July 23, 2014
Discovery Of Genetic Risk Factors Could Lead To New Schizophrenia Treatment
redOrbit Staff & Wire Reports - Your Universe Online
Scientists have discovered more than 100 genetic risk factors associated with schizophrenia in research that could provide new insight into how the condition is caused and could be the catalyst for new treatment options.Writing in the journal Nature, an international team of researchers led by Dr. Michael O'Donovan of the Cardiff University School of Medicine conducted what is being called the largest genomic study yet published on any type of psychiatric disorder.
Their efforts have revealed biological mechanisms and pathways that may be linked to schizophrenia, and could lead to the first significant new method of treating the disorder in more than six decades. The research was a multinational, collaborative effort involving over 300 scientists from 35 countries and several years of work.
According to Karen Weintraub of USA Today, the study confirmed that the genes which regulate the brain chemical dopamine were involved in schizophrenia, as experts had predicted. However, it also revealed that genes associated with the body’s immune system, as well as some linked with cigarette smoking, were also involved.
“Some are very familiar genes expressed in nerve cells, and some are results where you scratch your head and you know you have more work to do” in order to understand the role they play in the condition, researcher and Stanley Center for Psychiatric Research director Steven Hyman told Weintraub.
[ Watch the Video: Kick-Starting Schizophrenia Research At Cardiff University ]
He explained that the finding does not prove a causal relationship between schizophrenia and either smoking or inflammation, as genes could play one role in the immune system and a different one in the brain. In all, the genome-wide association study (GWAS) identified 108 specific locations in the human genome that was associated with an increased risk of schizophrenia – including 83 which had not previously been linked to the condition.
“Detecting biological risk factors on this scale shows that schizophrenia can be tackled by the same approaches that have already transformed outcomes for people with other diseases,” Sir Michael Owen, director of the university’s MRC Centre for Neuropsychiatric Genetics and Genomics, said in a statement. “We now believe they can also do so for schizophrenia which has, until now, been so poorly understood.”
“The fact that we were able to detect genetic risk factors on this massive scale shows that schizophrenia can be tackled by the same approaches that have already transformed our understanding of other diseases,” added Dr. O'Donovan in a separate statement. “The wealth of new findings has the potential to kick-start the development of new treatments in schizophrenia, a process which has stalled for the last 60 years.”
The research, which looked at 55 datasets from 40 contributors, also implicated genes active in pathways that control synaptic plasticity, which is a function essential to learning and memory, as well as those governing postsynaptic activity, including voltage-gated calcium channels (which play a role in signaling between cells in the brain).
Despite the promise the research holds, Dr. John Williams, head of neuroscience and mental health at the Wellcome Trust, wrote in The Telegraph that “it would be false to say that genomics work will lead to an imminent breakthrough in terms of a cure for mental illnesses.”
He added that the study reveals “how little we know about schizophrenia, and how far we are from biological tests and treatments for mental health disorders compared to other major diseases,” and that the answer to mental health illnesses such as schizophrenia would not be found solely in a genetic analysis.
“Understanding mental illness is about putting together a hugely complex jigsaw of different types of knowledge,” Dr. Williams concluded. “Gradually, as the picture we are forming becomes clearer, we can design interventions and therapy which will target individuals and their different matrix of symptoms more accurately.”