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Disruption in oligodendrocyte function indicated in schizophrenia

SPIS MedWire

Genome Biology 2001, 2:spotlight-20010426-01  doi:10.1186/gb-spotlight-20010426-01

The electronic version of this article is the complete one and can be found online at:

Published:26 April 2001

© 2001 BioMed Central Ltd

Research news

Myelin sheaths are critical for efficient signal transmission along axons. Their inactivation could explain some of the neuropathological deficits associated with schizophrenia.

In the April 10 Proceedings of the National Academy of Sciences, Yaron Hakak and colleagues of the Genomics Institute of the Novartis Research Foundation, San Diego, California used DNA microarray analysis to compare the gene-activation profiles in the postmortem dorsolateral prefrontal cortex of 12 schizophrenic and 12 nonschizophrenic individuals.

The team found that of 89 genes that were differentially activated in the schizophrenic group, only those involved in myelination were downregulated or activated at lower levels than normal. They emphasize that this suggests that oligodendrocytes could be a specific cell-type that is functionally impaired in schizophrenia.

Hakak's group stress that their findings support the observation that myelination of the prefrontal cortex occurs in late adolescence and early adulthood, the typical age of onset for schizophrenia. In addition, they point out the benefits of using microarray analysis in exploring the molecular basis of neuropsychiatric disorders and providing new insights into the cause of these diseases.


  1. [] webcite

    Hakak Y, Walker JR, Li C, Wong EH, Davis KL, Buxbaun JD, Haroutunian V, Fienberg AA: Genome-wide expression analysis reveals dysregulation of myelination-related genes in chronic schizophrenia. Proc Natl Acad Sci USA 2001, 98:4746-4751.

  2. [] webcite

    Genomics Institute of the Novartis Research Foundation