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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Source: University of Michigan

Medication abstract photo by shutterstock.

Although still considered an experimental therapy , direct brain stimulation (DBS) has been in practice for several years and has been tried out as a treatment for depression, obsessive-compulsive disorder and anxiety.

In the new study, transcranial stimulation was able to decrease auditory hallucinations in schizophrenia, and the effects lasted for up to 12 weeks. In addition, the treatment had a marked influence on some negative symptoms.

The researchers believe that one day patients may be able to use this treatment at home.

In this small study, the brains of patients with schizophrenia were stimulated in specific areas for about 20 minutes, twice a day for five consecutive days.  After five days, there was a significant lessening of auditory verbal hallucinations. The benefits of the treatment were still present at three months.

Unfortunately, no patient had complete recovery. The treatment had no effect on other symptoms of schizophrenia such as grandiosity, excitement or disorganization.

The researchers believe that perhaps those with schizophrenia who have symptoms that do not respond to medications may be candidates for transcranial direct stimulation.

Source: American Journal of Psychiatry

Past research has implied that the birth month of a child affects its mental health in later stages of life.

“For example, maternal infections — a mother may be more likely to have the flu over the winter. Does this increase risk?” said researcher Sreeram Ramagopalan, an epidemiologist at Queen Mary University of London.

“Or diet. Depending on the season, certain foods – fruits, vegetables — are more or less available, and this may impact on the developing baby. Or another key candidate is vitamin D, which is related to sunshine exposure. During the winter, with a lack of sunshine, moms tend to be very deficient in vitamin D.”

The study included almost 58,000 individuals with schizophrenia, bipolar disorder or recurrent depression as well as over 29 million people from England’s general population.

Mental disorders appeared season-based. Specifically, schizophrenia and bipolar disorder had statistically higher peaks in January and significant lows in July, August and September. Depression had an almost significant May peak and a significant November deficit.

“This result is further confirmation of seasonal variations in births of those later diagnosed with mental diseases,” said William Grant at the Sunlight, Nutrition and Health Research Center at San Francisco, who did not take part in this research.

“This implicates conditions during pregnancy. The two most likely factors are vitamin D status and temperature,” said Grant.

Source: Queen Mary University of London

“In medical research, we need to dissect events in biology so we can understand the precise mechanisms that give rise to neurodevelopmental traits,” said senior author Nicholas Katsanis, Ph.D., a professor of developmental biology, pediatrics and cell biology.

Katsanis said he knew that a region on chromosome 16 was one of the largest genetic contributors to autism and schizophrenia, but a conversation at a European medical meeting pointed him to information that changes within that same region also were related to changes in a newborn’s head size.

The problem was difficult to address because the region had large deletions and duplications in DNA, which are the most common mutations in humans, he said, adding, “Interpretation is harrowingly hard.”

That’s because a duplication of DNA or missing DNA usually involves several genes.

“It is very difficult to go from ‘here is a region with many genes, sometimes over 50′ to ‘these are the genes that are driving this pathology,’” Katsanis said.

Then he had a light bulb moment. The area of the genome the researchers were exploring gave rise to opposite defects in terms of brain cell growth.

“We realized that overexpressing a gene in question might give one phenotype — a smaller head — while shutting down the same gene might yield the other, a larger head,” he said.

The researchers transplanted a common duplication area of human chromosome 16 known to contain 29 genes into zebrafish embryos and then systematically turned up the activity to find which might cause a small head (microcephaly). They then suppressed the same gene set to see whether any of them caused the reciprocal defect: larger heads (macrocephaly).

The researchers knew that deletion of the region that contained these 29 genes occurred in 1.7 percent of children with autism, he said.

It took the team a few months to dissect such a “copy number variant” — an alteration of the genome that results in an abnormal number of one or more sections of chromosomal DNA, he reported.

“Now we can go from a genetic finding that is dosage-sensitive and start asking reasonable questions about this gene as it pertains to neurocognitive traits, which is a big leap,” Katsanis said, explaining neurocognitive refers to the ability to think, concentrate, reason, remember, process information, learn, understand and speak.

Katsanis concedes there are “major limitations in studying autistic or schizophrenic behavior in zebrafish, but we can measure head size, jaw size, or facial abnormalities.”

The gene in question, KCTD13, is responsible for driving head size in zebrafish by regulating the creation and destruction of new brain cells. This discovery let the team focus on the analogous gene in humans.

“This gene contributes to autism cases, and probably is associated with schizophrenia and also childhood obesity,” Katsanis said.

Once the gene has been uncovered, researchers can examine the protein it produces. “Once you have the protein, you can start asking valuable functional questions and learning what the gene does in the animal or human,” Katsanis said.

Copy number variants, such as the ones this team found on chromosome 16, are now thought to be one of the most common sources of genetic mutations. Hundreds, if not thousands, of such chromosomal deletions and duplications have been found in patients with a broad range of clinical problems, particularly neurodevelopmental disorders, the researcher said.

“Now we may have an efficient tool for dissecting them, which gives us the ability to improve both diagnosis and understanding of disease mechanisms,” Katsanis said.

The study was published online in the journal Nature.

Source: Duke University Medical Center

Led by scientists at Indiana University, the research team identified a group of genes most associated with schizophrenia. Using a functional genomics approach that incorporates a number of experimental techniques, the scientists were able to apply the gene test to data from other schizophrenia studies and successfully identify which patients had been diagnosed with schizophrenia, according to the study, which was published online by the journal Molecular Psychiatry.

The prototype test was able to predict whether a person was at a higher or lower risk of schizophrenia in about two-thirds of cases, researchers report.

The researchers also propose that schizophrenia is a disease emerging from a mix of genetic variations affecting brain development and neuronal connections, along with environmental factors, particularly stress.

“At its core, schizophrenia is a disease of decreased cellular connectivity in the brain, precipitated by environmental stress during brain development, among those with genetic vulnerability,” said principal investigator Alexander B. Niculescu III, M.D., Ph.D., associate professor of psychiatry and medical neuroscience at the IU School of Medicine and director of the Laboratory of Neurophenomics at the IU Institute of Psychiatric Research. “For the first time we have a comprehensive list of the genes that have the best evidence for involvement in schizophrenia.”

When the test estimating the risk for schizophrenia is refined, it could provide guidance to caregivers and health care professionals about young people in families with a history of the disease, prompting early intervention and treatment, Niculescu said.

He emphasized that a score indicating a higher risk of schizophrenia “doesn’t determine your destiny. It just means that your neuronal connectivity is different, which could make you more creative, or more prone to illness. It’s all on a continuum — these genetic variants are present throughout the population. If you have too many of them, in the wrong combination, in an environment where you are exposed to stress, alcohol and drugs, and so on, that can lead to the development of the clinical illness.”

To identify and prioritize the genes involved in schizophrenia, the researchers combined data from several types of studies, including genome-wide association studies, gene expression data derived from human tissue samples, genetic linkage studies, genetic evidence from animal models, and other work. This approach, called convergent functional genomics, has been pioneered by Niculescu and colleagues, and relies on multiple independent lines of evidence to implicate genes in clinical disorders.

The researchers noted that the results were stronger when analyses were performed using gene-level data, rather than analyses based on individual mutations — called single nucleotide polymorphisms, or SNPs — in those genes. Multiple SNPs can spark a gene’s role in the development of schizophrenia, so evidence for the genes, and the biological mechanisms in which they play a role, was much stronger from study to study than evidence for individual SNPs.

“By better understanding the genetic and biological basis of the illness, we can develop better tests for it, as well as better treatments,” he said.

Source: Indiana University School of Medicine

“Many neurological and psychiatric conditions are likely to involve problems with signaling in brain networks,” says co-author Dr. Maurizio Corbetta, a professor of neurology at Washington University in St. Louis. “Examining the temporal structure of brain activity from this perspective may be especially helpful in understanding psychiatric conditions like depression and schizophrenia, where structural markers are scarce.”

Scientists usually study brain networks using magnetic resonance imaging, which tracks blood flow, assuming that an increase in blood flow to part of the brain indicates increased activity in the cells of that region.

But MRI has its limitations, according to Corbetta. “It only allows us to track brain cell activity indirectly, and it is unable to track activity that occurs at frequencies greater than 0.1 hertz, or once every 10 seconds,” he said. “We know that some signals in the brain can cycle as high as 500 hertz, or 500 times per second.”

For the new study, conducted at the University Medical Center at Hamburg-Eppendorf, the researchers used magnetoencephalography (MEG) to analyze brain activity in 43 healthy volunteers. MEG detects very small changes in magnetic fields in the brain that are caused by many cells being active at once. It can detect these signals at rates up to 100 hertz.

“We found that different brain networks ticked at different frequencies, like clocks ticking at different speeds,” said lead author Joerg Hipp, Ph.D., of the University Medical Center at Hamburg-Eppendorf and the University of Tübingen, both in Germany.

Networks that included the hippocampus, a brain area critical for memory formation, tended to be active at frequencies around 5 hertz. Networks constituting areas involved in the senses and movement were active between 32 hertz and 45 hertz. Other brain networks were active at frequencies between 8 and 32 hertz.

“There have been a number of fMRI studies of depression and schizophrenia showing ‘spatial’ changes in the organization of brain networks,” Corbettta says. “MEG studies provide a window into a much richer ‘temporal’ structure. In the future, this might offer new diagnostic tests or ways to monitor the efficacy of interventions in these debilitating mental conditions.”

The research was published May 6 in Nature Neuroscience.

Source: Washington University School of Medicine 

The findings add to the growing body of evidence that several adult disorders may take root before and shortly after birth.

“Lifestyle and genes are not the only factors that shape disease risk, and factors and exposures before, during and after birth can help pre-program much of our adult health,” said investigator Robert Yolken, M.D., a neuro-virologist at Johns Hopkins Children’s Center.

“Our study is an illustrative example suggesting that a dietary sensitivity before birth could be a catalyst in the development of schizophrenia or a similar condition 25 years later.”

Infections and other inflammatory problems in the pregnant mother have long been associated with a greater risk for schizophrenia in the child but, the Swedish and U.S. researchers say, this is the first study that shows how a mother’s food sensitivity may potentially lead to the development of the disorder.

The findings demonstrate a strong link but do not mean that gluten sensitivity will invariably cause schizophrenia, say the researchers. The study, however, does provide an intriguing look into what drives up risk and could lead to the development of new prevention strategies.

“Our research not only underscores the importance of maternal nutrition during pregnancy and its lifelong effects on the offspring, but also suggests one potential cheap and easy way to reduce risk if we were to find further proof that gluten sensitivity exacerbates or drives up schizophrenia risk,” said study lead investigator Håkan Karlsson, M.D., Ph.D., a neuroscientist at Karolinska Institutet and former neuro-virology fellow at Johns Hopkins.

The study involved the examination of 764 birth records and neonatal blood samples of Swedes born between 1975 and 1985. About 211 of them eventually developed non-affective psychoses, such as schizophrenia and delusional disorders.

The researchers measured levels of IgG antibodies to milk and wheat in the stored neonatal blood samples. IgG antibodies are markers of immune system reactions triggered by the presence of certain proteins. Since the mother’s antibodies travel through the placenta during pregnancy to give immunity to the baby, a newborn’s higher IgG levels reveal a protein sensitivity in the mother.

Babies whose mothers had abnormally high levels of antibodies to the wheat protein gluten had almost double the risk of developing schizophrenia later in life, compared to children with normal levels of gluten antibodies.

The link persisted even after investigators accounted for other factors known to increase schizophrenia risk, including maternal age, gestational age, method of delivery and the mother’s immigration status. The risk for psychiatric disorders did not increase among those with elevated levels of antibodies to milk protein.

The researchers say the notion that a person’s psychiatric disorder may be linked to his mother’s food sensitivity began with an observation made by U.S. Army researcher F. Curtis Dohan, M.D. just after World War II. Dohan noticed that food scarcity in post-war Europe and wheat-poor diets led to notably fewer hospital admissions for schizophrenia. The link had been purely observational, but it has piqued the curiosity of scientists ever since.

Past research has also shown that people with schizophrenia have abnormally high rates of celiac disease, a rare autoimmune disorder characterized by gluten sensitivity. Although it is a hallmark of the condition, gluten sensitivity by itself is not enough to diagnose celiac disease.

Scientists note that other research has found that some people with schizophrenia have gluten sensitivity without having any other signs of celiac disease.

Yolken and Karlsson say the team is conducting followup studies to further investigate how gluten or gluten sensitivity increases schizophrenia risk and whether it only affects those already genetically predisposed.

The study is published in The American Journal of Psychiatry.

Source:  Karolinska Institutet

Researchers at McMaster University of Canada found that one-year-old babies who participate in interactive music classes with their parents smile more, communicate better, and show earlier and more sophisticated brain responses to music.

“Our results suggest that the infant brain might be particularly plastic with regard to musical exposure,” said Laurel Trainor, Ph.D., director of the McMaster Institute for Music and the Mind.

Trainor and David Gerry, a music educator and graduate student, received a grant from the Grammy Foundation in 2008 to study the effects of musical training in infancy. In the recent study, babies and their parents spent six months participating in one of two types of weekly music classes.

One class involved interactive music-making and learning lullabies, nursery rhymes and songs with actions. Parents and infants worked together to learn to play percussion instruments and sing specific songs.

In the other class, infants and parents played at various toy stations while recordings from the Baby Einstein series played in the background.

“Babies who participated in the interactive music classes with their parents showed earlier sensitivity to the pitch structure in music,” said Trainor.

“Specifically, they preferred to listen to a version of a piano piece that stayed in key, versus a version that included out-of-key notes. Infants who participated in the passive listening classes did not show the same preferences. Even their brains responded to music differently. Infants from the interactive music classes showed larger and/or earlier brain responses to musical tones.”

The non-musical differences between the two groups of babies were even more surprising, according to the researchers.

Babies from the interactive classes showed better early communication skills, like pointing at objects that are out of reach or waving goodbye. These babies also smiled more, were easier to soothe, and showed less distress when things were unfamiliar or didn’t go their way.

The findings were published recently in the scientific journals Developmental Science and Annals of the New York Academy of Sciences.

Source: McMaster University 

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

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

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

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

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

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

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

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

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

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

Source: Karolinska Institutet

Help me sign photo by shutterstock.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Source:  The Lancet

In the study, Finnish researchers determined individuals with epilepsy are more likely to have schizophrenia, and a family history of epilepsy is a risk factor for psychosis. However, investigators still do not know if the converse is true, i.e., whether a family history of psychosis is a risk factor for epilepsy.

Scandinavian countries are often optimal for genetic research because they maintain detailed population-based national registries that allow examination of medical and mental care extending for decades.

Past studies have used a variety of investigative techniques to determine that patients with schizophrenia and patients with epilepsy show some similar structural brain and genetic abnormalities. The commonalities suggest the conditions may share a common origin.

To investigate this possibility, researchers conducted a population-based study of parents and their children born in Helsinki, Finland. Using data available in two Finnish national registers, the study included 9,653 families and 23,404 offspring.

Researchers discovered that within this cohort, individuals with epilepsy had a 5.5-fold increase in the risk of having a psychotic disorder, a 6.3-fold increase in the risk of having bipolar disorder, and an 8.5-fold increase in the risk of having schizophrenia.

They also found that epilepsy and psychosis occurred within family clusters. Individuals with a parental history of epilepsy had a two-fold increase in the risk of developing psychosis, compared to individuals without a parental history of epilepsy.

Individuals with a parental history of psychosis had a 2.7-fold increase in the risk of having a diagnosis of epilepsy, compared to individuals without a parental history of psychosis.

Earlier theories that attempted to explain the relationship between epilepsy and psychosis have focused on the idea that epilepsy has a toxic effect on the brain. But researchers now believe that the findings of prior genetic and neurodevelopmental evidence suggest a much more complex association, which likely includes a shared genetic vulnerability.

“Our evidence that epilepsy and psychotic illness may cluster within some families indicates that these disorders may be more closely linked than previously thought. We hope that this epidemiological evidence may contribute to the ongoing efforts to disentangle the complex pathways that lead to these serious illnesses,” said Mary Clarke, Ph.D., first author of the study.

Dr. John Krystal, Editor of Biological Psychiatry, commented: “We have long known that particular types of epilepsy were associated with psychosis. However, the finding that a parental history of psychosis is associated with an increased risk of epilepsy in the offspring strengthens the mechanistic link between the two conditions.”

Source: Elsevier

In addition to shedding new light on how the brain works, the research, published May 2 in the Journal of Neuroscience, could have important implications for the treatment of attention-deficit disorder, depression, schizophrenia, and other forms of mental illness characterized by decreased motivation, according to the researchers from Vanderbilt University.

Using the brain mapping technique called positron emission tomography (PET scan), the researchers found that people who are willing to work hard for rewards had a higher release of dopamine in areas of the brain known to play a role in reward and motivation, the striatum and ventromedial prefrontal cortex.

On the other hand, those who were less willing to work hard for a reward had high dopamine levels in another area of the brain that plays a role in emotion and risk perception, the anterior insula.

The role of dopamine in the anterior insula came as a surprise, the researchers noted. It suggests that more dopamine in this area of the brain is associated with a reduced desire to work, even when it means earning less money.

The fact that dopamine can have opposing effects in different parts of the brain complicates the use of psychotropic medications that affect dopamine levels for the treatment of attention-deficit disorder, depression and schizophrenia because it questions the assumption that these drugs have the same effect throughout the brain, the researchers noted.

The study was conducted with 25 healthy volunteers ranging in age from 18 to 29. To determine their willingness to work for a monetary reward, the participants were asked to perform a button-pushing task. They were asked to select an easy or a hard task. Easy tasks earned $1, while the rewards for hard tasks ranged up to $4. The tasks lasted for about 30 seconds and participants were asked to perform them repeatedly for about 20 minutes.

While looking at just 20 minutes of behavior doesn’t conclusively show an individual’s potential for long-term achievement, it “does measure a trait variable such as an individual’s willingness to expend effort to obtain long-term goals,” said psychologist Dr. David Zald.

The research is part of a larger project designed to search for objective measures for depression and other psychological disorders where motivation is reduced, he said.

“Right now our diagnosis for these disorders is often fuzzy and based on subjective self-report of symptoms,” said Zald. “Imagine how valuable it would be if we had an objective test that could tell whether a patient was suffering from a deficit or abnormality in an underlying neural system. With objective measures we could treat the underlying conditions instead of the symptoms.”

Additional research is under way to examine whether individual differences in dopamine levels help explain the altered motivation seen in depression and addiction, he added.

Source: Vanderbilt University

Of the 33 genes, 22 were linked to autism for the first time.

“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,” said senior study author James Gusella, director of the Massachusetts General Hospital Center for Human Genetic Research. 

“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 analyzed the genomes of 38 people with autism or other neurodevelopmental disorders and found that a significant number of the genes linked to autism also seem 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,” said study author Michael Talkowski of Massachusetts General Hospital.

“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.”

Source:  Massachusetts General Hospital Center for Human Genetic Research

The research analyzed the findings from more than 30 years of studies looking at the association between childhood trauma and the development of psychosis.

The researchers looked at more than 27,000 research papers to extract data from three types of studies: those addressing the progress of children known to have experienced adversity; studies of randomly selected members of the population; and research on psychotic patients who were asked about their early childhood.

Across all three types of studies, the results led to similar conclusions, according to the researchers. Children who had experienced any type of trauma before the age of 16 were approximately three times more likely to become psychotic in adulthood compared to those selected randomly from the population.

Researchers also found a relationship between the level of trauma and the likelihood of developing illness in later life. Those who were severely traumatized as children were at a greater risk, in some cases up to 50 times increased risk, than those who experienced trauma to a lesser extent.

The Liverpool researchers also conducted a new study that looked at the relationship between specific symptoms and the type of trauma experienced in childhood. They found that different traumas led to different symptoms. For example, childhood sexual abuse was associated with hallucinations, while being brought up in a children’s home was associated with paranoia.

The findings suggest that a patient’s life experiences need to be considered, along with neurological and genetic factors, said researcher and psychologist Dr. Richard Bentall.

“We need to know, for example, how childhood trauma affects the developing brain, as well as whether there are genetic factors that increase vulnerability or resilience to traumatic events,” he said.

“These questions will need new research strategies, such as studies comparing traumatized children who grow up to be psychologically healthy and those who go on to develop mental illness. Looking at the brain or genes only is unlikely to tell us what we need to know in order to treat a patient effectively.”

The researchers will now look at the psychological and brain processes involved in the links between different types of trauma and particular psychotic symptoms.

Future research will also aim to discover why symptoms of psychosis may only be expressed in later life, when the initial trigger many have been many years before in childhood.

The research is published in Schizophrenia Bulletin.

Source: University of Liverpool

The UCLA-launched partnership is the largest study of human genes addressing mental health. In addition to defining genes that influence mental health, researchers discovered new genes that may explain individual differences in brain size and intelligence.

The study is published in the advance online edition of Nature Genetics.

“We searched for two things in this study,” said senior author Paul Thompson, Ph.D., professor of neurology at UCLA.

“We hunted for genes that increase your risk for a single disease that your children can inherit. We also looked for factors that cause tissue atrophy and reduce brain size, which is a biological marker for hereditary disorders like schizophrenia, bipolar disorder, depression, Alzheimer’s disease and dementia.”

Three years ago, Thompson’s lab partnered with geneticists Drs. Nick Martin and Margaret Wright at the Queensland Institute for Medical Research in Brisbane, Australia; and with geneticist Dr. Barbara Franke of Radboud University Nijmegen Medical Centre in the Netherlands.

The collaboration resulted in Project ENIGMA (Enhancing Neuro Imaging Genetics through Meta-Analysis), an initiative to recruit brain-imaging labs around the world to pool their brain scans and genomic data.

“Our individual centers couldn’t review enough brain scans to obtain definitive results,” said Thompson, who is also a professor of psychiatry at the Semel Institute for Neuroscience and Human Behavior at UCLA.

“By sharing our data with Project ENIGMA, we created a sample large enough to reveal clear patterns in genetic variation and show how these changes physically alter the brain.”

In the past, neuroscientists screened the genomes of people suffering from a specific brain disease and combed their DNA to uncover a common variant.

In this study, Project ENIGMA researchers measured the size of the brain and its memory centers in thousands of MRI images from 21,151 healthy people while simultaneously screening their DNA.

“Earlier studies have uncovered risk genes for common diseases, yet it’s not always understood how these genes affect the brain,” explained Thompson. “This led our team to screen brain scans worldwide for genes that directly harm or protect the brain.”

In the study, Project ENIGMA researchers explored whether any genetic variations correlated to brain size. Scientists focused on gene variants that deplete brain tissue beyond normal in a healthy person.

The large scope of the project allowed the team to unearth new genetic variants in people who have bigger brains as well as differences in regions critical to learning and memory.

When the scientists zeroed in on the DNA of people whose images showed smaller brains, they found a consistent relationship between subtle shifts in the genetic code and diminished memory centers.

Furthermore, the same genes affected the brain in the same ways in people across diverse populations from Australia, North America and Europe, suggesting new molecular targets for drug development.

“Millions of people carry variations in their DNA that help boost or lower their brains’ susceptibility to a vast range of diseases,” said Thompson.

“Once we identify the gene, we can target it with a drug to reduce the risk of disease. People also can take preventive steps through exercise, diet and mental stimulation to erase the effects of a bad gene.”

In an intriguing twist, Project ENIGMA investigators also discovered genes that explain individual differences in intelligence. They found that a variant in a gene called HMGA2 affected brain size as well as a person’s intelligence.

DNA is comprised of four bases: A, C, T and G. People whose HMGA2 gene held a letter “C” instead of “T” on that location of the gene possessed larger brains and scored more highly on standardized IQ tests.

“This is a really exciting discovery: that a single letter change leads to a bigger brain,” said Thompson. “We found fairly unequivocal proof supporting a genetic link to brain function and intelligence. For the first time, we have watertight evidence of how these genes affect the brain. This supplies us with new leads on how to mediate their impact.”

Researchers will next search for genes that affect how the brain is wired – an issue central to development of Alzheimer’s, autism and schizophrenia.

Source: UCLA