Schizophrenia and bipolar disorder may arise from reduced gene expression for myelin
Schizophrenia and bipolar disorder may have a similar genetic
cause in reduced expression of genes responsible for myelin production
in the central nervous system, according to an article in the September
6th issue of the Lancet.
Previous research has suggested abnormalities in expression of lipid-
and myelin-related genes in schizophrenia. Oligodendrocytes produce
the myelin (which is 80 percent lipid and 20 percent protein) that
sheaths axons in the central nervous system and makes possible efficient
conduction of nerve impulses.
Sabine Bahn, PhD, and her British colleagues investigated oligodendrocyte-specific
gene expression related to myelin and myelination 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.
The investigators used sensitive mRNA-based techniques (namely,
polymerase chain reaction 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 expression of key oligodendrocyte-related
and myelin-related genes in the brains of patients with schizophrenia
or bipolar disorder; the gene-expression changes showed a high degree
of overlap for the 2 disorders. There was strong correlation with
results obtained with microarray analysis compared with those obtained
by quantitative polymerase chain reaction.
Sabine Bahn commented, "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, Dr. Kenneth L Davis stated, "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."
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