Posts tagged science

June 25, 2012

The same neurological mechanism involved in the transition from habitual to compulsive drug use could underlie less severe, but still harmful, compulsive behaviours.

"We’re trying to understand individuality in addictive behaviour. Many people can be exposed to drugs with addictive potential, for instance, but not everyone will become addicted,” explains Eric Dumont, an associate professor in the Department of Biomedical and Molecular Sciences. “We believe we’ve identified a mechanism that makes certain people predisposed to developing addictions, and it’s possible that the same mechanism underlies many - perhaps most - compulsive behaviours.”

The mechanism occurs in a reward pathway of the brain. In this pathway, the brain maintains a delicate balance between pleasure and aversion, ensuring that moment-to-moment desires and dislikes remain in sync with the biological needs of the body.

Dr. Dumont and his team found unusual activity in this pathway when modeling drug addiction in rats, which exhibit a genetic predisposition to addiction comparable to humans. They believe that the pathway’s balance is prone to becoming unbalanced in a certain percentage of the population. The signal to stop an activity reverses to a green light.

The team hopes that by identifying this mechanism, and possibly others like it, they will allow researchers to better understand and monitor a range of compulsive behaviours. Accordingly, Dr. Dumont’s team collaborates with Dr. Cella Olmstead, associate professor of Psychology at Queen’s, who recently developed an animal model of compulsive sucrose intake.

Dr. Dumont and this team were recently awarded a $520,000 operating grant from Canadian Institutes of Health Research (CIHR) to support their work for the next five years in understanding the neurological processes behind addiction behaviour.

Provided by Queen’s University

Source: medicalxpress.com

ScienceDaily (June 25, 2012) — The hot flashes and night sweats that most women experience early in menopause are not linked to increased levels of cardiovascular disease risk markers unless the symptoms persist or start many years after menopause begins. These new study results were presented June 23 at The Endocrine Society’s 94th Annual Meeting in Houston.

"Our study provides reassurance that the common experience of menopausal symptoms in early menopause is not associated with increases in blood pressure or other risk markers for cardiovascular disease," said lead researcher Emily Szmuilowicz, MD, an assistant professor at Northwestern University’s medical school in Chicago.

Researchers have questioned whether vasomotor menopausal symptoms such as hot flashes and night sweats reflect poor cardiovascular health. However, a 2011 study by Szmuilowicz and co-workers found that women who experienced menopausal symptoms only at the onset of menopause were less likely to have a stroke or heart attack or to die than were women who experienced hot flashes late in menopause or who did not have hot flashes at all.

Their new study focused on markers in the body that have been linked to a raised risk of cardiovascular disease. The risk markers examined were blood pressure, cholesterol, insulin, glucose (blood sugar) and blood markers of abnormal blood vessel function. Because inflammation is common in people with heart disease or stroke, the group also looked at blood markers of inflammation, including white blood cell count — the number of disease-fighting cells.

This study used retrospective data from nearly 60,000 postmenopausal women who participated in the Women’s Health Initiative Observational Study. The ongoing study, funded by the National Institutes of Health, is examining the relationships between health outcomes and new risk indicators for disease.

The researchers grouped women into four categories based on timing of their menopausal symptoms of hot flashes and night sweats: only at the start of menopause (early-onset menopausal symptoms), only years later in menopause (late-onset menopausal symptoms), both time periods (persistent menopausal symptoms), and not at all.

The investigators found no association between early-onset vasomotor menopausal symptoms and increased levels of any cardiovascular risk markers. However, both persistent and late-onset menopausal symptoms were associated with higher blood pressure and higher white blood cell count compared with women without menopausal symptoms, they reported. Persistent menopausal symptoms also correlated with higher levels of glucose and insulin, which are markers for diabetes.

It is unclear why women who experience menopausal symptoms at different stages of menopause may have differing levels of cardiovascular disease risk, Szmuilowicz said She speculated that “if menopausal symptoms occur long after menopause begins, this may signal a blood vessel abnormality that could also affect cardiovascular health.”

Source: Science Daily

ScienceDaily (June 25, 2012) — Deep brain stimulation reduces binge eating in mice, suggesting that this surgery, which is approved for treatment of certain neurologic and psychiatric disorders, may also be an effective therapy for obesity. Presentation of the results took place June 25 at The Endocrine Society’s 94th Annual Meeting in Houston.

"Doing brain surgery for obesity treatment is a controversial idea," said the study’s presenting author, Casey Halpern, MD, a fifth-year neurosurgery resident physician at the University of Pennsylvania, Philadelphia. "However, binge eating is a common feature of obese patients that frequently is associated with suboptimal treatment outcomes."

Currently the U.S. Food and Drug Administration has approved deep brain stimulation for use in various conditions that affect the brain, including Parkinson’s disease and essential tremor. The procedure does not destroy any part of the brain and typically does not cause pain, Halpern said.

Available treatments of obesity may inadequately address the neural basis of this compulsive overeating behavior, he suggested. A region of the brain called the nucleus accumbens is known to be dysregulated in both rodents and people who binge eat. Therefore, Halpern and his co-workers targeted that brain region with deep brain stimulation in a strain of obesity-prone mice.

The surgery involved implanting an electrode in the nucleus accumbens. Wires connected the electrode to an external neurostimulator, a device similar to a pacemaker. When switched on, the stimulator triggers the electrode to deliver continuous electrical pulses to the brain.

After recovery from surgery, the mice received high-fat food at the same time every day for one hour, and the researchers measured their food consumption. Binge eating was defined as consuming 25 percent or more of the usual daily caloric intake during this period.

For one week, mice consistently binged, eating almost half of their daily calories during this one hour, the authors reported. Then on alternating days, the investigators turned on the stimulator. On the days that deep brain stimulation was administered, or “on,” the scientists observed a significant (approximately 60 percent) decrease in consumption of the high-fat diet. On the alternate days when they turned off the stimulator, binge eating returned, Halpern said.

The researchers then studied how deep brain stimulation might work to improve binge eating. With medications, they blocked various receptors of dopamine neurons, or nerve cells. Dopamine is a brain neurotransmitter, a chemical messenger, whose release in the brain is linked to the desire for rewarding behaviors such as eating high-fat food, according to Halpern.

Only one of the medications had an effect. Raclopride, which blocks the type 2 dopamine receptor, weakened the beneficial effect of deep brain stimulation by 50 percent.

Their results, Halpern said, showed that “at least one way that deep brain stimulation functions to suppress binge eating might be by modulating activity of neurons expressing the type 2 dopamine receptor.”

Source: Science Daily

June 25, 2012 By Rick Nauert

A new study involving children with Williams syndrome (WS) suggests that improved regulation of oxytocin and vasopressin may someday improve care for autism, anxiety, post-traumatic stress disorder and WS.

WS results when certain genes are absent because of a faulty recombination event during the development of sperm or egg cells. Virtually everyone with WS has exactly the same set of genes missing (25 to 28 genes are missing from one of two copies of chromosome 7).

“The genetic deficiencies allow researchers to examine the genetic and neuronal basis of social behavior,” said Ursula Bellugi, Ph.D., a co-author on the paper.

“This study provides us with crucial information about genes and brain regions involved in the control of oxytocin and vasopressin, hormones that may play important roles in other disorders.”

In the study, scientists at the Salk Institute for Biological Studies and the University of Utah, found that people with WS flushed with the hormones oxytocin and arginine vasopressin (AVP) when exposed to emotional triggers.

Children with WS love people, despite being challenged with numerous health problems. WS kids are extremely gregarious, irresistibly drawn to strangers, and insist on making eye contact.

They have an affinity for music. But they also experience heightened anxiety, have an average IQ of 60, experience severe spatial-visual problems, and suffer from cardiovascular and other health issues.

Yet despite their desire to befriend people, WS kids have difficulty creating and maintaining social relationships — an issue that obviously affects many people without WS.

In the new study, led by Julie R. Korenberg, M.D., 21 participants, 13 who have WS and a control group of eight people without the disorder were evaluated at the Cedars-Sinai Medical Center in Los Angeles. Because music is a known strong emotional stimulus, the researchers asked participants to listen to music.

Before the music was played, the participants’ blood was drawn to determine a baseline level for oxytocin. Remarkably, those with WS had three times as much of the hormone as those without the syndrome.

Blood also was drawn at regular intervals while the music played and was analyzed afterward to check for real-time, rapid changes in the levels of oxytocin and AVP.

While other studies have examined how oxytocin affects emotion when artificially introduced into people, such as through nasal sprays, this is one of the first significant studies to measure naturally occurring changes in oxytocin levels in rapid, real time as people undergo an emotional response.

Although the WS participants displayed little outward response to the music, an analyses of blood samples showed that the oxytocin levels, and to a lesser degree AVP, had increased sharply while they had listened to the music.

In contrast, among those without WS, both the oxytocin and AVP levels remained largely unchanged as they listened to music.

Korenberg believes the blood analyses strongly indicate that oxytocin and AVP are not regulated correctly in people with WS, and that the behavioral characteristics unique to people with WS are related to this problem. “This shows that oxytocin quite likely is very involved in emotional response,” she said.

In addition to listening to music, study participants already had taken three social behavior tests that evaluate willingness to approach and speak to strangers, emotional states, and various areas of adaptive and problem behavior.

Those test results suggest that increased levels of oxytocin are linked to both increased desire to seek social interaction and decreased ability to process social cues, a double-edged message that may be very useful at times, for example, during courtship, but damaging at others, as in WS.

“The association between abnormal levels of oxytocin and AVP and altered social behaviors found in people with Williams Syndrome points to surprising, entirely unsuspected deleted genes involved in regulation of these hormones and human sociability,” Korenberg said.

“It also suggests that the simple characterization of oxytocin as ‘the love hormone’ may be an overreach. The data paint a far more complicated picture.”

Overall, the researchers say, their findings paint a hopeful picture, and the study holds promise for speeding progress in treating WS, and perhaps autism and anxiety through regulation of these key players in human brain and emotion, oxytocin and vasopressin.

Source: PsychCentral

ScienceDaily (June 25, 2012) — Researchers have discovered how a hormone in the gut slows the rate at which the stomach empties and thus suppresses hunger and food intake. Results of the animal study were presented June 25 at The Endocrine Society’s 94th Annual Meeting in Houston.

"The gut hormone glucagon-like peptide 2, or GLP-2, functions as a neurotransmitter and fine-tunes gastric emptying through — as suspected — its receptor action in the brain," said the lead investigator, Xinfu Guan, PhD, assistant professor of pediatrics and medicine at Baylor College of Medicine in Houston.

The researchers found that this action occurs in the GLP-2 receptor specifically in a key group of nerve cells in the brain, called pro-opiomelanocortin, or POMC, neurons. These neurons are in the hypothalamus, the part of the brain that produces appetite-controlling neuropeptides.

In their study using molecular methods, mice lacking this GLP-2 receptor in the POMC neurons showed late-onset obesity and higher food intake compared with normal wild-type mice. The mutant, or GLP-2 receptor “knockout,” mice also had accelerated gastric emptying after a liquid meal, as found on a noninvasive breath test. The faster the gastric emptying, the higher the food intake, scientists know.

Therefore, obese people may have something wrong with this hormone receptor, which alters their gastric emptying rate, Guan speculated. Many studies have shown that nondiabetic, obese humans have accelerated gastric emptying.

The researchers also found that this receptor quickly activated the PI3K intracellular signaling pathway in the POMC neurons. This, in turn, induces neuronal excitation (transmission of signals) and gene expression, according to Guan.

These findings, Guan said, show that in the central nervous system the GLP-2 receptor plays an important physiological role in the control of food intake and gastric emptying.

"This study has advanced our understanding of the brain-gut neural circuits that mediate eating behavior via modulating gastric emptying, which contributes to the control of body weight," he said.

Source: Science Daily

ScienceDaily (June 25, 2012) — Women with moderate to severe depression had substantial improvement in their symptoms of depression after they received treatment for their vitamin D deficiency, a new study finds.

The case report series was presented June 23 at The Endocrine Society’s 94th Annual Meeting in Houston.

Because the women did not change their antidepressant medications or other environmental factors that relate to depression, the authors concluded that correction of the patients’ underlying shortage of vitamin D might be responsible for the beneficial effect on depression.

"Vitamin D may have an as-yet-unproven effect on mood, and its deficiency may exacerbate depression," said Sonal Pathak, MD, an endocrinologist at Bayhealth Medical Center in Dover, Del. "If this association is confirmed, it may improve how we treat depression."

Pathak presented the research findings in three women, who ranged in age from 42 to 66. All had previously diagnosed major depressive disorder, also called clinical depression, and were receiving antidepressant therapy. The patients also were being treated for either Type 2 diabetes or an underactive thyroid (hypothyroidism).

Because the women had risk factors for vitamin D deficiency, such as low vitamin D intake and poor sun exposure, they each underwent a 25-hydroxyvitamin D blood test. For all three women, the test found low levels of vitamin D, ranging from 8.9 to 14.5 nanograms per milliliter (ng/mL), Pathak reported. Levels below 21 ng/mL are considered vitamin D deficiency, and normal vitamin D levels are above 30 ng/mL, according to The Endocrine Society.

Over eight to 12 weeks, oral vitamin D replacement therapy restored the women’s vitamin D status to normal. Their levels after treatment ranged from 32 to 38 ng/mL according to the study abstract.

After treatment, all three women reported significant improvement in their depression, as found using the Beck Depression Inventory. This 21-item questionnaire scores the severity of sadness and other symptoms of depression. A score of 0 to 9 indicates minimal depression; 10 to 18, mild depression; 19 to 29, moderate depression; and 30 to 63, severe depression.

One woman’s depression score improved from 32 before vitamin D therapy to 12, a change from severe to mild depression. Another woman’s score fell from 26 to 8, indicating she now had minimal symptoms of depression. The third patient’s score of 21 improved after vitamin D treatment to 16, also in the mild range.

Other studies have suggested that vitamin D has an effect on mood and depression, but there is a need for large, good-quality, randomized controlled clinical trials to prove whether there is a real causal relationship, Dr Pathak said.

"Screening at-risk depressed patients for vitamin D deficiency and treating it appropriately may be an easy and cost-effective adjunct to mainstream therapies for depression," she said.

Source: Science Daily

ScienceDaily (June 25, 2012) — Widely available EEG testing can distinguish children with autism from neurotypical children as early as age 2, finds a study from Boston Children’s Hospital. The study is the largest, most rigorous study to date to investigate EEGs as a potential diagnostic tool for autism, and offers hope for an earlier, more definitive test.

Widely available EEG testing can distinguish children with autism from neurotypical children as early as age 2, finds a new study. The study is the largest, most rigorous study to date to investigate EEGs as a potential diagnostic tool for autism, and offers hope for an earlier, more definitive test. (Credit: © dule964 / Fotolia)

Researchers Frank H. Duffy, MD, of the Department of Neurology, and Heidelise Als, PhD, of the Department of Psychiatry at Boston Children’s Hospital, compared raw EEG data from 430 children with autism and 554 control subjects, ages 2 to 12, and found that those with autism had consistent EEG patterns indicating altered connectivity between brain regions — generally, reduced connectivity as compared with controls.

While altered connectivity occurred throughout the brain in the children with autism, the left-hemisphere language areas stood out, showing reduced connectivity as compared with neurotypical children, consistent with neuroimaging research. Findings were published June 26 in the online open-access journal BMC Medicine.

Duffy and Als focused on children with “classic” autism who had been referred for EEGs by neurologists, psychiatrists or developmental pediatricians to rule out seizure disorders. Those with diagnosed seizure disorders were excluded, as were children with Asperger’s syndrome and “high functioning” autism, who tend to dominate (and skew) the existing literature because they are relatively easy to study. The researchers also excluded children with genetic syndromes linked to autism (such as Fragile X or Rett syndrome), children being treated for other major illnesses, those with sensory disorders like blindness and deafness and those taking medications.

"We studied the typical autistic child seeing a behavioral specialist — children who typically don’t cooperate well with EEGs and are very hard to study," says Duffy. "No one has extensively studied large samples of these children with EEGs, in part because of the difficulty of getting reliable EEG recordings from them."

The researchers used techniques developed at Boston Children’s Hospital to get clean waking EEG recordings from children with autism, such as allowing them to take breaks. They used computer algorithms to adjust for the children’s body and eye movements and muscle activity, which can throw off EEG readings.

To measure connectivity in the brain, Duffy and Als compared EEG readings from multiple electrodes placed on the children’s scalps, and quantified the degree to which any two given EEG signals — in the form of waves — are synchronized, known as coherence. If two or more waves rise and fall together over time, it indicates that those brain regions are tightly connected. (Duffy likens coherence to two people singing “Mary Had a Little Lamb” together. If they can see and hear each other, they are more likely to sing in synchrony — so their coherence is high.)

In all, using computational techniques, the researchers generated coherence readings for more than 4,000 unique combinations of electrode signals, and looked for the ones that seemed to vary the most from child to child. From these, they identified 33 coherence “factors” that consistently distinguished the children with autism from the controls, across all age groups (2 to 4, 4 to 6, and 6 to 12 years).

Duffy and Als repeated their analysis 10 times, splitting their study population in half different ways and using half to identify the factors, and the other half to test and validate them. Each time, the classification scheme was validated.

"These factors allowed us to make a discriminatory rule that was highly significant and highly replicable," says Duffy. "It didn’t take anything more than an EEG — the rest was computational. Our choice of variables was completely unbiased — the data told us what to do."

The researchers believe the findings could be the basis for a future objective diagnostic test of autism, particularly at younger ages when behavior-based measures are unreliable. Their most immediate goal is to repeat their study in children with Asperger’s syndrome and see if its EEG patterns are similar to or different from autism. They also plan to evaluate children whose autism is associated with conditions such as tuberous sclerosis, fragile X syndrome and extremely premature birth.

Source: Science Daily

June 25, 2012 By Traci Pedersen

Scientists have found improvements on memory tests and an increase in brain volume in Chinese seniors who practice tai chi three times a week, according to an article published in the Journal of Alzheimer’s Disease.

The trial also showed increases in brain volume and smaller cognitive improvements in individuals that participated in lively discussions three times per week over the same time period.

Researchers from the University of South Florida and Fudan University in Shanghai conducted an eight-month randomized controlled trial involving a group of seniors who practiced tai chi as well as a group who participated in lively conversations.  Researchers compared these to a control group who received no intervention.

Previous studies have shown an increase in brain volume in people who participated in aerobic exercise, and in one of these trials, memory was improved as well.

However, this was the first trial to prove that a less aerobic form of exercise, tai chi, as well as stimulating discussion, led to similar increases in brain volume and improvements on psychological tests of memory and thinking.

Volunteers who did not participate in the interventions showed brain shrinkage during this time period, consistent with what generally has been observed for persons in their 60s and 70s.

Several studies have shown that dementia and the gradual cognitive decline that precedes it is linked to increasing shrinkage of the brain as nerve cells and their connections are slowly lost.

“The ability to reverse this trend with physical exercise and increased mental activity implies that it may be possible to delay the onset of dementia in older persons through interventions that have many physical and mental health benefits,” said lead author James Mortimer, Ph.D., professor of epidemiology at the University of South Florida College of Public Health.

Research suggests that aerobic exercise is associated with increased production of brain growth factors. It has been undetermined whether forms of exercise like tai chi that include an important mental exercise component could lead to similar changes in brain development.

“If this is shown, then it would provide strong support to the concept of ‘use it or lose it’ and encourage seniors to stay actively involved both intellectually and physically,” Mortimer said.

One question raised by the research is whether sustained physical and mental exercise can help prevent Alzheimer’s disease.

“Epidemiologic studies have shown repeatedly that individuals who engage in more physical exercise or are more socially active have a lower risk of Alzheimer’s disease,” Mortimer said. “The current findings suggest that this may be a result of growth and preservation of critical regions of the brain affected by this illness.”

Source: PsychCentral

ScienceDaily (June 25, 2012) — A team of researchers led by an epidemiologist at Mount Sinai School of Medicine and University of Iceland has found a correlation between the age at which children with attention-deficit/hyperactivity disorder (ADHD) begin taking medication, and how well they perform on standardized tests, particularly in math.

The study, titled, “A Population-Based Study of Stimulant Drug Treatment of ADHD and Academic Progress in Children,” appears in the July, 2012, edition of Pediatrics, and can be viewed online on June 25. Using data from the Icelandic Medicines Registry and the Database of National Scholastic Examinations, the researchers studied 11,872 Icelandic children born between 1994 and 1996. The children started medication for ADHD at different times between fourth and seventh grades.

The findings showed that children who began drug treatment within 12 months of their fourth-grade test declined 0.3 percent in math by the time they took their seventh-grade test, compared with a decline of 9.4 percent in children who began taking medication 25-to-36 months after their fourth-grade test.

The data also showed that girls benefited only in mathematics, whereas boys had marginal benefits in math and language arts.

"Children who began taking medications immediately after their fourth-grade standardized tests showed the smallest declines in academic performance," said the study’s lead author Helga Zoega, PhD, Post Doctoral Fellow of Epidemiology at Mount Sinai’s Institute for Translational Epidemiology. "The effect was greater in girls than boys and also greater for children who did poorly on their fourth grade test."

Stimulants are widely used in the United States as a therapeutic option for children with inattention, impulsivity, and hyperactivity associated with ADHD. The medications are less frequently used in Europe, although their use in Iceland most closely resembles the U.S. Long-term follow-up studies of stimulant use and academic performance are scarce, according to the researchers.

Source: Science Daily

June 25, 2012

The Allen Institute for Brain Science convened the first ever Allen Brain Atlas Hackathon last week, opening its doors to a diverse group of programmers and informatics experts for a non-stop week of collaboration, learning and coding based on its public online platform of data, tools and source code. The event brought together more than 30 participants from top universities and institutes ranging from the Baylor College of Medicine in Houston to the Nencki Institute of Experimental Biology in Poland, as well as from start-ups and established technology companies, to develop data analysis strategies and tools based on the newly enhanced Allen Brain Atlas application programming interface (API).

"This hackathon stems from our longstanding, open approach to science and our belief that putting our data-rich resources in the hands of the many and varied experts around the globe is the most effective way to drive progress in brain research,” said Chinh Dang, Chief Technology Officer of the Allen Institute for Brain Science. “The hackathon projects delivered innovative ways of handling data, offering direct contributions to the informatics and programming communities as well as to neuroscience. We hope that this event serves as a springboard for others out in the community to use our API, and we look forward to seeing what can be done with it.”

The Allen Institute for Brain Science is one of the biggest data producers in neuroscience, with rapidly growing data stores in the petabyte range that it makes publicly available through its Web-based Allen Brain Atlas resources. These resources include, among others, anatomically and genomically comprehensive maps of genes at work in the mouse and human brains and receive approximately 50,000 visits each month from researchers around the globe.

The public API was created as an additional form of data sharing to spur community technology development and further empower scientists to make groundbreaking discoveries about the brain in health and disease—including insights into learning, cognition, development, Alzheimer’s, obesity, schizophrenia, autism, and more—that will deliver better treatment options sooner. The hackathon coincided with the public release of the full Allen Brain Atlas API earlier this month, and a key goal of the event was to ignite community momentum and interest in using it.

Using the Allen Brain Atlas API, developers can create entirely new software applications, mashups and novel data mining tools for making sense of the large and ever-growing volumes of neuroscience data. The API offers data access across species, ages, disease and control states, providing a powerful means to compare many types of data (e.g., histology images, gene expression, and MRI) among many types of samples (e.g., ages, species or diseases).

"The Allen Institute is a leader in large-scale open science, known for providing high-quality data and online tools that advance brain research," said Sean Hill, Executive Director of the International Neuroinformatics Coordinating Facility (INCF). "With the Allen Brain Atlas Hackathon and their public API, they are bringing the same collaborative, community-focused approach to technology development and innovation that is at the core of INCF’s mission."

The hackathon program was designed to provide scientists and programmers a solid foundation in using the Allen Brain Atlas API for data mining, data analysis and tools development. The event featured a handful of speakers from the Allen Institute, as well as external experts who had leveraged earlier versions of the API in their work. As a hands-on workshop, participants spent most of the time working on projects of their choice. The Allen Institute development team actively participated throughout the week to provide specific examples of API usage, as well as to team up with community participants to develop collaborative projects. Participants’ presentations throughout the week showcased their projects and progress, stimulating new ideas and benefiting from the collective feedback and troubleshooting power of the entire group.

Projects ranged from practical applications, such as using a list of glioblastoma-related genes to discover biological patterns that could shed new light on the biology of the disease and developing strategies to use gene expression data with functional brain scanning technologies, to purely creative applications, including translating genomic data into music.

The Allen Brain Atlas Hackathon was hosted by the Allen Institute for Brain Science and funded jointly with the International Neuroinformatics Coordinating Facility (INCF).

Provided by Allen Institute for Brain Science

Source: medicalxpress.com