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August

Bipolar Disorder genetic consortium discover genes which increase the risk of developing Bipolar Affective Disorder

AUGUST 17, 2008

In a major paper titled Collaborative genome-wide association analysis of 10,596 individuals supports a role for Ankyrin-G (ANK3) and the L-type voltage-gated calcium channel (CACNA1C) in bipolar disorder, published on the 17th August 2008 in the online edition of the journal Nature Genetics, a consortium led by Professor Pamela Sklar of Harvard Medical School and Professor Nick Craddock of the School of Medicine, Cardiff University and combining samples from the Wellcome Trust Case Control Consortium, Systematic Treatment Enhancement Program for Bipolar Disorder, University College London, University of Edinburgh and University of Dublin samples, has identified susceptibility genes for bipolar affective disorder. The study included contributions from the Institute of Psychiatry at King’s College London, from Professors Peter McGuffin, Anne Farmer, David Collier and Dr Gerome Breen. 

It has been known for many years that bipolar affective disorder has inherited causes, and indeed more than 80% of the risk of the disorder is thought to involve genetic factors, but despite decades of research it has proven very difficult to identify the exact genes involved. The reason for this appears to be that there are many genes which increase risk of this disorder, and the effect of each one is very small, making them very difficult to detect above the 'noise' of general human gene variation.  

In order to detect these genes the consortium put together a huge group of volunteer subjects with bipolar disorder and people without the illness, resulting in 4,387 bipolar disorder cases and 6,209 controls. Using the latest genetic technology the group identified a strong association with the Ankyrin-G gene and the L-type voltage-gated calcium channel gene, CACNA1C and the findings confirm that bipolar affective disorder is caused by changes in the way electrical signals are transmitted in nerve cells. 

The local investigators, David Collier, of the Medical Research Council-funded Social, Genetic and Developmental Psychiatry Centre, and the Dean, Professor Peter McGuffin, said “These findings will improve our understanding of the underlying causes of this devastating mental illness, which will pave the way for improved and safer treatment for sufferers.  The discovery of the role of ion channels in the disorder has important implications for research and treatment of this illness, not least because ion channels can be specifically targeted by drugs.  Identifying the genes involved will improve treatment for the patient, and in the case of bipolar disorder this may mean the identification of better and safer drugs which can modulate the activity of ion channels. Since these genes have a very small effect on risk, at this stage it is less likely to allow us to better diagnose mental illness through genetic tests, however, it is always of major benefit to research and clinical treatment if the basic aetiology of a disorder is better understood.” 

Participation in this landmark research was made possible by the dedication and effort over many years of researchers in the UK, Ireland, Australia, the United States as well as other countries, and included the  the Social, Genetic and Developmental Psychiatry Centre at the Institute of Psychiatry, King’s College London. Essential funding to enable this work was provided by the Wellcome Trust, the US National Institute of Mental Health, NARSAD, Johnson & Johnson Pharmaceutical Research & Development, Sylvan C. Herman Foundation, Stanley Medical Research Institute, Dauten Family, Merck Genome Research Institute (E.M.S.); GSK and Medical Research Council (MRC), Australia (M.A.R.F.) and the Broad Institute Center for Genotyping and Analysis.
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