Over the past few years data has shown that exercise creates neurobiological changes, according to David Bucci, an associate professor in the department of psychological and brain sciences.

His latest research finds that the effects of exercise are different on memory, as well as on the brain, depending on whether the exerciser is an adolescent or an adult. Researchers have also identified a gene that seems to mediate the degree to which exercise has a beneficial effect, which has implications for the use of exercise as an intervention for mental illness, Bucci said.

He said he began his pursuit of the link between exercise and memory with ADHD, one of the most common childhood psychological disorders, noting he is concerned that the treatment of choice is medication.

“The notion of pumping children full of psycho-stimulants at an early age is troublesome,” Bucci said. “We frankly don’t know the long-term effects of administering drugs at an early age — drugs that affect the brain — so looking for alternative therapies is clearly important.”

Anecdotal evidence from colleagues at the University of Vermont pointed Bucci toward studying exercise and ADHD. Researchers observed that ADHD children in Vermont summer camps, athletes or team sports players were found to respond better to behavioral interventions than more sedentary children. While systematic empirical data is lacking, this association of exercise with a reduction of characteristic ADHD behaviors was persuasive enough for Bucci.

Coupled with his interest in learning and memory and their underlying brain functions, Bucci and teams of graduate and undergraduate students embarked upon a series of experiments to investigate the potential connection between exercise and brain function.

Early on, they found that laboratory rats that exhibit ADHD-like behavior demonstrated that exercise was able to reduce the extent of these behaviors. The researchers also found that exercise was more beneficial for female rats than males, similar to how it affects male and female children with ADHD.

Next they investigated a mechanism through which exercise seems to improve learning and memory called brain-derived neurotrophic factor (BDNF), which is involved in the growth of the developing brain. The degree of BDNF in exercising rats correlated positively with improved memory.

The researchers also found that it had longer-lasting effects in adolescents compared to adults.

“The implication is that exercising during development, as your brain is growing, is changing the brain in concert with normal developmental changes, resulting in your having more permanent wiring of the brain in support of things like learning and memory,” says Bucci. “It seems important to [exercise] early in life.”

Bucci’s latest paper was a move to take the studies of exercise and memory in rats and apply them to humans. The subjects in this new study were Dartmouth undergraduates and individuals recruited from the Hanover community.

According to Bucci, an interesting finding was that a person’s genotype for BDNF affected whether exercise benefited learning and memory.

“This could mean that you may be able to predict which ADHD child, if we genotype them and look at their DNA, would respond to exercise as a treatment and which ones wouldn’t,” he said.

The notion that exercise is good for health, including mental health, is not a huge surprise, he concludes. “The interesting question in terms of mental health and cognitive function is how exercise affects mental function and the brain,” he said.

Source: Dartmouth College

Child exercising photo by shutterstock.

Researchers from University of California – Davis found that mothers who had fevers during their pregnancies were more than twice as likely to have a child with autism or developmental delay than were mothers who did not have a fever or who took medication to counter its effect.

“Our study provides strong evidence that controlling fevers while pregnant may be effective in modifying the risk of having a child with autism or developmental delay,” said Ousseny Zerbo, Ph.D., lead author of the study. “We recommend that pregnant women who develop fever take anti-pyretic (fever-reducing) medications and seek medical attention if their fever persists.”

The study is published online in the Journal of Autism and Developmental Disorders, and is believed to be the first to consider how fever from any cause, including the flu, and its treatment during pregnancy could affect the likelihood of having a child with autism or developmental delay.

Researchers analyzed data from a large, case-control investigation known as the Childhood Autism Risk from Genetics and the Environment (CHARGE) Study. Another recent study based on CHARGE data found that mothers who were obese or diabetic had a higher likelihood of having children with autism.

Dr. Irva Hertz-Picciotto, a professor of public health sciences at UC Davis and principal investigator of CHARGE, pointed out that fever is produced by acute inflammation — the short-term, natural immune system reaction to infection or injury — and that chronic inflammation, which no longer serves a beneficial purpose and can damage healthy tissue, may be present in mothers with metabolic abnormalities like diabetes and obesity.

“Since an inflammatory state in the body accompanies obesity and diabetes as well as fever,” said Hertz-Picciotto, “the natural question is: Could inflammatory factors play a role in autism?”

Typically, when people are infected by bacteria or viruses, the body mounts a healing response that involves the release of pro-inflammatory cytokines from white blood cells into the bloodstream. Some cytokines are able to cross the placenta, and therefore could reach the fetal central nervous system, potentially altering neurotransmitters and brain development.

“We definitely think more research is necessary to pinpoint the ways that inflammation could alter brain development,” said Hertz-Picciotto.

CHARGE includes an ethnically diverse population of children aged 2 to 5 years born in California and living in Northern California. The current study included 538 children with autism, 163 children with developmental delay but not autism, and 421 typically developing children whose mothers answered standardized questionnaires about whether they had the flu and/or fever during pregnancy and if they took medications to treat their illnesses.

Interestingly, the results showed that flu during pregnancy was not associated with greater risks of having a child with autism or developmental delay. Fever from any cause during pregnancy, however, was far more likely to be reported by mothers of children with autism (2.12 times higher odds) or developmental delay (2.5 times higher odds), as compared with mothers of children who were developing typically.

For children of mothers who took anti-fever medication, the risk of autism was not different from the risk in children whose mothers reported no fever.

According to Hertz-Picciotto, the results are noteworthy because of the study’s large population-based sample and detailed information on participants.

Prior discoveries from the CHARGE evaluations suggest that taking prenatal vitamins prior to and during the first month of pregnancy may help prevent autism and that living near a freeway or in areas with high regional air pollution is associated with higher risk of autism in children.

“CHARGE has obtained a wealth of environmental, demographic and medical information on young children and their parents and provides a solid basis for a variety of epidemiologic studies,” said Hertz-Picciotto. “Those studies are helping us find ways to protect childhood neurodevelopment.”

Source: University of California – Davis Health System

Pregnant woman photo by shutterstock.

New research looks at risk factors for cognitive decline and dementia and how low to moderate alcohol consumption can serve to protect the brain from deterioration while heavy alcohol can destroy brain function.

A review paper by J.W. Kim in Psychiatry Investigation summarizes the potential ways alcohol may affect cognitive function and the risk of dementia, both adversely and favorably. The variance in outcomes depends on the dose (how much alcohol consumed) and the drinking pattern.

Using longitudinal and brain imaging studies, researchers have determined that excessive alcohol consumption may increase the risk of cognitive dysfunction and dementia in the elderly. But regular low to moderate alcohol intake may protect against cognitive decline and dementia and provide cardiovascular benefits.

Currently there is no proven method to prevent cognitive decline or dementia, although a number of studies have shown a lower risk of such conditions among light to moderate drinkers in comparison with non-drinkers.

Other studies have found that beneficial effects are seen only among certain subgroups of subjects. A recent review of subjects over the age of 65 concluded that light-to-moderate alcohol consumption, in comparison with abstinence, was associated with approximately 35-45 percent lower risk of cognitive decline or dementia.

In the current study, the authors state that their intent is to determine if there is an “optimal pattern of drinking” that may protect the elderly against cognitive dysfuntion.

At present, the way by which the moderate intake of wine and other alcoholic beverages reduces the risk of cardiovascular diseases is much better defined than the protective or detrimental effect of alcohol on the brain.

Experts believe further research is needed to evaluate the potential role that alcohol may play in reducing the risk of dementia. And, since the bio-pharmacological protective pathway is not well-defined, researchers believe it would be premature to recommend light-to-moderate drinking for reducing the risk of dementia.

“On the other hand, current biomedical data supports the concept that regular, moderate intake of ethanol is not simply less dangerous for cognitive function, but is positively protective. This is the same conclusion reached by epidemiologic studies,” the authors said.

Source: Boston University Medical Center

Elderly couple drinking wine photo by shutterstock.

At the same forum, cognitive-behavioral therapy receives less attention even though emerging evidence suggests “talk therapy” can be as effective as pharmaceutical for illnesses such as depression.

In the study, psychiatrists from the University of Michigan and Yale University, analyzed the presentations given at two recent meetings of the American Psychiatric Association.

Findings from the analysis are published in the Journal of Clinical Psychopharmacology.

In a study of APA annual meetings held in 2009 and 2010, researchers discovered that of the 278 studies comparing at least two medicines against each other, 195 had been supported by industry, and 83 funded by other means.

The authors then evaluated the studies without knowing which kind of support each one had.

Of the industry-supported studies, 97.4 percent reported results that were positive toward the medicine that the study was designed to test, and 2.6 percent reported mixed results. Remarkably, no industry-sponsored studies with negative results were presented.

In contrast, when industry was not the source of funding, 68.7 percent of the presentations were positive, and 24.1 percent contained mixed results, while 7.2 percent contained negative results.

This “presentation bias,” in which mostly good news about medicines gets reported at meetings, echoes the “publication bias” that has been documented in research published in major journals, said Srijan Sen, M.D., Ph.D., an assistant professor of psychiatry at the U-M Medical School who led the study.

Sen and his colleague discovered the annual meeting of the American Psychiatric Association, which typically draws 16,000 participants, is characterized by a large industry presence with emphasis on research involving medicines that were still “on patent” and being actively marketed to both psychiatrists attending the conference.

Sen teamed with Yale psychiatrist Maya Prabhu, M.D., M.Sc., to do the formal review.

“This analysis suggests that the APA meeting might be being used as an opportunity to make drugs seem more effective than they are,” he said. At the same time, research discussing the efficacy of “talk therapy” treatments was found to receive much less attention – probably because this intervention does not receive industry backing.

Researchers believe this slanted presentation of new research may influence clinical practice patterns because the APA meeting is a major source of continuing medical education credit for psychiatrists, and a hub for psychiatry residents just starting out in the field.

Sen noted that the research journals and funding agencies have tried to confront research bias in journal articles by requiring pharmaceutical companies to register the clinical trials they are conducting and include the registration number when publishing the study.

This opens up which trials are being reported in the medical literature, and whether the trial results are interpreted according to the original study design. For instance, if a drug trial is designed to test long-term results from a particular treatment, but a paper is published showing positive results over a much shorter term, that could be an indication of bias.

Research meetings could require a similar practice, Sen said. And the APA could be more selective in accepting poster presentation submissions.

If nothing else, Sen said, attendees at the APA’s meeting – and perhaps other large gatherings of psychiatrists – should be aware of the positive bias of the research they will hear about at the meeting. And non-industry funding for research – especially research to compare older “off patent” drugs that aren’t being marketed by industry – is also important, he says.

The federal government has funded large comparison studies in depression, schizophrenia and bipolar disorder, he said – and these mostly showed that the generic medications that have lost their patent protection are just as effective as newer, patent-protected ones.

Even so, psychiatrists prescribe the generic ones far less often than the brand-name patent-protected ones.

Source: University of Michigan

Medication abstract photo by shutterstock.

Policymakers have questioned whether the increased opportunity to participate in genetic testing would appreciably drive up or diminish test recipients’ demand for potentially costly followup health services.

The study by researchers at the National Institutes of Health and colleagues at other institutions allay, at least temporarily, cost concerns at a time when health care cost escalation is a significant national issue.

The study is published in the online issue of Genetics in Medicine.

Genetic tests are available from a growing number of commercial producers. Health care providers and policymakers have been uncertain whether people who received information only about risk would follow up by demanding diagnostic testing to monitor for predicted illnesses.

The study is the first to use electronic health records — rather than self-reported behavior — to measure the impact of genetic testing on the subsequent consumption of health services by commercially insured, healthy adults.

Self-reports, which can be affected by memory lapses and other problems, tend to be less accurate.

“We need to understand the impact of genomic discoveries on the health care system if these powerful technologies are going to improve human health,” said Dan Kastner, M.D., Ph.D., scientific director and head of the National Human Genome Research Institute’s (NHGRI) Division of Intramural Research.

“We are still learning how to integrate new genomic discoveries into clinical care effectively and efficiently.”

“There are a lot of unanswered questions about how genetic test results can be used to guide people toward making positive lifestyle and health behavior changes,” said Colleen McBride, Ph.D., chief of NHGRI’s Social and Behavioral Research Branch.

“This study goes a long way toward bringing data to these debates and shows that people are not likely to make inappropriate demands of health delivery systems if they are properly informed about the limitations of genetic tests.”

Genetic tests, such as those used in this study, can detect common variants of genes associated with modest alterations in the chances of developing particular diseases. The term multiplex refers to simultaneously performing multiple genetic tests on a single blood sample.

Researchers followed 217 healthy people between the ages of 25 and 40 who elected to participate in genetic susceptibility testing offered by their health plan.

Health care usage by the participants was monitored for the 12 months before genetic testing and the 12 months following the testing. Investigator also compared the test group’s behavior with a group of about 400 similar plan members who declined the testing offer.

The researchers counted the number of physician visits and laboratory tests or procedures the people received, particularly those services associated with four of the eight conditions tested by the multiplex panel.

Researchers discovered that most of the procedures or screening tests that were counted were not among those currently recommended for people in this age group who don’t have symptoms.

Saliently, researchers found that participants in genetic testing did not change their overall use of health care services compared with those not tested.

All of the individuals who elected to undergo the multiplex test carried at least one at-risk genetic marker, with the majority carrying an average of nine at-risk variants.

The tests performed for the Multiplex Initiative include a set of genetic variants reliably associated with an increase in disease risk and for which some corrective health behavior has been shown to prevent illness.

Having a risk version of one of the 15 genes on the multiplex genetic test does not mean that a person is certain to get the condition — only that he or she might have a slightly greater chance of developing the health condition, explained Dr. McBride.

There are many things other than genetics that contribute to the risk of common diseases, including lifestyle factors such as diet, exercise, smoking and sun exposure.

“Much is written about using genetics to personalize health care,” said co-author Lawrence C. Brody, Ph.D., chief of NHGRI’s Genome Technology Branch.

“Some think that this new generation of genetic tests will be a very positive addition to medicine; others believe they have the potential to make things worse.”

Dr. Brody designed the panel of genetic tests used in the Multiplex Initiative, consisting of 15 genetic markers that play roles in eight common diseases, including type 2 diabetes, coronary heart disease, high blood cholesterol, high blood pressure, osteoporosis, lung cancer, colorectal cancer and melanoma.

Source: NIH/National Human Genome Research Institute

Components found in kudzu root can reduce alcohol consumption without adverse side effects, said David Penetar, Ph.D., of the Behavioral Psychopharmacology Research Laboratory at McLean Hospital, and the lead author of the study.

In the study, published in the latest issue of Drug and Alcohol Dependence, researchers looked at one of the major components of the kudzu root — the isoflavone puerarin — to determine whether it would reduce alcohol consumption.

According to Penetar, puerarin was selected over other kudzu root components because its safety and efficacy have already been established in humans, particularly in China where it is approved for intravenous injection to treat coronary heart disease, myocardial infarction, and angina. Puerarin is also less potent than other parts of the kudzu plant, so it has few side effects and has none of the estrogenic activity found in other components, making it safe for women, he added.

In the study, the researchers recruited 10 men and women, all in their 20s, who reported regularly consuming alcohol. A laboratory was set up as an apartment, with TV, DVD player, reclining chair, and other amenities, including a refrigerator stocked with each subject’s favorite beer and other non-alcoholic beverages.

In an initial 90-minute session in the “apartment,” each subject was allowed to consume as many beers as he or she wanted — up to a maximum of six. After the session, each was given either puerarin or a placebo and told to take it daily for a week. Then, they returned to do the experiment again. Two weeks later, the subjects returned for a third session to see if they had returned to their baseline drinking levels. After that, each subject was given the pill he or she didn’t get the first time and told to take it for a week. Each then returned for a fourth and final drinking session.

The study showed that subjects taking puerarin drank fewer beers, dropping from 3.5 beers on average to 2.4.

“This was a simulation of a binge drinking opportunity and not only did we see the subjects drinking less, we noted that their rate of consumption decreased, meaning they drank slower and took more sips to finish a beer,” said Penetar.

“While we do not suggest that puerarin will stop drinking all together, it is promising that it appears to slow the pace and the overall amount consumed. Further research is needed, but this botanical medication may lead to additional methods to treat alcohol abuse and dependence.”

Source: McLean Hospital

While testing the role of a gene called Glo1 in anxiety, scientists uncovered a new inhibitory factor in the brain: the metabolic byproduct methylglyoxal (MG). The study, published in the Journal of Clinical Investigation, found that animals with multiple copies of the Glo1 gene were more likely to exhibit anxiety-like behavior in laboratory tests, said Abraham Palmer, Ph.D., assistant professor of human genetics at the University of Chicago Medicine and senior author of the study.

“We showed that Glo1 was causally related to anxiety-like behavior, rather than merely correlated,” he said.

Further experiments showed that Glo1 increased anxiety-like behavior by lowering levels of MG. When researchers inhibited Glo1 or raised MG levels, it reduced anxiety behaviors.

In 2005, a comparison of different mouse strains found a link between anxiety-like behaviors and Glo1, the gene encoding the metabolic enzyme glyoxylase 1. However, subsequent studies questioned the link, and the lack of an obvious connection between glyoxylase 1 and brain function or behavior made some scientists skeptical, according to the researcher.

“When people discover a gene, they’re always most comfortable when they discover something they already knew,” Palmer said. “The alarming thing here was there was a discovery of something that nobody knew, and therefore it seemed less likely to actually be correct.”

A 2009 study from Palmer’s laboratory suggested that differences in Glo1 expression between mouse strains were due to copy number variants, where the segment of the genome containing the gene is repeated multiple times. To test this hypothesis, lead author Margaret Distler inserted two, eight or 10 copies of the Glo1 gene into mouse lines. She then ran experiments, such as the open field test, in which researchers measure how much time a mouse spends in the center of an arena versus along the walls, to detect changes in anxiety.

The results confirmed that mice with more copies of the Glo1 gene exhibited higher anxiety-like behavior, the researchers said.

“It’s the first study to show that it’s the copy number variant that has the potential to change Glo1 expression and behavior,” said Distler, an M.D./Ph.D. student in the Pritzker School of Medicine’s Medical Scientist Training Program.

The researchers then set about solving the mystery of how Glo1 influences anxiety-like behaviors. The primary function of Glo1 is to metabolize and lower cellular levels of MG, a waste product of glycolysis. Distler produced the opposite effect by injecting MG to artificially increase its levels in the brain, finding that raising MG levels quickly reduced anxiety symptoms in mice.

“Methylglyoxal changed behavior within 10 minutes of administration, which means it’s a rapid onset. It’s not changing gene expression, and it’s not having long-term downstream effects,” Distler said. “That was our first breakthrough.”

The short time suggested that MG might have a direct effect on neuronal activity, she said. MG also demonstrated sedative effects at high doses, a hallmark of drugs that activate inhibitory GABA receptors on neurons, the researchers add. In collaboration with Leigh Plant, Ph.D., now at Brandeis University, the researchers demonstrated that MG activated GABA-A receptors on neurons, a previously unknown inhibitory mechanism.

“It’s a completely different system that is tying neuronal inhibitory tone into metabolic activity,” Palmer said. “It turns out now that methylglyoxal, which has been around ever since glycolysis evolved, was also acting at these receptors, and nobody knew that.”

Anxiety is usually treated with drugs that activate the GABA-A receptor, such as benzodiazepines and barbiturates, which are prone to abuse and dangerous side effects. The researchers theorized that targeting the Glo1/MG interaction could provide a more selective strategy for reducing anxiety by subtly influencing inhibitory tone.

“The GABA-A receptor agents already out there have a lot of side effects, such as sedation and hypothermia, as well as a high abuse liability,” Distler said. “It’s possible that taking a Glo1 inhibitor will increase only MG levels to a certain maximum. You could have the potential for more specificity, given that you’re activating a system that’s already in place, not just dumping methylglyoxal or some other GABA-A receptor agent throughout the brain.”

Preliminary experiments with a small molecule inhibitor of Glo1 supported the theory. Injections of the inhibitor, developed by John Termini at the Beckman Research Institute of the City of Hope, reduced anxiety-like symptoms in mice.

“It’s a different way of hitting these GABA-A receptors,” Palmer said. “We have yet to determine if that’s a better way of doing it, but it’s certainly different, and it gives us a unique angle of attack on this system and potential advantages that we have yet to evaluate.”

Such a drug may also be useful in treating epilepsy and sleep disorders, where GABA-A drugs have shown success, he added.

While the therapeutic potential is yet to be determined, the research clears the fog around the role of Glo1 in anxiety by adding behavioral and cellular evidence, the researchers note.

“What’s neat is that we started with exploratory, open-ended genetic studies in mice, and we’ve now gotten into some fundamental new physiology that nobody had appreciated or put together before,” Palmer said. “Now we’re starting to reap some of the fruit from those types of genetic studies to enrich our understanding of more classical aspects of biology.”

Source: University of Chicago Medical Center

The study “underscores that fact that sleepwalking is much more prevalent in adults than previously appreciated,” noted Maurice Ohayon, M.D., D.Sc., Ph.D., professor of psychiatry and behavioral sciences, who is the lead author of the paper. It will appear in the May 15 issue of Neurology, the medical journal of the American Academy of Neurology.

Sleepwalking, a disorder “of arousal from non-REM sleep,” can have serious consequences, resulting in injuries to the sleepwalker or others, as well as impaired psychosocial functioning, the researchers noted.

It is thought that the use of medication and certain psychological and psychiatric conditions can trigger sleepwalking, but the exact causes are unknown, the researchers added. Also unknown to experts in the field: its prevalence.

“Apart from a study we did 10 years ago in the European general population, where we reported a prevalence of 2 percent of sleepwalking, there are nearly no data regarding the prevalence of nocturnal wanderings in the adult general population,” the researchers said in their published paper. “In the United States, the only prevalence rate was published 30 years ago.”

The latest study was the first to use a large, representative sample of the U.S. population to demonstrate the number of sleepwalkers, according to the researchers, who also aimed to evaluate the importance of medication use and mental disorders associated with sleepwalking. Ohayon and his colleagues secured a sample of 19,136 individuals from 15 states and then used phone surveys to gather information on mental health, medical history, and medication use.

Participants were asked specific questions related to sleepwalking, including frequency of episodes during sleep, duration of the sleep disorder, and any inappropriate or potentially dangerous behaviors during sleep. Those who didn’t report any episodes in the last year were asked if they had sleepwalked during their childhood. Participants were also asked whether there was a family history of sleepwalking and whether they had other symptoms, such as sleep terrors and violent behaviors during sleep.

The researchers determined that as many as 3.6 percent of the sample reported at least one episode of sleepwalking in the previous year, with 1 percent saying they had two or more episodes in a month. Because of the number of respondents who reported having episodes during childhood or adolescence, lifetime prevalence of sleepwalking was found to be 29.2 percent.

The study also showed that people with depression were 3.5 times more likely to sleepwalk than those without, and people dependent on alcohol or who had obsessive-compulsive disorder were also significantly more likely to have sleepwalking episodes. Additionally, people taking SSRI antidepressants were three times more likely to sleepwalk twice a month or more than those who didn’t.

“There is no doubt an association between nocturnal wanderings and certain conditions, but we don’t know the direction of the causality,” said Ohayon. “Are the medical conditions provoking sleepwalking, or is it vice versa? Or perhaps it’s the treatment that is responsible.”

Although more research is needed, the work could help raise awareness of this association among primary care physicians, he added. “We’re not expecting them to diagnose sleepwalking, but they might detect symptoms that could be indices of sleepwalking,” said Ohayon.

Among the researchers’ other findings:

• The duration of sleepwalking was mostly chronic, with just over 80 percent of those who have sleepwalked reporting they’ve done so for more than five years.
• Sleepwalking was not associated with gender and seemed to decrease with age.
• Nearly one-third of individuals with nocturnal wandering had a family history of the disorder.
• People using over-the-counter sleeping pills had a higher likelihood of reporting sleepwalking episodes at least two times per month.

Source: The Stanford University School of Medicine

“It appears from our research that administering Vitamin K2 could possibly help patients with Parkinson’s. However, more work needs to be done to understand this better,” said Patrik Verstreken, who is associated with The Flanders Institute for Biotechnology and KU Leuven. He also worked with colleagues at Northern Illinois University on the research, which has been published online in the journal Science.

Verstreken uses a factory to explain what happens with Parkinson’s patients: “If we looked at cells as small factories, then mitochondria would be the power plants responsible for supplying the energy for their operation. In Parkinson’s patients, the activity of mitochondria and the transport of electrons have been disrupted, resulting in the mitochondria no longer producing sufficient energy for the cell. This has major consequences as the cells in certain parts of the brain will start dying off, disrupting communication between neurons. The results are the typical symptoms of Parkinson’s: Lack of movement (akinesia), tremors and muscle stiffness.

While the exact cause of Parkinson’s is not known, scientists have been able to pinpoint several genetic defects found in Parkinson’s patients, including the so-called PINK1 and Parkin mutations, which both lead to reduced mitochondrial activity, the researcher said.

For their research, Verstreken and his team used fruit flies with a genetic defect in PINK1 or Parkin that is similar to the one associated with Parkinson’s. They found that the flies with a PINK1 or Parkin mutation lost their ability to fly.

Upon closer examination, they discovered that the mitochondria in these flies were defective, just as in Parkinson’s patients. Because of this they generated less intracellular energy – energy the insects needed to fly. When the flies were given Vitamin K2, the energy production in their mitochondria was restored and the insects’ ability to fly improved. The researchers determined that the energy production was restored because the Vitamin K2 had improved electron transport in the mitochondria.

Because defective mitochondria are also found in Parkinson’s patients with a PINK1 or Parkin mutation, Vitamin K2 potentially offers hope for a new treatment for Parkinson’s, the researcher concludes.

Source: The Flanders Institute for Biotechnology

The results, based on nationwide surveys of nearly 120,000 U.S. teens, suggest prevention programs may need to be introduced in childhood and early adolescence, said James C. Anthony, Ph.D., of MSU’s Department of Epidemiology and Biostatistics.

Getting out information on the risks of prescription painkillers has become all the more important. Earlier this year, the U.S. Centers for Disease Control and Prevention found that the death toll from overdoses of prescription painkillers has more than tripled in the past decade.

“While much of the previous thinking was that misuse of these drugs emerged in the final year of high school and during the college-age years, we found that for adolescents the peak risk of starting to misuse these painkillers generally occurs earlier, not during the post-secondary school years,” Anthony said.

The researchers analyzed data from the 2004 through 2008 National Surveys on Drug Use and Health to identify when young people are most likely to start using prescription pain relievers to get high or for other unapproved uses.

The results show about 1 in 60 young people between 12 and 21 years old starts misusing prescription pain relievers each year. Peak risk is at about 16 years, when roughly 1 in 30 to 40 young people start to use painkillers to get high or for other reasons not intended by the prescriber.

“Getting a firm grasp of when the first onset occurs is very important when we try to take public health action to prevent first occurrence,” Anthony said. “With the peak risk at age 16 years and a notable acceleration in risk between ages 13 and 14 years, any strict focus on college students or 12th graders might be an example of too little too late.”

The results reveal a need to strengthen prescribing guidelines and introduce early school-based prevention programs, he said.

He added there also is an opportunity to work with pharmaceutical specialists who sometimes can reformulate these drugs so their effects are blunted when misused.

But it all starts with the prescription. He suggests prescribers should first try nonopioid pain relievers, such as ibuprofen, for kids. When opioid pain killers are prescribed for adolescents — or the drugs are in the reach of teens — the number of tablets should be limited or kept under lock and key, he advised.

“Patients in transient pain are often given a larger opioid prescription than is needed,” he said. “It can end up stacked in the medicine cabinet, available to anyone in or visiting the household.”

The study was published in the Archives of Pediatrics & Adolescent Medicine.

Source: Michigan State University

“Alcohol abuse is a huge problem, and this is a big step forward in identifying a potential new treatment,” said senior author Howard L. Fields, M.D., Ph.D., professor of neurology and director of the Wheeler Center for the Neurobiology of Addiction at UCSF.

Study participants were seeking treatment for smoking, not drinking, and were randomly given either varenicline or a placebo. By the end of the study, volunteers taking varenicline had reduced their average number of drinks per week by 36 percent compared to those taking placebo.

Researchers found no link between the average number of drinks each participant consumed per week with the average number of cigarettes smoked, suggesting that the drug’s effects on drinking behavior were separate from its effects on smoking.

Although researchers noted that more studies are needed to further examine potential side effects, they are hopeful that varenicline will be used as a treatment for heavy drinking.

“The drug is already widely used by smokers to help them quit,” said Fields. “Many heavy drinkers also smoke, and this study indicated that, in this group, varenicline was effective in reducing both the number of cigarettes smoked and the number of drinks consumed.”

Interestingly, during the study, participants drank the same number of times per week as they did before, said lead author Jennifer Mitchell, Ph.D., clinical project director at the Gallo Center and an adjunct assistant professor of neurology at UCSF.

“People initiated drinking at the same rate, but they drank less once they started,” she said. “If your usual pattern was to come home and have a few beers, you would still do that, but you might have one or two instead of four or five.”

A drug that could reliably decrease alcohol consumption would be of great value in reducing the harm caused by alcohol abuse, said Mitchell.

“If you currently drink seven drinks a night, and we can turn that into two or three, then you’re not only drinking at a level that’s going to harm you less, you’re less likely to harm others, as well.

“If we could lower the rates of drunk driving, spousal and child abuse and other secondary effects of alcoholism, that would be tremendous.”

Researchers noted that the study confirms earlier research by the Gallo Center by showing that alcohol and nicotine work through a common pathway in areas of the brain that offer a feeling of pleasure and reward. Varenicline works by blocking the pleasurable effects of nicotine in the brain.

Few negative side effects were reported, suggesting that the drug can be well-tolerated, said Fields. However, researchers warned that the absence of significant side effects could be because study participants were thoroughly screened for mental disorders such as depression, anxiety and suicidal ideation, as well as alcoholism, before the study began.

They suggest that the drug be tested in populations with co-existing psychiatric conditions, as well as with nonsmoking alcohol abusers.

The study was published in the journal Psychopharmacology.

Source:  University of California, San Francisco

Smoking and alcohol photo by shutterstock.

But giving a patient several antipsychotics simultaneously seemed to have no effect at all on mortality.

“We weren’t aware that the beneficial effects of antidepressants were so powerful,” said Jari Tiihonen, professor of clinical psychiatry at Karolinska Institutet’s Department of Clinical Neuroscience, who led the study.

The study followed 2,588 Finns who had developed schizophrenia from the time of their initial admission to the hospital over an average of four years. The researchers were able to ascertain the effects of different drug combinations on the group’s mortality risk.

During the study, 160 people died. While external causes, such as drowning, poisoning or violent crime, claimed 57 people, 35 of the deaths were suicides, which made it and cardiovascular disease the two main causes of death.

The researchers found that when taking benzodiazepines, the participants ran a 91 percent higher risk of early death than when these drugs were not used. Most deaths occurred with patients who had been taking benzodiazepines for longer than four weeks.

“The increased suicide risk for patients with long-standing benzodiazepine use may be partly attributable to the possible development of withdrawal symptoms when the drugs run out,” said Tiihonen.

“These symptoms, which can be severe anxiety and insomnia, might have affected some of the patients’ decisions to commit suicide. It’s therefore extremely important that bensodiazepines are discontinued gradually rather than abruptly over a period of weeks or months and in consultation with a doctor.”

During the periods the participants took antidepressants, they ran a 43 percent lower mortality risk than when these drugs were not used. The decrease in suicide risk was 85 percent, the researcher notes. Antipsychotics had no effect on mortality if the patients were on multiple prescriptions simultaneously, he added.

“People think that it’s dangerous to treat patients with schizophrenia with more than one antipsychotic drug, but there is nothing to back that up,” Tiihonen said.

“I believe that most doctors prescribe several antipsychotics if their patients are not helped by just one kind, and our study finds no link between this and increased mortality during a four-year followup. But it does mean more adverse effects, such as the risk of weight gain, which also impacts the health in the long run, so the recommended attitude is still one of restraint.”

Source: Karolinska Institutet

Help me sign photo by shutterstock.

The data from the study stretches back 50 years and “is consistent with what we see in clinical practice — that we are very well able to keep our patients functioning better and out of the hospital when they consistently take these medications,” said Dr. Roberto Estrada, attending psychiatrist at Lenox Hill Hospital in New York City.

For the study, German researchers searched through findings from 65 clinical trials reported in 116 articles published between 1959 and 2011. The trials involved nearly 6,500 patients with schizophrenia.

Researchers found that, after one year, relapse rates were 27 percent among patients who took antipsychotic drugs and 64 percent among those who took an inactive placebo. For patients taking antipsychotics, rates of hospital readmission were 10 percent compared to 26 percent for those taking placebo.

Five studies showed evidence that patients who took antipsychotic drugs behaved less aggressively, and findings from three studies suggested that they have a better quality of life.

Antipsychotic drugs are the main type of treatment for schizophrenia, but they can cause serious side effects. Researchers found that patients who took antipsychotic drugs had more negative side effects than those who took a placebo, including movement disorders (16 percent vs 9 percent), sedation (13 percent vs 9 percent), and weight gain (10 percent vs 6 percent).

Antipsychotic drugs can also be expensive, said the authors. In 2010, about $18.5 billion was spent worldwide on antipsychotic drugs, according to a journal news release.

“The cost and adverse effects associated with antipsychotics remain major impediments to achieving more successful treatment of schizophrenia,” said Estrada.  ”Further work needs to be done to develop more effective treatments for schizophrenia that are better-tolerated and thus likely to improve patients’ adherence to taking these medications.”

Still, the overall message from the new study is clear, noted the study authors.

“Antipsychotic maintenance treatment substantially reduces relapse risk in all patients with schizophrenia for up to two years of follow-up,” said psychiatrist Dr. Stefan Leucht, from the Technical University of Munich, and colleagues in a journal news release.

“The effect was robust in important subgroups such as patients who had only one episode, those in remission,” he added.

Benefits were witnessed regardless of whether patients took older or newer forms of antipsychotic drugs, Leucht added. However, for many patients “the drugs seemed to lose their effectiveness with time,” he said.

Although the medications have drawbacks, they have eased the suffering of those with schizophrenia.

“This study confirms clinical observations going back to the early 1950s — that is, antipsychotic drugs are effective in reducing the symptoms associated with schizophrenia. The decreased number of patients in long-term mental health facilities, such as state mental hospitals, is a testimonial to this,” said Dr. Norman Sussman, a psychiatrist at NYU Langone Medical Center and professor at the NYU School of Medicine in New York City.

“Hopefully, even better treatments will emerge in the near future that have fewer adverse effects and more robust therapeutic impact on cognition and social functioning,” Sussman said.

The findings are published in the online edition of The Lancet.

Source:  The Lancet

Parkinson’s is defined by a gradual loss of nerve cells of neurons that produce a chemical called dopamine. Dopamine is essential for normal function of muscles and other body organs.

Researchers have learned that changes in a gene known as DJ-1 also leads to an accelerated loss of dopaminergic neurons and results in the onset of Parkinson’s symptoms at a young age.

Although people naturally lose dopamine-producing neurons as part of the aging process, Parkinson’s patients experience a rapid loss of these neurons from the onset of the disease, leading to much more drastic deficiencies in dopamine than the average person.

The ability to modify the activity of DJ-1 could change the progress of the disease, said Dr. Nirit Lev, a researcher at Tel Aviv University. Working in collaboration with Profs. Dani Offen and Eldad Melamed, she has now developed a peptide which mimics DJ-1′s normal function, thereby protecting dopamine-producing neurons.

Preserving dopamine-producing neurons can mean the difference between living life as a Parkinson’s patient or aging normally, Lev said.

The peptide can be easily delivered by daily injections or absorbed into the skin through an adhesive patch.

The new peptide is structured from DJ-1 and has been shown to stop neurodegeneration, reducing problems with mobility and leading to greater protection of neurons and higher dopamine levels in the brain.

Lev said that this method, which has been published in a number of journals including the Journal of Neural Transmission, could be developed as a preventative therapy.

In the study, researchers set out to develop a therapy based on the protective effects of DJ-1, using a short peptide based on the healthy version of DJ-1 itself as a vehicle.

“We attached the DJ-1-related peptide to another peptide that would allow it to enter the cells, and be carried to the brain,” said Lev.

In preclinical trials, the treatment was tested on mice utilizing well-established toxic and genetic models for Parkinson’s disease. From both a behavioral and biochemical standpoint, the mice that received the peptide treatment showed remarkable improvement.

Symptoms such as mobility dysfunctions were reduced significantly, and researchers noted the preservation of dopamine-producing neurons and higher dopamine levels in the brain.

Preliminary tests indicate that the peptide is a viable treatment option. Though many peptides have a short life span and degrade quickly, this one does not. Additionally, it provides a safe treatment option because peptides are organic to the body itself.

Lev believes the peptide could fill a gap in the treatment of Parkinson’s disease. “Current treatments are lacking because they can only address symptoms — there is nothing that can change or halt the disease,” she said. “Until now, we have lacked tools for neuroprotection.”

Source: American Friends of Tel Aviv University

Psychologists Geoffrey Brookshire and Dr. Daniel Casasanto of The New School for Social Research have published their study in the journal PLoS ONE.

Researchers have long considered motivation, or the drive to approach or withdraw from physical and social stimuli, as the basic building block of human emotion.

Scientists have also operated on the premise that motivation is computed mainly in the left hemisphere of the brain, and withdraw motivation in the right hemisphere.

In the new study, Brookshire and Casasanto’s challenge this idea, as they determine a well-established pattern of brain activity, found across dozens of studies in right-handers, completely reverses in left-handers.

The researchers used electroencepahlography (EEG) to compare activity in participants’ right and left hemispheres during rest. After having their brain waves measured, participants completed a survey measuring their level of approach motivation, a core aspect of our personalities.

In right-handers, stronger approach motivation was associated with greater activity in the left hemisphere than the right, consistent with previous studies. Left-handers showed the opposite pattern: approach motivation was associated with greater activity in the right hemisphere than the left.

However, most cognitive functions do not reverse with handedness. Language, for example, is mainly in the left hemisphere for the majority of right- and left-handers.

Nevertheless, the finding of contralateral approach motivation activity was not unexpected.

“We predicted this hemispheric reversal because we observed that people tend to use different hands to perform approach- and avoidance-related actions,” says Casasanto.

Approach actions are often performed with the dominant hand, and avoidance actions with the non-dominant hand.

“Approach motivation is computed by the hemisphere that controls the right hand in right-handers, and by the hemisphere that controls the left hand in left-handers,” says Casasanto.

“We don’t think this is a coincidence. Neural circuits for motivation may be functionally related to circuits that control hand actions – emotion may be built upon neural circuits for action, in evolutionary or developmental time.”

The authors caution that these data show a correlation between emotional motivation and motor control, and that further studies are needed to establish a causal link.

Investigators believe the findings are important because of the current method to treat depression and anxiety with neural stimulation. Currently, brain stimulation is used to increase neural activity in the patient’s left hemisphere, long believed to the ‘approach hemisphere.”

“Given what we show here,” says Brookshire, “this treatment, which helps right-handers, may be detrimental to left-handers — the exact opposite of what they need.” The discovery that approach motivation reverses with handedness may lead to safer, more effective neural therapies for left-handers, according to Brookshire, “it’s something we’re investigating now.”

Source: The New School for Social Research