FUNCTIONAL GENOMICS STUDIES OF BIPOLAR DISORDER

 

FUNCTIONAL GENOMICS

STUDIES OF BIPOLAR DISORDER

 

Sabine

Bahn and Colleagues

 

Babraham

Institute, Cambridge, UK

Stanley

Laboratories, Johns Hopkins, Baltimore, MD, USA and Bethesda, MD, USA

 

 

 

Results

of microarray studies on human post-mortem tissue have suggested abnormalities

in lipid- and myelin-related genes in the prefrontal cortex of schizophrenia1-3

Recently we found that key oligodendrocyte and myelination genes, including

transcription factors known to regulate these genes, were altered not only in

schizophrenia, but also in bipolar disorder.  Although the notion that these

apparently diverse disorders may be related and may share common genetic and/or

epigenetic pathways has been considered for the last 100 years, the molecular

evidence supporting this assumption was still surprising.  Thus, we now

undertook an extensive microarray investigation coupled with proteomics

(Fluorescent 2-D gels with biological variation analysis) and metabolomics

(high-resolution NMR) studies comparing the molecular signatures of a total of

150 post-mortem brains (50 schizophrenia, 50 bipolar and 50 control samples from

the Stanley brain collection; all prefrontal cortex) to further examine the

shared and disease-specific alterations at the gene, protein and metabolite

level.  We will present results from the different functional genomics tiers

outlining both shared and distinct alterations in schizophrenia and bipolar

disorder.

 

1Hakah

Y. et al (2001) Genome-wide expression analysis reveals dysregulation of

myelination-related genes in chronic schizophrenia. Natl Acad Sci USA

98(8), 4746-4751.

 

2Pongrac

J. et al (2002) Gene expression profiling with DNA microarrays: advancing our

understanding of psychiatric disorders. Neurochem Res 27 (10), 1049-1063

 

3Mimmack

M.L. et al (2002) Gene expression analysis in schizophrenia: reproducible

up-regulation of several members of the apolipoprotein L family located in a

high-susceptibility locus for schizophrenia on chromosome 22. Proc Natl Acad

Sic USA 99 (7):4680-4685