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Schizophrenia and bipolar disorder could have similar genetic causes (pp 758, 798)
September 03, 2003Issue 6 September 2003
Embargoed 0001 h (London time) 5 September 2003.
Authors of a study in this week's issue of THE LANCET provide strong evidence that schizophrenia and bipolar disorder have a similar genetic cause arising from reduced expression of genes responsible for myelin development of the central nervous system.
Schizophrenia and bipolar disorder are two major psychotic illnesses, affecting about 2% of the population. Previous research has suggested abnormalities in expression of lipid and myelin-related genes in schizophrenia. Oligodendrocytes produce the Myelin sheaths, which insulate nerve cells. Myelin is 80% lipid and 20% protein and enables the efficient conduction of electrical impulses down the axon.
Sabine Bahn from the University of Cambridge, UK, and colleagues investigated the oligodendrocyte-specific and myelination-associated gene expression in schizophrenia and bipolar disorder. The investigators used sensitive mRNA-based techniques (polymerase chain reaction[PCR] and microarray assessment) to compare gene expression in the preserved brains of 15 people who had had schizophrenia, 15 who had had bipolar disorder, and a control group of 15 brains from people who had not had either disorder.
There was a clear reduction of key oligodendrocyte-related and myelin-related genes in schizophrenia and bipolar patients; gene-expression changes for both disorders showed a high degree of overlap. There was strong correlation with results obtained with microarray analysis compared with those obtained by quantitative PCR.
Sabine Bahn comments: "We believe that our results provide strong evidence for oligodendrocyte and myelin dysfunction in schizophrenia and bipolar disorder. Expression profiles of most known oligodendrocyte-specific and myelin-associated genes were greatly reduced, and several transcription factors known to coordinate myelin gene expression showed corresponding alterations. The high degree of correlation between the expression changes in schizophrenia and bipolar disorder provide compelling evidence for common pathophysiological pathways that may govern the disease phenotypes of schizophrenia and bipolar disorder. I would like to add that this research would not have been possible without the support of the Stanley Medical Research Institute."
In an accompanying Commentary (p 758), Kenneth L Davis from the Mount Sinai School of Medicine, New York, USA, states: "The observation that at least some myelin-related gene- expression deficits are common between individuals with schizophrenia and bipolar disorder is intriguing because schizophrenia and bipolar disorder have different symptom profiles and require treatment based on quite different neurotransmitter systems.'
Lancet
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