Sleep deprivation can lead to symptoms of schizophrenia

Research shows that sleep deprivation for 24 hours can lead to a person developing symptoms of schizophrenia.

Twenty-four hours of sleep deprivation can lead to conditions in healthy persons similar to the symptoms of schizophrenia. This discovery was made by an international team of researchers under the guidance of the University of Bonn and King's College London. The scientists point out that this effect should be investigated more closely in persons who have to work at night. In addition, sleep deprivation may serve as a model system for the development of drugs to treat psychosis. The results have now been published in The Journal of Neuroscience.

In psychosis, there is a loss of contact with reality and this is associated with hallucinations and delusions. The chronic form is referred to as schizophrenia, which likewise involves thought disorders and misperceptions. Affected persons report that they hear voices, for example. Psychoses rank among the most severe mental illnesses. An international team of researchers under the guidance of the University of Bonn has now found out that after 24 hours of sleep deprivation in healthy patients, numerous symptoms were noted which are otherwise typically attributed to psychosis or schizophrenia. "It was clear to us that a sleepless night leads to impairment in the ability to concentrate," says Prof. Dr. Ulrich Ettinger of the Cognitive Psychology Unit in the Department of Psychology at the University of Bonn. "But we were surprised at how pronounced and how wide the spectrum of schizophrenia-like symptoms was."

The scientists from the University of Bonn, King's College London (England) as well as the Department of Psychiatry and Psychotherapy of the University of Bonn Hospital examined a total of 24 healthy subjects of both genders aged 18 to 40 in the sleep laboratory of the Department of Psychology. In an initial run, the test subjects were to sleep normally in the laboratory. About one week later, they were kept awake all night with movies, conversation, games and brief walks. On the following morning, subjects were each asked about their thoughts and feelings. In addition, subjects underwent a measurement known as prepulse inhibition.

Unselected information leads to chaos in the brain

"Prepulse inhibition is a standard test to measure the filtering function of the brain," explains lead author Dr. Nadine Petrovsky from Prof. Ettinger's team. In the experiment, a loud noise is heard via headphones. As a result, the test subjects experience a startle response, which is recorded with electrodes through the contraction of facial muscles. If a weaker stimulus is emitted beforehand as a "prepulse," the startle response is lower. "The prepulse inhibition demonstrates an important function of the brain: Filters separate what is important from what is not important and prevent sensory overload," says Dr. Petrovsky.

In our subjects, this filtering function of the brain was significantly reduced following a sleepless night. "There were pronounced attention deficits, such as what typically occurs in the case of schizophrenia," reports Prof. Ettinger. "The unselected flood of information led to chaos in the brain." Following sleep deprivation, the subjects also indicated in questionnaires that they were somewhat more sensitive to light, color or brightness. Accordingly, their sense of time and sense of smell were altered and mental leaps were reported. Many of those who spent the night even had the impression of being able to read thoughts or notice altered body perception. "We did not expect that the symptoms could be so pronounced after one night spent awake," says the psychologist from the University of Bonn.

Sleep deprivation as a model system for mental illnesses

The scientists see an important potential application for their results in research for drugs to treat psychoses. "In drug development, mental disorders like these have been simulated to date in experiments using certain active substances. However, these convey the symptoms of psychoses in only a very limited manner," says Prof. Ettinger. Sleep deprivation may be a much better model system because the subjective symptoms and the objectively measured filter disorder are far more akin to mental illnesses. Of course, the sleep deprivation model is not harmful: After a good night's recovery sleep, the symptoms disappear. There is also a need for research with regard to persons who regularly have to work at night. "Whether the symptoms of sleep deprivation gradually become weaker due to acclimatization has yet to be investigated," says the psychologist from the University of Bonn.

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All About Obama's BRAIN Initiative

This article discusses the new BRAIN Initiative, , and how the initiative's bureaucracy is structured at the NIH.

Today at the White House, President Barack Obama unveiled the "BRAIN" Initiative -- a bold new research effort to revolutionize our understanding of the human mind and uncover new ways to treat, prevent, and cure brain disorders like Alzheimer's, schizophrenia, autism, epilepsy, and traumatic brain injury.

The NIH Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative is part of a new Presidential focus aimed at revolutionizing our understanding of the human brain. By accelerating the development and application of innovative technologies, researchers will be able to produce a revolutionary new dynamic picture of the brain that, for the first time, shows how individual cells and complex neural circuits interact in both time and space. Long desired by researchers seeking new ways to treat, cure, and even prevent brain disorders, this picture will fill major gaps in our current knowledge and provide unprecedented opportunities for exploring exactly how the brain enables the human body to record, process, utilize, store, and retrieve vast quantities of information, all at the speed of thought.

Why is the NIH BRAIN Initiative needed?

With nearly 100 billion neurons and 100 trillion connections, the human brain remains one of the greatest mysteries in science and one of the greatest challenges in medicine. Neurological and psychiatric disorders, such as Alzheimer's disease, Parkinson's disease, autism, epilepsy, schizophrenia, depression, and traumatic brain injury, exact a tremendous toll on individuals, families, and society. Despite the many advances in neuroscience in recent years, the underlying causes of most of neurological and psychiatric conditions remain largely unknown, due to the vast complexity of the human brain. If we are ever to develop effective ways of helping people suffering from these devastating conditions, researchers will first need a more complete arsenal of tools and information for understanding how the brain functions both in health and disease.

Why is now the right time for the NIH BRAIN Initiative?

In the last decade alone, scientists have made a number of landmark discoveries that now create the opportunity to unlock the mysteries of the brain. We have witnessed the sequencing of the human genome, the development of new tools for mapping neuronal connections, the increasing resolution of imaging technologies, and the explosion of nanoscience. These discoveries have yielded unprecedented opportunities for integration across scientific fields. For instance, by combining advanced genetic and optical techniques, scientists can now use pulses of light in animal models to determine how specific cell activities within the brain affect behavior. What's more, through the integration of neuroscience and physics, researchers can now use high-resolution imaging technologies to observe how the brain is structurally and functionally connected in living humans.

While these technological innovations have contributed substantially to our expanding knowledge of the brain, significant breakthroughs in how we treat neurological and psychiatric disease will require a new generation of tools to enable researchers to record signals from brain cells in much greater numbers and at even faster speeds. This cannot currently be achieved, but great promise for developing such technologies lies at the intersections of nanoscience, imaging, engineering, informatics, and other rapidly emerging fields of science.

How will the NIH BRAIN Initiative work?

Given the ambitious scope of this pioneering endeavor, it is vital that planning for the NIH BRAIN Initiative be informed by a wide range of expertise and experience. Therefore, NIH is establishing a high level working group of the Advisory Committee to the NIH Director (ACD) to help shape this new initiative. This working group, co-chaired by Dr. Cornelia "Cori" Bargmann (The Rockefeller University) and Dr. William Newsome (Stanford University), is being asked to articulate the scientific goals of the BRAIN initiative and develop a multi-year scientific plan for achieving these goals, including timetables, milestones, and cost estimates.

As part of this planning process, input will be sought broadly from the scientific community, patient advocates, and the general public. The working group will be asked to produce an interim report by fall 2013 that will contain specific recommendations on high priority investments for Fiscal Year (FY) 2014. The final report will be delivered to the NIH Director in June 2014.

How will the NIH BRAIN Initiative be supported?

In total, NIH intends to allocate $40 million in FY14. Given the cross-cutting nature of this project, the NIH Blueprint for Neuroscience Research -- an initiative spanning 14 NIH Institutes and Centers -- will be the leading NIH contributor to its implementation in FY14. Of course, a goal this audacious will require ideas from the best scientists and engineers across many diverse disciplines and sectors. Therefore, NIH is working in close collaboration with other government agencies, including the Defense Advanced Research Projects Agency (DARPA) and the National Science Foundation (NSF). Strong interest has also been expressed by several private foundations, including the Howard Hughes Medical Institute, the Allen Institute for Brain Science, and The Kavli Foundation, and the Salk Institute for Biological Studies. Private industries have also expressed a high level of interest in participation in this groundbreaking initiative.

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Yoga may help with depression and sleep problems

A review of studies on yoga shows that yoga may benefit those with depression and sleep problems. People with ADHD or schizophrenia may also benefit.

Some people with certain psychiatric conditions may benefit from yoga, according to a new review.

The review, which examined results from 16 well-designed studies of yoga's effect on mental illness, concluded that yoga may have positive effects for people with depression and sleep complaints even if they don't take medication, as well as for people suffering from schizophrenia and ADHD who are taking medication.

However, the review did not find a benefit for people with eating or cognitive disorders.

Studies that have looked at yoga suggest the practice influences chemical messengers in the brain, inflammation in the body, and other biological factors in much the same way antidepressants and psychotherapy do, said study researcher Dr. P. Murali Doraiswamy, a professor of psychiatry and medicine at Duke University Medical Center in. [See The Science of Yoga and Why It Works.]

However, the studies in the review had limitations. Most of the studies on depression included patients with mild depression, so it's not clear if the results will apply to those with more severe forms of the disorder. Also, in many of the studies, people performed yoga in groups, and it's difficult to separate the effect of yoga from that of social interaction, Doraiswamy said.

In one study of 69 older adults with mild depression, weekly yoga sessions reduced depression scores by 40 percent at six months. A comparison group of adults who didn't take yoga, and a group that practiced a form of complementary medicine called Ayurveda, did not show changes in depression scores.

In another study of 39 adults who were sleeping poorly (they were receiving chemotherapy), seven weeks of yoga improved sleep quality and reduced the need for sleep aids. People who did not take the yoga sessions (control group) did not have an improvement in sleep.

The National Center for Complementary and Alternative Medicine (NCCAM) says people should not  replace conventional medical care with yoga. Nor should people who practice yoga postpone seeing a health care provider. Patients should tell their doctor about any complementary health practices they use. Anyone with a medical condition should check with a health care provider before starting yoga, NCCAM says.

Pass it on: Yoga may have positive effects for people with depression, complaints, schizophrenia or ADHD.

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Poor sleep may worsen schizophrenia symptoms

Neuroscientists found that some symptoms of schizophrenia can worsen with irregular sleep cycles or poor sleep quality.

The possible link between poor sleep and schizophrenia prompted the research team, led by scientists from the University of Bristol, the Lilly Centre for Cognitive Neuroscience and funded by the Medical Research Council (MRC), to explore the impact of irregular sleep patterns on the brain by recording electrical brain activity in multiple brain regions during sleep.

For many people, sleep deprivation can affect mood, concentration and stress levels. In extreme cases, prolonged sleep deprivation can induce hallucinations, memory loss and confusion all of which are also symptoms associated with schizophrenia.

Dr Ullrich Bartsch, one of the study’s researchers, said: “Sleep disturbances are well-documented in the disease, though often regarded as side effects and poorly understood in terms of their potential to actually trigger its symptoms.”

Using a rat model of the disease, the team’s recordings showed desynchronisation of the waves of activity which normally travel from the front to the back of the brain during deep sleep. In particular the information flow between the hippocampus — involved in memory formation, and the frontal cortex — involved in decision-making, appeared to be disrupted. The team’s findings reported distinct irregular sleep patterns very similar to those observed in schizophrenia patients.

Dr Matt Jones, the lead researcher from the University’s School of Physiology and Pharmacology, added: “Decoupling of brain regions involved in memory formation and decision-making during wakefulness are already implicated in schizophrenia, but decoupling during sleep provides a new mechanistic explanation for the cognitive deficits observed in both the animal model and patients: sleep disturbances might be a cause, not just a consequence of schizophrenia. In fact, abnormal sleep patterns may trigger abnormal brain activity in a range of conditions.”

Cognitive deficits — reduced short term memory and attention span, are typically resistant to medication in patients. The findings from this study provide new angles for neurocognitive therapy in schizophrenia and related psychiatric diseases.

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Study: Schizophrenia and autism may be linked in families

Families with a history of schizophrenia or bipolar disorder are also more likely to have a child with autism, new research from Sweden and Israel suggests.

Researchers found that kids whose parents or siblings had been diagnosed with schizophrenia were almost three times more likely to have an autism spectrum disorder, including autism and Asperger syndrome.

The link was weaker for bipolar disorder, but still consistent, according to findings published this week in the Archives of General Psychiatry.

"Most people with a family history of one of these disorders actually get nothing - the vast majority in fact," said Dr. Patrick Sullivan, the study's lead author from the University of North Carolina at Chapel Hill.

Still, he told Reuters Health, "Maybe there is something that is more fundamental but common to both," such as certain changes in gene patterns that are passed from parents to children.

The number of autism diagnoses in the United States has been rising, and the Centers for Disease Control and Prevention now estimates one in 88 kids has an autism spectrum disorder. That's up from one in 150 a decade ago.

One of the questions in recent autism research has been how much genetics is involved in who gets the condition, versus the prenatal or early childhood environment.

Sullivan and his colleagues note that autism used to be considered the childhood version of schizophrenia, before researchers learned more about the two disorders. And some research has continued to suggest certain genetic changes are common in both conditions, as well as in bipolar disorder.

So for the new study, the researchers analyzed information from three separate databases, including two that tracked kids and families in Sweden and their medical diagnoses and a third that recorded data on all Israeli citizens entering the army draft, including sibling pairs.

All in all, Sullivan's team had data on more than 30,000 young people with autism.

The researchers found that in the Swedish studies, kids whose parent or sibling had been diagnosed with schizophrenia, according to family medical records, were 2.6 to 2.9 times more likely to have autism. The trend was the same for siblings of teens with schizophrenia in Israel.

When a parent had bipolar disorder, on the other hand, kids were 1.6 to 1.9 times more likely to have autism or another autism spectrum disorder.

"It's been questioned for many years, whether there's a relationship" between schizophrenia and autism, said Dr. Andrew Zimmerman, a neurologist from the Lurie Center for Autism at MassGeneral Hospital for Children in Lexington, Massachusetts.

"In fact, I think those of us that see a lot of patients with autism have seen this relationship in relatives for a long time," he added.

Sullivan said there are certain rare genetic mutations that seem to predispose people to both autism and schizophrenia.

And there could be other gene variations, he said, where differences in a person's environment in the womb or growing up could influence whether the same mutation ends up leading to schizophrenia, autism or nothing.

"Just because two things share a risk factor doesn't mean that they're the same thing," Sullivan added. "The needs of people with autism and schizophrenia, and the treatments that we know work for one or the other, don't overlap very well."

Zimmerman, who wasn't involved in the current research, told Reuters Health there are still many questions about how the conditions may be related.

The new study "is important because it makes us think," he said. "It doesn't tell us whether (autism and schizophrenia) are genetic or environmental - certainly both are still possible - but it makes us think there might be relationships between the two."

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Genes Associated With Autism Also Related to Schizophrenia

Scientists have identified 33 genes associated with autism and related disorders, and they say several of the genes also appear to be altered in people with schizophrenia.

Of the 33 genes, 22 were identified as associated with autism for the first time, according to the study, which currently appears online and is scheduled for publication in the April 27 print issue of the journal Cell.

"By sequencing the genomes of a group of children with neurodevelopmental abnormalities, including autism, who were also known to have abnormal chromosomes, we identified the precise points where the DNA strands are disrupted and segments exchanged within or between chromosomes," senior study author James Gusella, director of the Massachusetts General Hospital Center for Human Genetic Research, said in a hospital news release. "As a result, we were able to discover a series of genes that have a strong individual impact on these disorders."

"We also found that many of these genes play a role in diverse clinical situations -- from severe intellectual disability to adult-onset schizophrenia -- leading to the conclusion that these genes are very sensitive to even subtle perturbations," Gusella added.

The researchers screened the genomes of 38 people with autism or other neurodevelopmental disorders. A significant number of the genes linked with autism also appear to be associated with schizophrenia and other psychiatric disorders.

"The theory that schizophrenia is a neurodevelopmental disorder has long been hypothesized, but we are just now beginning to uncover specific portions of the genetic underpinnings that may support that theory," study author Michael Talkowski, also of Massachusetts General Hospital, said in the news release.

"We also found that different gene variations -- deletion, duplication or inactivation -- can result in very similar effects, while two similar changes at the same site might have very different neurodevelopmental manifestations," Talkowski said. "We suspected that the genetic causes of autism and other neurodevelopmental abnormalities are complex and likely to involve many genes, and our data support this."

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Study Compares Traits of Autism, Schizophrenia

A UT Dallas professor is studying the differences between the social impairments found in autism and schizophrenia to help develop better treatments for people with both disorders.

Autism spectrum disorder (ASD) and schizophrenia are distinct disorders with unique characteristics, but they share similarities in social dysfunction. For many years, this similarity resulted in confusion in diagnosis. Many young people with ASD were thought to have a childhood version of schizophrenia, said Dr. Noah Sasson, assistant professor in the UT Dallas School of Behavioral and Brain Sciences.

Sasson points out that clear differences exist between people diagnosed with schizophrenia and ASD. Symptoms of ASD can be seen from very early in life, while the onset of schizophrenia typically occurs in young adulthood. And individuals who have schizophrenia often experience hallucinations and delusional thoughts, which are far less common in individuals with ASD.

An overlapping problem for both clinical groups is a difficulty with social interaction. Both groups are known to be poor at recognizing social cues. They often have difficulty identifying emotion in other people, so their reactions may seem inappropriate. By not picking up on the subtle cues in interactions, adults with ASD or schizophrenia may alienate other people and have trouble making friends or getting along with classmates or co-workers.

Along with collaborators at Southern Methodist University, Sasson is conducting new research at the UT Dallas Callier Center for Communication Disorders that compares the basis for social interaction impairments between adults with ASD and adults with schizophrenia. He is attempting to understand the mechanisms that underlie their social limitations.

"Because the two disorders are different in so many ways, it is likely that the basis for their social impairments differs as well," he said. "Understanding these differences will be key for developing effective treatments. What works well for individuals with ASD might be very different than those with schizophrenia."

In previous research, Sasson and his colleagues used eye-tracking technology and found that neither adults with ASD nor adults with schizophrenia look at social information in the same way as those without either disorder. His colleagues also found that parts of the brain that process social information are underactive in those with ASD and schizophrenia. But the researchers have also found differences. Individuals with ASD do not spontaneously orient to emotional information, while individuals with schizophrenia do. While both groups show aspects of paranoia in social situations, Sasson and his colleagues are discovering that the root cause of the paranoia is different for each disorder.

"People with schizophrenia have a much higher likelihood than the general population to attribute ill will to others, and this is likely tied to their delusions," he said. "On the other hand, people with autism are more 'socially cynical.' They seem to be exhibiting fairly realistic responses to people as a result of the challenges they've faced in life because of their condition."

By differentiating between schizophrenia and autism, and by examining how patients react in social settings, Sasson said he hopes researchers can develop new ways to counteract the negative social experiences of patients. This could result in a profound improvement in their ability to navigate life successfully.

Read more: http://www.sciencedaily.com/releases/2012/02/120228114312

Schizophrenia Diagnosis Associated With Progressive Brain Changes Among Adolescents

Adolescents diagnosed with schizophrenia and other psychoses appear to show greater decreases in gray matter volume and increases in cerebrospinal fluid in the frontal lobe compared to healthy adolescents without a diagnosis of psychosis, according to a report in the January issue of Archives of General Psychiatry, one of the JAMA/Archives journals.

"Progressive loss of brain gray matter (GM) has been reported in childhood-onset schizophrenia; however, it is uncertain whether these changes are shared by pediatric patients with different psychoses," the authors write as background information in the study.

Celso Arango, M.D., Ph.D., of the Hospital General Universitario Gregorio Marañón, Madrid, Spain, and colleagues, examined the progression of brain changes in first-episode early-onset psychosis and the relationship to diagnosis and prognosis at two-year follow-up among patients at six child and adolescent psychiatric units in Spain. The authors performed magnetic resonance imaging (MRI) of the brain for 61 patients (25 diagnosed with schizophrenia, 16 with bipolar disorder and 20 with other psychoses) and 70 healthy control participants. MRI scans were conducted at study baseline and after two years of follow-up.

Compared with control patients, those diagnosed with schizophrenia showed greater gray matter volume loss in the frontal lobe during the two-year follow-up. Patients with schizophrenia also showed cerebrospinal fluid increase in the left frontal lobe. Additionally, changes for total brain gray matter and left parietal gray matter were significantly different in patients with schizophrenia compared with patients in the control group.

Among patients with schizophrenia, progressive brain volume changes in certain areas were related to markers of poorer prognosis, such as more weeks of hospitalization during follow-up and less improvement in negative symptoms. Greater left frontal gray matter volume loss was related to more weeks of hospitalization whereas severity of negative symptoms correlated with cerebrospinal fluid increase in patients with schizophrenia.

The authors did not find any significant changes in patients with bipolar disorder compared to control patients, and longitudinal brain changes in the control group were consistent with the expected pattern described for healthy adolescents.

"In conclusion, we found progression of gray matter volume loss after a two-year follow-up in patients who ended up with a diagnosis of schizophrenia but not bipolar disease compared with healthy controls," the authors write. "Some of these pathophysiologic processes seem to be markers of poorer prognosis. To develop therapeutic strategies to counteract these pathologic progressive brain changes, future studies should focus on their neurobiological underpinnings."

Read more: http://www.sciencedaily.com/releases/2012/01/120102180842

Brain Cell Malfunction in Schizophrenia Identified

Scientists at The Scripps Research Institute have discovered that DNA stays too tightly wound in certain brain cells of schizophrenic subjects. The findings suggest that drugs already in development for other diseases might eventually offer hope as a treatment for schizophrenia and related conditions in the elderly.

The research, now available online in the new Nature journal, Translational Psychiatry, shows the deficit is especially pronounced in younger people, meaning treatment might be most effective early on at minimizing or even reversing symptoms of schizophrenia, a potentially devastating mental disorder associated with hallucinations, delusions, and emotional difficulties, among other problems.

"We're excited by the findings," said Scripps Research Associate Professor Elizabeth Thomas, a neuroscientist who led the study, "and there's a tie to other drug development work, which could mean a faster track to clinical trials to exploit what we've found."

A Promising New Field

Over the past few years, researchers have increasingly recognized that cellular-level changes not tied to genetic defects play important roles in causing disease. There is a range of such so-called epigenetic effects that change the way DNA functions without changing a person's DNA code.

One critical area of epigenetic research is tied to histones. These are the structural proteins that DNA has to wrap around. "There's so much DNA in each cell of your body that it could never fit in your cells unless it was tightly and efficiently packed," said Thomas. Histone "tails" regularly undergo chemical modifications to either relax the DNA or repack it. When histones are acetylated, portions of DNA are exposed so that the genes can be used. The histone-DNA complexes, known as chromatin, are constantly relaxing and condensing to expose different genes, so there is no single right or wrong configuration. But the balance can shift in ways that can cause or exacerbate disease.

DNA is the guide that cellular machinery uses to construct the countless proteins essential to life. If portions of that guide remain closed when they shouldn't because histones are not acetylated properly, then genes can be effectively turned off when they shouldn't be with any number of detrimental effects. Numerous research groups have found that altered acetylation may be a key factor in other conditions, from neurodegenerative disorders such as Huntington's disease and Parkinson's disease to drug addiction.

A Good Idea

Thomas had been studying the roles of histone acetylation in Huntington's disease and began to wonder whether similar mechanisms of gene regulation might also be important in schizophrenia. In both diseases, past research in the Thomas lab had shown that certain genes in sufferers were much less active than in healthy people. "It occurred to me that we see the same gene alterations, so I thought, 'Hey, let's just try it,'" she said.

Working with lead author Bin Tang, a postdoctoral fellow in her lab, and Brian Dean, an Australian colleague at the University of Melbourne, Thomas obtained post-mortem brain samples from schizophrenic and healthy brains held at medical "Brain Banks" in the United States and Australia. The brains come from either patients who themselves agreed to donate some or all of their bodies for scientific research after death, or from patients whose families agreed to such donations.

A great deal of epigenetic research has focused on chemical alterations to DNA itself. Histone alterations have been much more difficult to study because such research requires that the histones and DNA remain chemically intact. Many researchers feared that these bonds were disrupted in the brain after death. However, Thomas's group was able to develop a technique for maintaining the histone-DNA interactions. "While many people thought this was lost, we were able to show that indeed these interactions are preserved in post-mortem brain, allowing us to carry out these studies," said Thomas.

Compared to healthy brains, the brain samples from subjects with schizophrenia showed lower levels of acetylation in certain histone portions that would block gene expression. Another critical finding was that in younger subjects with schizophrenia, the problem was much more pronounced.

Need for New Treatment Options

Just what causes the acetylation defects among schizophrenic subjects -- what keeps certain pages of the DNA guide closed -- isn't clear, but from a medical perspective it doesn't matter. If researchers can reliably show that acetylation is a cause of the problem, they can look for ways to open the closed guide pages and hopefully cure or improve the condition in patients.

Thomas sees great potential. Based on the more pronounced results in younger brains, she believes that treatment with histone deacetylase inhibitors might well prove helpful in reversing or preventing the progression of the condition, especially in younger patients. Current drugs for schizophrenia tend to treat only certain symptoms, such as hallucinations and delusions, and the drugs have major side effects including movement problems, weight gain, and diabetes. If deacetylase inhibitors effectively treat a root cause of the disease and prove sufficiently non-toxic, they might improve additional symptoms and provide a major expansion of treatment options.

Interestingly, some of the cognitive deficits that plague elderly people look quite similar biologically to schizophrenia, and the two conditions share at least some brain abnormalities. So deacetylase inhibitors might also work as a treatment for age-related problems, and might even prove an effective preventive measure for people at high risk of cognitive decline based on family history or other indicators.

Read more: http://www.sciencedaily.com/releases/2011/12/111228111731

Putting the Body Back Into the Mind of Schizophrenia

A study using a procedure called the rubber hand illusion has found striking new evidence that people experiencing schizophrenia have a weakened sense of body ownership and has produced the first case of a spontaneous, out-of-body experience in the laboratory.

These findings suggest that movement therapy, which trains people to be focused and centered on their own bodies, including some forms of yoga and dance, could be helpful for many of the2.2 million people in the United States who suffer from this mental disorder.

The study, which appears in the Oct. 31 issue of the scientific journalPublic Library of Science One, measured the strength of body ownership of 24 schizophrenia patients and 21 matched control subjects by testing their susceptibility to the "rubber hand illusion" or RHI. This tactile illusion, which was discovered in 1998, is induced by simultaneously stroking a visible rubber hand and the subject's hidden hand.

"After a while, patients with schizophrenia begin to 'feel' the rubber hand and disown their own hand. They also experience their real hand as closer to the rubber hand." said Sohee Park, the Gertrude Conaway Vanderbilt Chair of Psychology and Psychiatry, who conducted the study with doctoral candidate Katharine Thakkar and research analysts Heathman Nichols and Lindsey McIntosh.

"Healthy people get this illusion too, but weakly," Park said. "Some don't get it at all, and there is a wide range of individual differences in how people experience this illusion that is related to a personality trait called schizotypy, associated with psychosis-proneness."

Read more: http://www.sciencedaily.com/releases/2011/10/111031220259

Found in the Developing Brain: Mental Health Risk Genes and Gender Differences

Most genes associated with psychiatric illnesses are expressed before birth in the developing human brain, a massive study headed by Yale University researchers discovered. In addition, hundreds of genetic differences were found between males and females as their brains take shape in the womb, the study in the Oct. 27 issue of the journal Natureshows.

The creation of a hundred billion brain cells and the incalculable number of connections between them is such a complex task that 86 percent of 17,000 human genes studied are recruited in the effort. The study tracked not only what genes are involved in development, but where and when they are expressed, or activated.

"We knew many of the genes involved in the development of the brain, but now we know where and when they are functioning in the human brain," said Nenad Sestan, associate professor of neurobiology, researcher for the Kavli Institute for Neuroscience and senior author of the study. "The complexity of the system shows why the human brain may be so susceptible to psychiatric disorders."

The study identified genes expressed in the human brain, and when and where in the brain they were expressed in 1340 tissue samples taken from 57 subjects aged from 40 days after conception to 82 years. The analysis of 1.9 billion data points gives an unprecedented map of genetic activity in the brain at different stages of development. In dramatic fashion, the findings show just how much of the human brain is shaped prior to birth.

For instance, the team analyzed genes and variants previously linked with autism and schizophrenia, the symptoms of which are evident in the first few years of life or during early adulthood, respectively. The new analysis shows molecular evidence of expression of these suspect genes prior to birth.

"We found a distinct pattern of gene expression and variations prenatally in areas of the brain involving higher cognitive function," Sestan said. "It is clear that these disease-associated genes are developmentally regulated."

The team also looked for differences in brains of males and females. They expected to find clear differences in Y chromosome genes that are possessed only by males. However, they also demonstrated that men and women showed distinct differences in many genes that are shared by both sexes -- both in whether the gene was expressed and the level of the gene's activity. Most of the differences were noted prenatally.

Read more: http://www.sciencedaily.com/releases/2011/10/111026143723

Bidirectional Relationship Between Schizophrenia and Epilepsy, Study Finds

Researchers from Taiwan have confirmed a bidirectional relation between schizophrenia and epilepsy. The study published in Epilepsia, a journal of the International League Against Epilepsy (ILAE), reports that patients with epilepsy were nearly 8 times more likely to develop schizophrenia and those with schizophrenia were close to 6 times more likely to develop epilepsy.

Prior clinical studies have shown a prevalence of psychosis among epilepsy patients and studies of psychiatric illness have found a strong relationship between schizophrenia and epilepsy, suggesting a shared susceptibility between the diseases that may be a result of genetic, environmental or neurobiological causes. While a number of studies have established a bidirectional relationship between depression, mood disorder and epilepsy, the current study is the first to investigate this type of relation between schizophrenia and epilepsy.

"Our research results show a strong bidirectional relation between schizophrenia and epilepsy," said lead author I-Ching Chou, M.D., with China Medical University Hospital and Associate Professor with China Medical University in Taichung, Taiwan. "This relationship may be due to common pathogenesis in these diseases such as genetic susceptibility and environmental factors, but further investigation of the pathological mechanisms are needed."

Read more: http://www.sciencedaily.com/releases/2011/09/110919074244.htm