Genome-wide expression analysis reveals dysregulation of myelination-related genes in chronic schizophrenia

Yaron Hakak(Genomics Institute of the Novartis Research Foundation), John R. Walker(Genomics Institute of the Novartis Research Foundation), Cheng Li(Genomics Institute of the Novartis Research Foundation), Wing Hung Wong(Genomics Institute of the Novartis Research Foundation), Kenneth L. Davis(Genomics Institute of the Novartis Research Foundation), Joseph D. Buxbaum(Genomics Institute of the Novartis Research Foundation), Vahram Haroutunian(Genomics Institute of the Novartis Research Foundation), Allen A. Fienberg(Genomics Institute of the Novartis Research Foundation)
Proceedings of the National Academy of Sciences
April 10, 2001
Cited by 1,200Open Access
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Abstract

Neuropathological and brain imaging studies suggest that schizophrenia may result from neurodevelopmental defects. Cytoarchitectural studies indicate cellular abnormalities suggestive of a disruption in neuronal connectivity in schizophrenia, particularly in the dorsolateral prefrontal cortex. Yet, the molecular mechanisms underlying these findings remain unclear. To identify molecular substrates associated with schizophrenia, DNA microarray analysis was used to assay gene expression levels in postmortem dorsolateral prefrontal cortex of schizophrenic and control patients. Genes determined to have altered expression levels in schizophrenics relative to controls are involved in a number of biological processes, including synaptic plasticity, neuronal development, neurotransmission, and signal transduction. Most notable was the differential expression of myelination-related genes suggesting a disruption in oligodendrocyte function in schizophrenia.


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