Posts tagged science

ScienceDaily (May 7, 2012) — Antipsychotic medications are increasingly prescribed in the US, but they can cause serious side effects including rapid weight gain, especially in children. In the first study of its kind, researchers at Zucker Hillside Hospital and the Feinstein Institute for Medical Research identified a gene that increases weight gain in those treated with commonly-used antipsychotic drugs.

These findings were published in the May issue of Archives of General Psychiatry.

Second-generation antipsychotics (SGAs) were used as the treatment in this study. SGAs are commonly used to treat many psychotic and nonpsychotic disorders. However, it is important to note that these SGAs are associated with substantial weight gain, including the development of obesity and other cardiovascular risk factors. The weight gain side effect of SGAs is significant because it often results in a reduced life expectancy of up to 30 years in those who suffer from chronic and severe mental illnesses. The weight gain also prompts some to stop taking the medication, adversely impacting their quality of life.

In this genome-wide association study (GWAS), researchers first evaluated a group of pediatric patients in the US being treated for the first time with antipsychotics. They then replicated the result in three independent groups of patients who were in psychiatric hospitals in the United States and Germany or participating in European antipsychotic drug trials. The gene that was identified to increase weight gain, MC4R or melanocortin 4 receptor, has been previously identified as being linked to obesity and type 2 diabetes. In the new study, it was found that patients gained up to 20 pounds when on treatment.

"This study offers the prospect of being able to identify individuals who are at greatest risk for severe weight gain following antipsychotic treatment," said Anil Malhotra, MD, investigator at the Zucker Hillside Hospital Department of Psychiatry Research and Feinstein Institute for Medical Research. "We hope that those who are at risk could receive more intensive or alternative treatment that would reduce the potential for weight gain and we are currently conducting studies to identify such treatment."

Additional Details About the Study

Researchers conducted the first GWAS of SGA-induced weight gain in patients carefully monitored for medication adherence who were undergoing initial treatment with SGAs. To confirm results, they next assessed three independent replication cohorts: 1) a cohort of adult subjects undergoing their first treatment with a single SGA (clozapine), 2) a cohort of adult subjects treated with the same SGAs as in our discovery sample, and 3) a cohort of adult subjects in the first episode of schizophrenia and enrolled in a randomized clinical trial of antipsychotic drugs. The discovery cohort consisted of 139 pediatric patients undergoing first exposure to SGAs. The 3 additional cohorts consisted of 73, 40, and 92 subjects. Patients in the discovery cohort were treated with SGAs for 12 weeks. Additional cohorts were treated for 6 and 12 weeks.

This GWAS yielded 20 single-nucleotide polymorphisms at a single locus exceeding a statistical threshold of P10-5. This locus, near the melanocortin 4 receptor (MC4R) gene, overlaps a region previously identified by large-scale GWAS of obesity in the general population. Effects were recessive, with minor allele homozygotes gaining extreme amounts of weight during the 12-week trial. These results were replicated in 3 additional cohorts, with rs489693 demonstrating consistent recessive effects; meta-analysis revealed a genome-wide significant effect. Moreover, consistent effects on related metabolic indices, including triglyceride, leptin, and insulin levels were observed.

Source: Science Daily

ScienceDaily (May 7, 2012) — Depressive symptoms that are present in midlife or in late life are associated with an increased risk of developing dementia, according to a report in the May issue of Archives of General Psychiatry, a JAMA Network publication.

Nearly 5.3 million individuals in the United States have Alzheimer disease (AD) and the resulting health care costs in 2010 were roughly $172 billion, the authors write as background information in the study. “Prevalence and costs of AD and other dementias are projected to rise dramatically during the next 40 years unless a prevention or a cure can be found. Therefore, it is critical to gain a greater understanding of the key risk factors and etiologic underpinnings of dementia from a population-based perspective,” the authors write.

Deborah E. Barnes, Ph.D., M.P.H., of the University of California, San Francisco and the San Francisco Veterans Affairs Medical Center, and colleagues evaluated data from 13,535 long-term Kaiser Permanente members and examined depressive symptoms assessed in midlife (1964-1973) and in late life (1994-2000) and risks of developing dementia, Alzheimer disease (AD) and vascular dementia (VaD; dementia resulting from brain damage from impaired blood flow to the brain).

Depressive symptoms were present in 14.1 percent of study participants in midlife only, 9.2 percent in late life only and 4.2 percent in both. During six years of follow-up, 22.5 percent of patients were diagnosed with dementia; 5.5 percent with Alzheimer disease and 2.3 percent with VaD.

When examining AD and VaD separately, patients with late-life depressive symptoms had a two-fold increase in AD risk, and patients with midlife and late-life symptoms had more than a three-fold increase in VaD risk.

"Our findings suggest that chronic depression during the life course may be etiologically associated with an increased risk of dementia, particularly VaD, whereas depression that occurs for the first time in late life is likely to reflect a prodromal stage of dementia, in particular AD," the authors conclude.

Source: Science Daily

ScienceDaily (May 7, 2012) — The deletion of part of a gene that plays a role in the synthesis of carnitine — an amino acid derivative that helps the body use fat for energy — may play a role in milder forms of autism, said a group of researchers led by those at Baylor College of Medicine and Texas Children’s Hospital.

"This is a novel inborn error of metabolism," said Dr. Arthur Beaudet, chair of molecular and human genetics at BCM and a physician at Texas Children’s Hospital, and the senior author of the report that appears online in the Proceedings of the National Academy of Sciences. "How it is associated with the causes of autism is as yet unclear. However, it could point to a means of treatment or even prevention in some patients."

Deletion leads to imbalance

Beaudet and his international group of collaborators believe the gene deletion leads to an imbalance in carnitine in the body. Meat eaters receive about 75 percent of their carnitine from their diet. However, dietary carnitine levels are low in vegetarians and particularly in vegans. In most people, levels of carnitine are balanced by the body’s ability to manufacture its own carnitine in the liver, kidney and brain, starting with a modified form of the amino acid lysine.

Carnitine deficiency has been identified when not enough is absorbed through the diet or because of medical treatments such as kidney dialysis. Genetic forms of carnitine deficiency also exist, which are caused when too much carnitine is excreted through the kidneys.

In this new inborn error, there is a deletion in the second exon — the protein-coding portion of a gene — of the TMLHE gene, which includes the genetic code for the first enzyme in the synthesis of carnitine (TMLHE stands for trimethyllysine epsilon which encodes the enzyme trimethyllysine dioxygenase).

Studies in the laboratory that identified the deletion were led by Dr. Patricia B.S. Celestino-Soper, as a graduate student in Beaudet’s laboratory at BCM, and by Dr. Sara Violante, a graduate student in the laboratory of Dr. Frédéric M. Vaz of the Academic Medical Center in Amsterdam.

Frequency of deletion

To determine the frequency of the gene deletion, Beaudet and his colleagues tested male autism patients who were the only people with the disorder in their families (simplex families) from the Simons Simplex Collection, the South Carolina Early Autism Project and Houston families. In collaboration with laboratories and researchers in Nashville, Los Angeles, Paris, New York, Toronto and Cambridge (United Kingdom), they tested affected male siblings in families with more than one male case of autism (multiplex families).

When they looked at the TMLHE genes in males affected by autism and compared them to normal controls, they found that the gene alteration is a fairly common one, occurring in as many as one in 366 males unaffected by autism. It was not significantly more common in males within families in which there is only one person with autism. However, it is nearly three times more common in families with two or more boys with autism.

No syndromic form

Beaudet said most of the affected males with the deletion did not have syndromic autism that is frequently associated with other serious diseases. In many instances, syndromic autism affects physical development as well as cognitive, which is reflected in their facial features as well as other parts of their bodies. None of the six boys affected with autism (where information was available) had the syndromic form of disease. Their intelligence quotients and cognitive scores varied, with some being far below normal and others normal.

"Most of the males we identified with the TMLHE deficiency were apparently normal as adults," said Beaudet, although detailed information on learning and behavior was not available on these "control" males. "The gene deletion is neither necessary nor sufficient in itself to cause autism."

"TMLHE deficiency itself is likely to be a weak risk factor for autism, but we need to do more studies to replicate our results," Beaudet said. He estimated that at the rates found in his study, the deficiency might be a factor in about 170 males born with autism per year in the United States. This would equate to about one-half of one percent of autism cases.

The authors from Amsterdam found major increases in some carnitine-related chemicals and absence of others in both urine and plasma. These metabolic alterations were found to be predictive of the dysfunction of the TMLHE gene and therefore can be used to identify males with this disorder.

It remains uncertain whether TMLHE deficiency is benign or causes autism by affecting the function of neurons through toxic accumulation or deficiency of a variety of chemical metabolites.

"We believe that the most attractive hypothesis at this time is that the increased risk of autism is modified by dietary intake of carnitine from birth through the first few years of life," said Beaudet.

He and his colleagues are undertaking three studies to further their understanding of the TMLHE deficiency. In one, they will attempt to replicate the findings in multiplex families. In a second, they will study carnitine levels in the cerebrospinal fluid of infants with autism — both those who have the gene deficiency and those who do not. In a third study, they plan to begin giving boys under age 5 with autism carnitine or a related supplement and determine whether this improves the behavior of those with the TMLHE deficiency and those without.

Source: Science Daily

ScienceDaily (May 7, 2012) — One of the world’s most important fossils has a story to tell about the brain evolution of modern humans and their ancestors, according to Florida State University evolutionary anthropologist Dean Falk.

Taung surrounded by a juvenile chimp skull and human skull, the latter having a fontanelle and metopic suture. The metopic suture is visible on the frontal lobe of Taung’s endocast. (Credit: CT-based images by M. Ponce de León and Ch. Zollikofer, University of Zurich)

The Taung fossil — the first australopithecine ever discovered — has two significant features that were analyzed by Falk and a group of anthropological researchers. Their findings, which suggest brain evolution was a result of a complex set of interrelated dynamics in childbirth among new bipeds, were published May 7 in the Proceedings of the National Academy of Sciences.

"These findings are significant because they provide a highly plausible explanation as to why the hominin brain might grow larger and more complex," Falk said.

The first feature is a “persistent metopic suture,” or unfused seam, in the frontal bone, which allows a baby’s skull to be pliable during childbirth as it squeezes through the birth canal. In great apes — gorillas, orangutans and chimpanzees — the metopic suture closes shortly after birth. In humans, it does not fuse until around 2 years of age to accommodate rapid brain growth.

The second feature is the fossil’s endocast, or imprint of the outside surface of the brain transferred to the inside of the skull. The endocast allows researchers to examine the brain’s form and structure.

After examining the Taung fossil, as well as huge numbers of skulls belonging to apes and humans, as well as corresponding 3-D CT (three-dimensional computed tomographic) scans, and taking into account the fossil record for the past 3 million years, Falk and her colleagues noted three important findings: The persistent metopic suture is an adaptation for giving birth to babies with larger brains; is related to the shift to a rapidly growing brain after birth; and may be related to expansion in the frontal lobes.

"The persistent metopic suture, an advanced trait, probably occurred in conjunction with refining the ability to walk on two legs," Falk said. "The ability to walk upright caused an obstretric dilemma. Childbirth became more difficult because the shape of the birth canal became constricted while the size of the brain increased. The persistent metopic suture contributes to an evolutionary solution to this dilemma."

The later fusion of the metopic suture is most likely an adaptation of hominins who walked upright to be able to more easily give birth to babies with relatively large brains. The unfused seam is also related to the shift to rapidly growing brains after birth, an advanced human-like feature as compared to apes.

"The later fusion was also associated with evolutionary expansion of the frontal lobes, which is evident from the endocasts of australopithecines such as Taung," Falk said.

The Taung fossil, which is estimated to be around 2½ million years old, was discovered in 1924 in Taung, South Africa. It became the “type specimen,” or main model, of the genus Australopithecus africanus when it was announced in 1925.

An australopithecine is any species of the extinct generaAustralopithecus or Paranthropus that lived in Africa, walked on two legs and had relatively small brains.

Source: Science Daily

May 7, 2012

A study on a handful of people with suspected mild Alzheimer’s disease (AD) suggests that a device that sends continuous electrical impulses to specific “memory” regions of the brain appears to increase neuronal activity. Results of the study using deep brain stimulation, a therapy already used in some patients with Parkinson’s disease and depression, may offer hope for at least some with AD, an intractable disease with no cure.

"While our study was designed mainly to establish safety, involved only six people and needs to be replicated on a larger scale, we don’t have another treatment for AD at present that shows such promising effects on brain function," said the study’s first author, Gwenn Smith, Ph.D., a professor in the Department of Psychiatry and Behavioral Sciences at the Johns Hopkins University School of Medicine. The research, published in the Archives of Neurology, was conducted while Smith was on the faculty at the University of Toronto, and will be continuing at Toronto, Hopkins and other U.S. sites in the future. The study was led by Andres M. Lozano, chairman of the Department of Neurosurgery at the University of Toronto.

One month and one year after implanting a device that allows for continuous electrical impulses to the brain, Smith and her colleagues performed PET scans that detect changes in brain cells’ metabolism of glucose, and found that patients with mild forms of AD showed sustained increases in glucose metabolism, an indicator of neuronal activity. The increases, the researchers say, were larger than those found in patients who have taken the drugs currently marketed to fight AD progression. Other imaging studies have shown that a decrease in glucose metabolism over the course of a year is typical in AD. Alzheimer’s disease cannot be precisely diagnosed by brain biopsies until after death.

The team observed roughly 15 percent to 20 percent increases in glucose metabolism after one year of continuous stimulation. The increases were observed, to a greater extent, in patients with better outcomes in cognition, memory and quality of life. In addition, the stimulation increased connectivity in brain circuits associated with memory.

Deep brain stimulation (DBS) requires surgical implantation of a brain pacemaker, which sends electrical impulses to specific parts of the brain. For the study, surgeons implanted a tiny electrode able to deliver a low-grade electrical pulse close to the fornix, a key nerve tract in brain memory circuits. The researchers — most with the University of Toronto — reported few side effects in the six subjects they tested. Just as importantly, says Smith, was seeing that DBS appeared to reverse the downturn in brain metabolism that typically comes with AD.

AD is a progressive and lethal dementia that mostly strikes the elderly. It affects memory, thinking and behavior. Estimates vary, but experts suggest that as many as 5.1 million Americans may have AD and that, as baby boomers age, prevalence will skyrocket. Smith says decades of research have yet to lead to clear understanding of its causes or to successful treatments that stop progression.

The trial of DBS came about, Smith reports, when Lozano used DBS of the fornix to treat an obese man. The procedure, designed to target the regions of the brain involved in appetite suppression, unexpectedly had significant increases in his memory. Inspired, the scientists persisted through rigorous ethical and scientific approvals before their AD phase I safety study could begin.

Smith, who also is director of the Division of Geriatric Psychiatry and Neuropsychiatry at Johns Hopkins Bayview Medical Center, is an authority on mapping the brain’s glucose metabolism in aging and psychiatric disease. It was Smith’s earlier analysis of AD patients’ PET scans that revealed their distinct pattern of lowered brain metabolism. She determined that specific parts of the temporal and parietal cerebral cortex — memory network areas of the brain where AD’s earliest pathology surfaces— became increasingly sluggish with time.

Provided by Johns Hopkins Medical Institutions

Source: medicalxpress.com

ScienceDaily (May 7, 2012) — Badly controlled diabetes are known to affect the brain causing memory and learning problems and even increased incidence of dementia, although how this occurs is not clear. But now a study in mice with type 2 diabetes has discovered how diabetes affects a brain area called hippocampus causing memory loss, and also how caffeine can prevent this. 

Curiously, the neurodegeneration that Rodrigo Cunha  from the Centre for Neuroscience and Cell Biology of the University of Coimbra in Portugal see caused by diabetes is the same that occurs at the first stages of several neurodegenerative diseases, including Alzheimer’s and Parkinson’s, suggesting that caffeine (or drugs with similar mechanism) could help them too.

 Type 2 diabetes (which accounts for about 90%of all diabetic cases) is a full blown public health disaster – 285 million people affected worldwide (6.4% of the world population) with numbers expected to almost double by 2030. And this without counting pre-diabetic individuals. The problem is that the disease is triggered by obesity, sedentary lifestyle and bad eating habits (although there is also a genetic predisposition), all of which are increasingly widespread. 

Diabetes is caused by high levels of sugar in the blood, and in type 2 this occurs because the body becomes increasingly resistant to insulin –the hormone that allows the cells to take the sugar from the blood to use it as “fuel” – resulting in toxic high levels of sugar  in the blood that damage nerves and blood vessels and, with time, cause severe complications

 In the study out now in the journal PLoS , João Duarte, Rodrigo Cunha and colleagues take advantage of a new mouse model of diabetes type 2, which, like humans, develops the disease in adults as result of a high-fat diet, to look at one of the least understood complications of diabetes – the disease effect on the brain, more specifically, on memory. They also investigate a possible protective effect by caffeine as this psychostimulant has been suggested to prevent memory loss in a series of neurodegenerative diseases, maybe even in diabetes, although how this happens is not known. And when we consider that coffee is the world leading beverage right after water, with about 500 billion cups consumed annually, this, if true, needs to be better understood.

With that aim  the Portuguese researchers compared four groups of mice - diabetic or normal animals without or with caffeine (equivalent to 8 cups of coffee a day) in their water – to find that long-term consumption of caffeine not only diminished the weight gain and the high levels of blood sugar typical of diabetes, but also prevented the mice’s memory loss (diabetic animals had significantly poorer memory than normal ones). This confirmed that caffeine could, in fact, protect against diabetes as well as prevent memory impairment, probably by interfering with the neurodegeneration caused by toxic sugar levels.

To investigate this, next, the researchers looked at a brain region linked to memory and learning, which is often atrophied in diabetics, called hippocampus. And in fact, diabetic mice had abnormalities in this area showing synaptic degeneration (synapses are the structures at the end of each neuron used to communicate between neurons) and astrogliosis (an abnormal increase of the cells that surround neurons normally as result of the deathof nearby neurons). Both phenomena are known to affect memory and caffeine consumption  prevented the abnormalities.

But to be able to develop drugs based on caffeine’s protective effect, it was necessary to understand its molecular mechanisms. So next the researchers looked at the only brain molecules known to respond to caffeine – the adenosine receptors A1R and A2AR - in the hippocampus. And here, A2AR seemed to be the key for caffeine’s memory rescue since its density - which increases with noxious insults - was high in diabetic animals but normal in those treated with caffeine. This agrees with the previous studies that showed that A2AR inhibition protected against synaptic degeneration and memory dysfunction.

In conclusion, Duarte and Cunha’s work – using an animal model of diabetes type 2 that closely mimics the human form of the disease – suggests that diabetes affects memory by causing synaptic degeneration, astrogliosis and increased levels of A2AR. The study indicates as well that chronic consumption of caffeine can prevent the neurodegeneration and the memory impairment. And this not only in diabetes, since synaptic degeneration and astrogliosis are both part of a cascade of events common to several neurodegenerative diseases, suggesting that caffeine (or similar drugs) could help them too through the same mechanisms.

So does this means that we should drink eight cups of coffee a day to prevent memory loss in old age or diabetes? 

Not really as Rodrigo Cunha, the team leader explains: “Indeed, the dose of caffeine shown to be effective is just too excessive. All we can take from here is that a moderate consumption of caffeine should afford a moderate benefit, but still a benefit. Such experimental design is common in pre-clinical studies: in order to highlight a clear benefit, one dramatises the tested doses. But it’s an important first step. Our ultimate goal is the design of a drug more potent and selective (i.e. with less potential side effects) than caffeine itself; animal studies enable us to pinpoint the likely target of caffeine with protective benefits in type 2 diabetes. So now we will be testing chemical derivates of caffeine, which act as selective adenosine A2A receptor antagonists,to try to prevent diabetic encephalopathy. It might turn out to be a therapeutic breakthrough for this devastating disease”. 

And a breakthrough in a disease that is already affecting 6.4% of the population and growing can never come too soon.

Source: Science Daily

ScienceDaily (May 7, 2012) — Elderly people with pre-diabetes and type 2 diabetes suffer from an accelerated decline in brain size and mental capacity in as little as two years according to new research presented at the joint International Congress of Endocrinology/European Congress of Endocrinology in Florence, Italy. 

An Australian research team led by Associate Professor Katherine Samaras (Garvan Institute of Medical Research) found that the aging brain is vulnerable to worsening blood sugar levels even before type 2 diabetes is diagnosable.

While some brain volume loss is a normal part of aging, the researchers found that elderly people with blood sugar levels in flux, as well as type 2 diabetes, lost almost two and a half times more brain volume than their peers over two years. The reduction in size of the frontal lobe — associated with higher mental functions like decision-making, emotional control, and long term memory — has a significant impact on cognitive function and quality of life.

Diabetes is a very common disorder caused by high levels of sugar in the bloodstream. It affects 6.4% (285 million) of the worldwide population and is associated with an increased risk of heart attacks, stroke and damage to the eyes, feet and kidneys. In type 2 diabetes, which accounts for 90% of all cases, insulin — a hormone that allows cells to take sugar from the bloodstream and store it as energy — does not work properly. 344 million people also have pre-diabetes, a condition with mildly elevated blood sugar levels that gives them a 50% risk of developing the disease over ten years.

This research — a follow-up of 312 participants from the Sydney Memory and Ageing Study — compared MRI scans taken from the beginning and end of a two-year period. The participants were elderly community-dwelling Australians aged between 70 and 90 years old (average age 78, 54% male) and free from dementia. At the start of the study 41% had pre-diabetes and 13% had type 2 diabetes.

At the end of the study the participants were divided into four groups: (1) those with normal, stable glucose levels (102 people); (2) those with stable pre-diabetes (120 people); (3) those whose glucose levels had worsened (57 people); and finally, (4) those with type 2 diabetes from the start (33 people).

The MRI scans showed that the normal group lost an average of 18.4 cm3 total brain volume over two years. In comparison, the stable pre-diabetic group lost 1.4 times more brain volume (26.6 cm3). Both the third group (worsening glucose levels) and fourth group (type 2 diabetes) lost 2.3 times the stable group’s brain volume loss (41.7 cm3 and 42.3 cm3, respectively).

The researchers — using statistical models that accounted for other variables — concluded that a person’s blood sugar status after two years can significantly predict their decline in brain volume.

Associate Professor Katherine Samaras, from the Garvan Institute of Medical Research, said:

"These findings highlight the importance of prevention of diabetes. They also emphasise that, in the elderly, clinicians and allied health professionals need to understand that the complexity of diabetes care needs to accommodate expected declines in cognitive function.

"We need to understand why these changes in cognition and brain size occur. Is it due merely to higher blood sugars? Is the brain subject to the toxic effects of glucose, just as peripheral nerves are? To what extent do other factors associated with diabetes also contribute to the decline in brain size and function, for example inflammation or blood fat levels?

"We also need to learn how we can prevent or deter the negative effects of diabetes on the brain."

Source: Science Daily

ScienceDaily (May 7, 2012) — A Kansas State University graduate student is creating a schoolyard that can become a therapeutic landscape for children with autism.

Chelsey King, master’s student in landscape architecture, St. Peters, Mo., is working with Katie Kingery-Page, assistant professor of landscape architecture, to envision a place where elementary school children with autism could feel comfortable and included.

"My main goal was to provide different opportunities for children with autism to be able to interact in their environment without being segregated from the rest of the school," King said. "I didn’t want that separation to occur."

The schoolyard can be an inviting place for children with autism, King said, if it provides several aspects: clear boundaries, a variety of activities and activity level spaces, places where the child can go when overstimulated, opportunities for a variety of sensory input without being overwhelming and a variety of ways to foster communication between peers.

"The biggest issue with traditional schoolyards is that they are completely open but also busy and crowded in specific areas," King said. "This can be too overstimulating for a person with autism."

King researched ways that she could create an environment where children with autism would be able to interact with their surroundings and their peers, but where they could also get away from overstimulation until they felt more comfortable and could re-enter the activities.

"Through this research, I was able to determine that therapies and activities geared toward sensory stimulation, cognitive development, communication skills, and fine and gross motor skills — which traditionally occur in a classroom setting — could be integrated into the schoolyard," King said.

King designed her schoolyard with both traditional aspects — such as a central play area — and additional elements that would appeal to children with autism, including:

* A music garden where children can play with outdoor musical instruments to help with sensory aspects.

* An edible garden/greenhouse that allows hands-on interaction with nature and opportunities for horticulture therapy.

* A sensory playground, which uses different panels to help children build tolerances to difference sensory stimulation.

* A butterfly garden to encourage nature-oriented learning in a quiet place.

* A variety of alcoves, which provide children with a place to get away when they feel overwhelmed and want to regain control.

King created different signs and pictures boards around these schoolyard elements, so that it was easier for children and teachers to communicate about activities. She also designed a series of small hills around the central play areas so that children with autism could have a place to escape and watch the action around them.

"It is important to make the children feel included in the schoolyard without being overwhelmed," King said. "It helps if they have a place — such as a hill or an alcove — where they can step away from it and then rejoin the activity when they are ready.

King and Kingery-Page see the benefits of this type of schoolyard as an enriching learning environment for all children because it involves building sensory experience and communication.

"Most children spend seven to nine hours per weekday in school settings," Kingery-Page said. "Designing schoolyards that are educational, richly experiential, with potentially restorative nature contact for children should be a community concern."

The researchers collaborated with Jessica Wilkinson, a special education teacher who works with children with autism. King designed her schoolyard around Amanda Arnold Elementary School, which is the Manhattan school district’s magnet school for children with autism.

"Although there are no current plans to construct the schoolyard, designing for a real school allowed Chelsey to test principles synthesized from literature against the actual needs of an educational facility," Kingery-Page said. "Chelsey’s interaction with the school autism coordinator and school principal has grounded her research in the daily challenges of elementary education for students with autism."

Source: Science Daily

May 7, 2012 

(Medical Xpress) — An international study led by the University of Sydney and published in the Annals of Neurology has the potential to improve the design of clinical trials for the treatment of Charcot-Marie-Tooth disease, a disorder which affects the peripheral nervous system.

Charcot-Marie-Tooth disease (CMT) is among the most common inherited neurological disorders, affecting one in 2500 people. Symptoms such as leg weakness, foot pain, trips and falls develop in the first two decades of life, with some patients wheelchair bound by 21 years. Currently there is no treatment for any form of this disease, but clinical trials are increasingly occurring.

"While it is very positive that clinical trials are taking place in this area, it is vital that trials are based on appropriately selected patients and carefully chosen outcome measures," says Associate Professor Joshua Burns, Chief Investigator from the University of Sydney and The Children’s Hospital at Westmead. "This relies on being able to measure disease severity accurately, and in turn the patient’s response to treatment, which we were previously unable to do in children."

In response, Associate Professor Burns and colleagues from the USA, UK and Italy designed the CMT Pediatric Scale (CMTPedS), a patient-centred multi-item rating scale of disability for children with CMT.

"Rating scales used for adult patients are inappropriate for children and since most forms of CMT affect children there was an obvious need for a new clinical tool.

"Furthermore, it is during childhood that we anticipate that treatments for CMT may be most effective - before the disease progresses and makes repair more difficult."

During a 14-month test period the CMTPedS was administered to more than 170 children aged three to 20 with varying types of CMT in Australia and internationally via the Inherited Neuropathies Consortium. Analysis of these data supported the viability of CMTPedS as a reliable, valid and sensitive global measure of disability for children with CMT from the age of three years.

The CMTPedS can be completed in 25 minutes and will have broad application in clinical trials of rehabilitative, pharmacological and surgical interventions.

"There is growing international support for the rating scale to be implemented as the primary outcome measure in studies of children with CMT because the quality of the measure has the potential to influence the outcome of clinical trials and patient care," says Associate Professor Burns.

Provided by University of Sydney

Source: medicalxpress.com

May 7, 2012

Many of us love massages, but imagine a massage so deep that tissues, organs and cells could also be ‘massaged’.

That’s exactly what Vibroacoustic Therapy, a low frequency sound massage, is clinically proven to do, and new research at U of T suggests that it may help people with debilitating diseases.

“It is basically stimulating the body with very low sound – like sitting on a subwoofer,” said Professor Lee Bartel of the Faculty of Music.  “But it requires special speakers that carry sound almost too low to hear in a way that changes it basically to something you feel instead of hear.”

Bartel and his team in the new Music and Health Research Collaboratory (MaHRC) are exploring the medical effects of low frequency sound and have shown that this therapy can play a key role in reducing the symptoms of Parkinson’s disease.

Vibroacoustic therapy (VAT) consists of low sound frequencies that are transmitted to the body and mind through special transducers that convert the sound to inner body massage. MaHRC associates Heidi Ahonen and Quincy Almeida treated two groups of Parkinson’s patients (20 with dominant tremor symptoms and 20 with slow/rigid movement symptoms) with five minutes of 30 Hz vibration.

Both groups showed improvements in all symptoms, including less rigidity and better walking speed with bigger steps and less tremor.

“There have been several studies using vibration from sound with Parkinson’s,” said Bartel   “It has been known for over 100 years that vibration (like riding in a wagon on cobblestones) helped relieve some symptoms. So the scientific study of the effect of low frequency sound was a natural connection. Also known is that 40 Hz brain waves seem to be carriers of information between the parts of the brain that control movement. So adding extra stimulation in that zone should help that communication and so assist in movement control.”

Bartel, Founding and Acting Director of MaHRC, says the goal of low frequency sound studies with Parkinson’s is to determine which approach is most effective, how much and how often treatment is needed, and whether medication can be reduced. Vibroacoustic Therapy frequencies, between 20 and 100 Hz or pulses per second, correspond to brainwave activities and function that are currently being explored in neuroscience. 

But the effects of Vibroacoustic Therapy extend beyond the brain. It also provides deep physical cellular stimulation to skin, muscles and joints, resulting in decreased pain and increased mobility. Like hand/mechanical massage, vibroacoustic therapy aids circulation, relaxes muscles, and feels good.

Bartel points to research that shows that “several medical conditions including Parkinson’s and neuralgic pain like fibromyalgia, may be related to a common brain mechanism – a brain rhythm disorientation between the inner brain and the outer cortex. Since the rhythmic pulses of music can drive and stabilize these, we speculate that low frequency sound might help in fibromyalgia as well as Parkinson’s.”

Bartel’s team is now looking at the role of vibroacoustic therapy as a treatment for patients with fibromyalgia.

“Although it is too early to form any conclusions, there is encouraging data indicating that treating fibromyalgia patients with doses of 40 Hz sound seems to reduce pain.” 

“It is truly an exciting time for music medicine – the idea of developing audioceuticals (prescribable sound) points to a whole new direction for music therapy, and the potential for MaHRC to lead in this is very exciting for me” said Bartel.      

Provided by University of Toronto

Source: medicalxpress.com