to establish a direct relationship between what they observed in the brain and the performance of the animal.

Researchers believe the experiment shows that synchronized brain oscillations are important for the communication and interaction of different brain regions.

Investigators say that almost all multi-faceted cognitive acts, such as visual recognition, arise from a complex interplay of specialized and distributed neural networks. Research is ongoing in an effort to understand how the brain communicates both internal and external information.

Source: Max-Planck-Gesellschaft

Prior studies have linked the virus to mental illnesses such as bipolar disorder, schizophrenia, anxiety disorder and dementia. Investigators were open-minded to the possibility as genetic fragments and antibodies to this RNA virus causes behavior disorders in a range of mammals and birds.

Moreover, although the results have been inconclusive, traces of the virus have been found to be prevalent in psychiatric patients.

But Mady Hornig, M.D., director of translational research at the Center for Infection and Immunity (CII) at Columbia University, said, “Our study provides compelling evidence that bornaviruses do not play a role in schizophrenia or mood disorders.”

Hornig and collaborators at seven other institutions in the U.S, Germany and Australia, published their findings online in the journal Molecular Psychiatry.

As part of the study, scientists evaluated 198 patients in California with schizophrenia, bipolar disorder and major depressive disorder. They then carefully matched each one of them with a healthy control of the same sex, age, region and socio-economic status, and tested blood of patients and controls for the presence of BDV genetic material and antibodies to BDV.

The investigators hypothesized that if the virus was, in fact, associated with a psychiatric disorder, genetic evidence of infection would be apparent in blood samples taken at the onset and/or at the peak of a psychiatric episode, and antibody evidence would be detectable several weeks afterward.

To test the hypothesis, blood samples were collected within six weeks of the onset of an acute mental episode or upon clinically significant worsening of symptoms. Blood samples were then taken again after six weeks to allow for changes in viral load or antibody levels.

Researchers found no evidence of active or historical infection with BDV in any of the subjects, nor did they discover a relationship between mental illness and bornavirus.

In a commentary in the same issue of the journal, Michael B.A. Oldstone, M.D., an expert in molecular virology and central nervous system infections at the Scripps Research Institute, observes that the design and experimental procedures carried out in the Hornig study provide a gold standard for investigating links between persistent viral infection and human disease.

CII director, W. Ian Lipkin, M.D., senior author of the paper, notes that “it was concern over the potential role of BDV in mental illness and the inability to identify it using classical techniques led us to develop molecular methods for pathogen discovery.

“Ultimately these new techniques enabled us to refute a role for BDV in human disease. But the fact remains that we gained strategies for the discovery of hundreds of other pathogens that have important implications for medicine, agriculture and environmental health.”

Source: Columbia University