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Human Molecular Genetics Advance Access originally published online on May 10, 2006
Human Molecular Genetics 2006 15(12):1949-1962; doi:10.1093/hmg/ddl118
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© 2006 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Genome-wide expression analysis detects eight genes with robust alterations specific to bipolar I disorder: relevance to neuronal network perturbation

Noriaki Nakatani1, Eiji Hattori1, Tetsuo Ohnishi1, Brian Dean3, Yoshimi Iwayama1, Izuru Matsumoto4, Tadafumi Kato2, Noriko Osumi5,6, Teruhiko Higuchi7, Shin-Ichi Niwa8 and Takeo Yoshikawa1,6,*

1Laboratory for Molecular Psychiatry, 2Laboratory for Molecular Dynamics of Mental Disorders, RIKEN Brain Science Institute, Saitama 351-0198, Japan, 3The Rebecca L. Cooper Research Laboratories, Mental Health Research Institute of Victoria, Parkville Victoria 3052, Australia, 4Department of Pathology, The University of Sydney, NSW 2006, Australia, 5Division of Developmental Neuroscience, Center for Translational and Advanced Animal Research, Tohoku University School of Medicine, Miyagi 980-8575, Japan, 6CREST, Japan Science and Technology Agency, Saitama 332-0012, Japan, 7Musashi Hospital, National Center of Neurology and Psychiatry, Tokyo 187-8551, Japan and 8Department of Neuropsychiatry, School of Medicine, Fukushima Medical University, Fukushima 960-1295, Japan

* To whom correspondence should be addressed. Tel: +81 484675968; Fax: +81 484677462; Email: takeo{at}brain.riken.jp

Received February 7, 2006; Revised March 28, 2006; Accepted April 28, 2006

The limited number of genome-wide transcriptome analyses using the postmortem brains of bipolar disorder sufferers has not produced a clear consensus on the molecular pathways affected by the disorder. To expand the knowledge in this area, we examined the expression levels of more than 12 000 genes in Brodmann's Area (BA), 46 (dorsolateral prefrontal cortex) from bipolar I disorder and control samples using Affymetrix GeneChips. This analysis detected 108 differentially expressed genes in bipolar brains. Validation studies using quantitative RT–PCR on the two original diagnostic cohorts plus tissue from schizophrenic subjects, confirmed the differential expressions of eight genes (RAP1GA1, SST, HLA-DRA, KATNB1, PURA, NDUFV2, STAR and PAFAH1B3) in a bipolar-specific manner and one gene (CCL3) which was downregulated in both bipolar and schizophrenic brains. Of these, protein levels of RAP1GA1 (RAP1 GTPase activating protein 1) showed a trend of increase in BA46 from bipolar brains, in keeping with mRNA transcript levels. Transmission disequilibrium analysis of the nine genes using 43 single nucleotide polymorphisms (SNPs) in 229 National Institute of Mental Health bipolar trios exposed nominal SNP association and modest empirical haplotypic association (P=0.033) between SST (somatostatin) and disease. Finally, gene network analysis using the currently obtained expression data highlighted cellular growth and nervous system development pathways as potential targets in the molecular pathophysiology of bipolar disorder.


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