Posts tagged mental illness
Articles and news from the latest research reports.
Evidence Mounts for Role of Mutated Genes in Development of Schizophrenia
Johns Hopkins researchers have identified a rare gene mutation in a single family with a high rate of schizophrenia, adding to evidence that abnormal genes play a role in the development of the disease.
The researchers, in a report published in the journal Molecular Psychiatry, say that family members with the mutation in the gene Neuronal PAS domain protein 3 (NPAS3) appear at high risk of developing schizophrenia or another debilitating mental illnesses.
Normally functioning NPAS3 regulates the development of healthy neurons, especially in a region of the brain known as the hippocampus, which appears to be affected in schizophrenia. The Johns Hopkins researchers say they have evidence that the mutation found in the family may lead to abnormal activity of NPAS3, which has implications for brain development and function.
"Understanding the molecular and biological pathways of schizophrenia is a powerful way to advance the development of treatments that have fewer side effects and work better than the treatments now available," says study leader Frederick C. Nucifora Jr., Ph.D., D.O., M.H.S., an assistant professor of psychiatry and behavioral sciences at the Johns Hopkins University School of Medicine. "We could definitely use better medicines."
Frontiers publishes systematic review on the effects of yoga on major psychiatric disorders
Yoga has positive effects on mild depression and sleep complaints, even in the absence of drug treatments, and improves symptoms associated with schizophrenia and ADHD in patients on medication, according to a systematic review of the exercise on major clinical psychiatric disorders.
Published in the open-access journal, Frontiers in Psychiatry, on January 25th, 2013, the review of more than one hundred studies focusing on 16 high-quality controlled studies looked at the effects of yoga on depression, schizophrenia, ADHD, sleep complaints, eating disorders and cognition problems.
(Image: Corbis)
Mouse Research Links Adolescent Stress and Severe Adult Mental Illness
Working with mice, Johns Hopkins researchers have established a link between elevated levels of a stress hormone in adolescence - a critical time for brain development - and genetic changes that, in young adulthood, cause severe mental illness in those predisposed to it.
The findings, reported in the journal Science, could have wide-reaching implications in both the prevention and treatment of schizophrenia, severe depression and other mental illnesses.
"We have discovered a mechanism for how environmental factors, such as stress hormones, can affect the brain’s physiology and bring about mental illness," says study leader Akira Sawa, M.D., Ph.D., a professor of psychiatry and behavioral sciences at the Johns Hopkins University School of Medicine. "We’ve shown in mice that stress in adolescence can affect the expression of a gene that codes for a key neurotransmitter related to mental function and psychiatric illness. While many genes are believed to be involved in the development of mental illness, my gut feeling is environmental factors are critically important to the process."
Sawa, director of the Johns Hopkins Schizophrenia Center, and his team set out to simulate social isolation associated with the difficult years of adolescents in human teens. They found that isolating healthy mice from other mice for three weeks during the equivalent of rodent adolescence had no effect on their behavior. But, when mice known to have a genetic predisposition to characteristics of mental illness were similarly isolated, they exhibited behaviors associated with mental illness, such as hyperactivity. They also failed to swim when put in a pool, an indirect correlate of human depression. When the isolated mice with genetic risk factors for mental illness were returned to group housing with other mice, they continued to exhibit these abnormal behaviors, a finding that suggests the effects of isolation lasted into the equivalent of adulthood.
"Genetic risk factors in these experiments were necessary, but not sufficient, to cause behaviors associated with mental illness in mice," Sawa says. "Only the addition of the external stressor - in this case, excess cortisol related to social isolation - was enough to bring about dramatic behavior changes."
The investigators not only found that the “mentally ill” mice had elevated levels of cortisol, known as the stress hormone because it’s secreted in higher levels during the body’s fight-or-flight response. They also found that these mice had significantly lower levels of the neurotransmitter dopamine in a specific region of the brain involved in higher brain function, such as emotional control and cognition. Changes in dopamine in the brains of patients with schizophrenia, depression and mood disorders have been suggested in clinical studies, but the mechanism for the clinical impact remains elusive.
Brain & Behavior Research Foundation Announces 10 Major Research Achievements of 2012
In 2012, the Brain & Behavior Research Foundation funded more than 200 new promising ideas through its NARSAD Grants to identify the causes, improve treatments and develop prevention strategies for mental illness. Many research projects also came to fruition in 2012, and the Foundation highlights ten significant findings.
'Smart' genes put us at risk of mental illness
Humans may be endowed with the ability to perform complex forms of learning, attention and function but the evolutionary process that led to this has put us at risk of mental illness.
Data from new research, published today in the journal Nature Neuroscience, was analysed by Dr Richard Emes, a bioinformatics expert from the School of Veterinary Medicine and Science at The University of Nottingham. The results showed that disease-causing mutations occur in the genes that evolved to make us smarter than our fellow animals.
Dr Emes, Director of The University of Nottingham’s Advanced Data Analysis Centre, conducted an analysis of the evolutionary history of the Discs Large homolog (Dlg) family of genes which make some of the essential building blocks of the synapse — the connection between nerve cells in the brain. He said: “This study highlights the importance of the synapse proteome — the proteins involved in the brains signalling processes — in the understanding of cognition and the power of comparative studies to investigate human disease.”
The study involved scientists from The University of Edinburgh, The Wellcome Trust Sanger Institute, the University of Aberdeen, The University of Nottingham and the University of Cambridge.
This cross-disciplinary team of experts carried out what they believe to be the first genetic dissection of the vertebrate’s ability to perform complex forms of learning, attention and function. They focussed on Dlg — a family of genes that humans shared with the ancestor of all backboned animals some 550 million years ago. Gene families like the Dlgs arose by duplication of DNA, changed by mutation over millions of years and now contribute to the complex cognitive processes we have today. However, this redundancy and subsequent accumulation of changes in the DNA may have led to increased susceptibility to some diseases.
Components of the human cognitive repertoire are routinely assessed by using computerised touch-screen methods. By using the same technique with mice researchers were able to probe the cognitive mechanisms conserved since humans and mice shared a common ancestor — around 100 million years ago. By comparing the effect of DNA changes on behavioural test outcomes this research showed a common cause of mutation and effect of learning changes in both mice and humans.
Dr Emes said: “This research shows the importance of discerning information from data and how the power of computational research combined with behavioural and cognitive studies can provide such novel insight into the basis of clinical disorders. This research provides continued support that discovery occurs at the boundary of disciplines by the integration of data.”
(Source: nottingham.ac.uk)
Origin of intelligence and mental illness linked to ancient genetic accident
Scientists have discovered for the first time how humans – and other mammals – have evolved to have intelligence. Researchers have identified the moment in history when the genes that enabled us to think and reason evolved.
This point 500 million years ago provided our ability to learn complex skills, analyse situations and have flexibility in the way in which we think. Professor Seth Grant, of the University of Edinburgh, who led the research, said: “One of the greatest scientific problems is to explain how intelligence and complex behaviours arose during evolution.”
The research, which is detailed in two papers in Nature Neuroscience, also shows a direct link between the evolution of behaviour and the origins of brain diseases. Scientists believe that the same genes that improved our mental capacity are also responsible for a number of brain disorders.
"This ground breaking work has implications for how we understand the emergence of psychiatric disorders and will offer new avenues for the development of new treatments," said John Williams, Head of Neuroscience and Mental Health at the Wellcome Trust, one of the study funders.
The study shows that intelligence in humans developed as the result of an increase in the number of brain genes in our evolutionary ancestors. The researchers suggest that a simple invertebrate animal living in the sea 500 million years ago experienced a ‘genetic accident’, which resulted in extra copies of these genes being made.
This animal’s descendants benefited from these extra genes, leading to behaviourally sophisticated vertebrates – including humans. The research team studied the mental abilities of mice and humans, using comparative tasks that involved identifying objects on touch-screen computers.
Researchers then combined results of these behavioural tests with information from the genetic codes of various species to work out when different behaviours evolved. They found that higher mental functions in humans and mice were controlled by the same genes.
Scientists identify depression and anxiety biomarker in youths
Scientists have discovered a cognitive biomarker – a biological indicator of a disease – for young adolescents who are at high risk of developing depression and anxiety. Their findings were published in the journal PLOS ONE.
The test for the unique cognitive biomarker, which can be done on a computer, could be used as an inexpensive tool to screen adolescents for common emotional mental illnesses. As the cognitive biomarker may appear prior to the symptoms of depression and anxiety, early intervention (which has proven to be one of the most effective ways of combatting mental illness) could then be initiated.
For the study, 15-18 year old participants underwent genetic testing and environmental assessment, an exercise which would currently be too expensive and take too long to use as a widespread method of screening. The adolescents were then given a computer test to gauge how they process emotional information. The test had the participants evaluate whether words were positive, negative or neutral (examples included ‘joyful’ for positive, ‘failure’ for negative, and ‘range’ for neutral).
Those adolescents with a variation of one gene (the short form of the serotonin transporter) as well as exposure to intermittent family arguments for longer than six months and violence between parents before the age of six were shown to have marked difficulty in evaluating the emotion within the words, indicating an inability to process emotional information. Previous research associated a maladjusted perception and response to emotions, as seen here, with a significantly increased risk of depression and anxiety.
Professor Ian Goodyer, Principal Investigator on the study from the University of Cambridge, said: “Whether we succumb to anxiety and depression depends in part on our tendencies to think well or poorly of ourselves at troubled times. How it comes about that some people see the ‘glass half full’ and think positively whereas other see the ‘glass half empty’ and think negatively about themselves at times of stress is not known.
The evidence is that both our genes and our early childhood experiences contribute to such personal thinking styles. Before there are any clinical symptoms of depression or anxiety, this test reveals a deficient ability to efficiently and effectively perceive emotion processes in some teenagers – a biomarker for low resilience which may lead to mental illnesses.”
Seeing Things? Hearing Things? Many of Us Do
are very startling and frightening: you suddenly see, or hear or smell something — something that is not there. Your immediate, bewildered feeling is, what is going on? Where is this coming from? The hallucination is convincingly real, produced by the same neural pathways as actual perception, and yet no one else seems to see it. And then you are forced to the conclusion that something — something unprecedented — is happening in your own brain or mind. Are you going insane, getting , having a ?
In other cultures, hallucinations have been regarded as gifts from the gods or the Muses, but in modern times they seem to carry an ominous significance in the public (and also the medical) mind, as portents of severe mental or neurological disorders. Having hallucinations is a fearful secret for many people — millions of people — never to be mentioned, hardly to be acknowledged to oneself, and yet far from uncommon. The vast majority are benign — and, indeed, in many circumstances, perfectly normal. Most of us have experienced them from time to time, during a or with the sensory monotony of a desert or empty road, or sometimes, seemingly, out of the blue.
Many of us, as we lie in bed with closed eyes, awaiting sleep, have so-called hypnagogic hallucinations — geometric patterns, or faces, sometimes landscapes. Such patterns or scenes may be almost too faint to notice, or they may be very elaborate, brilliantly colored and rapidly changing — people used to compare them to slide shows.
Single protein targeted as the root biological cause of several childhood psychiatric disorders
New research in The FASEB Journal suggests that dysfunction in the SRGAP3 protein may lead to schizophrenia, hydrocephalus, mental retardation and some forms of autism in childhood
A new research discovery has the potential to revolutionize the biological understanding of some childhood psychiatric disorders. Specifically, scientists have found that when a single protein involved in brain development, called “SRGAP3,” is malformed, it causes problems in the brain functioning of mice that cause symptoms that are similar to some mental health and neurological disorders in children. Because this protein has similar functions in humans, it may represent a “missing link” for several disorders that are part of an illness spectrum. In addition, it offers researchers a new target for the development of treatments that can correct the biological cause rather than treat the symptoms. This discovery was published in November 2012 print issue of The FASEB Journal.
"Developmental brain disorders such as schizophrenia, hydrocephalus, mental retardation and autism are among the most devastating diseases in children and young adults," said Dusan Bartsch, Ph.D., a researcher involved in the work from the Department of Molecular Biology at the Central Institute of Mental Health at the University of Heidelberg in Mannheim, Germany. "We hope that our findings will contribute to a better understanding, and in the end, to better treatments for these disorders."
Bartsch and colleagues made this discovery using mice with the SRGAP3 protein inactivated. Then they conducted several experiments comparing these mice to normal mice. The mice with inactive SRGAP3 showed clear changes in their brains’ anatomy, which resulted in altered behavior similar to certain symptoms in human neurological and psychiatric diseases. An involvement of SRGAP3 in different brain disorders could indicate that these disorders are possibly connected, as SRGAP3 is a key player in brain development. These different disorders could be connected via the SRGAP3 protein because they all emerge from disturbed development of the nervous system.
"Since Freud put biological psychiatry on the map, we’ve slowly increased our understanding of how mental health is dictated by chemistry," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "Eventually we’ll understand the complex biology underlying most psychiatric illnesses, from genes to proteins to cell signaling to overt behaviors. Along the way, as in this report, we’re likely to find single targets close to the roots of apparently different mental illnesses."
(Source: eurekalert.org)
Eye Movements and the Search for Biomarkers for Schizophrenia
There is a long history of research on impaired eye movements associated with schizophrenia. Using a series of simple viewing tests, researchers of a new paper in Biological Psychiatry explored the ability of these eye movement tests to distinguish people with and without the diagnosis of schizophrenia.
Using their complete dataset, they were able to develop a model that could discriminate all schizophrenia cases from healthy control subjects with an impressive 98.3% accuracy.
Drs. Philip Benson and David St. Clair, lead authors on the paper, agreed that their findings were remarkable: “It has been known for over a hundred years that individuals with psychotic illnesses have a variety of eye movement abnormalities, but until our study, using a novel battery of tests, no one thought the abnormalities were sensitive enough to be used as potential clinical diagnostic biomarkers.”
Their battery of tests included smooth pursuit, free-viewing, and gaze fixation tasks. In smooth pursuit, people with schizophrenia have well-documented deficits in the ability to track slow-moving objects smoothly with their eyes. Their eye movements tend to fall behind the moving object and then catch-up with the moving object using a rapid eye movement, called a saccade.. A picture is displayed in the free-viewing test, and where most individuals follow a typical pattern with their gaze as they scan the picture, those with schizophrenia follow an abnormal pattern. In a fixation task, the instruction is to keep a steady gaze on a single unmoving target, which tends to be difficult for individuals with schizophrenia.
As expected, the researchers found that the performance of individuals with schizophrenia was abnormal compared to the healthy volunteer group on each of the eye tests. At right is an example of the differences, with the eye tracking of a schizophrenia case in red and a healthy control in blue.
The researchers then used several methods to model the data. The accuracy of each of the created algorithms was then tested by using eye test data from another group of cases and controls. Combining all the data, one of the models achieved 98.3% accuracy.
"It is encouraging to see the high sensitivity of this model for the diagnosis of schizophrenia. It will be interesting to see the extent to which this approach enables clinical investigators to distinguish people with schizophrenia from individuals with other psychiatric disorders," commented Dr. John Krystal, Editor of Biological Psychiatry.
Benson and St Clair have already started that work, stating, “We now have exciting unpublished data showing that patterns of eye movement abnormalities are specific to different psychiatric subgroups, another key requirement for diagnostic biomarkers. The next thing we want to know is when the abnormalities are first detectable and can they be used as disease markers for early intervention studies in major mental illness?”
"We are also keen to explore how best our findings can be developed for use in routine clinical practice," they added. Typical neuropsychological assessments are time-consuming, expensive, and require highly trained individuals to administer. In comparison, these eye tests are simple, cheap, and take only minutes to conduct. This means that a predictive model with such precision could potentially be incorporated in clinics and hospitals to aid physicians by augmenting traditional symptom-based diagnostic criteria.
(Source: alphagalileo.org)