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	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Glial cells have been grossly neglected in schizophrenia research.¹ Hopefully, the publication of the oligodendrocyte hypothesis by Davis et al² in the May 2003 issue of the ARCHIVES and their excellent review of the supporting evidence will change the situation. Oligodendrocytes produce myelin and, together with astrocytes and microglia, were formerly thought to be merely glia ("glue") of the brain.

Additional evidence from genetic and other studies supports the oligodendrocyte hypothesis and further suggests a more general glial deficiency involving astrocytes. (1) Pooled linkage data and the colocalization of genes related to glial growth suggest that glial asthenia is an important factor in the liability to schizophrenia.³ (2) Genetic associations between schizophrenia and genes for neuregulin 1 and the rhesus factor have been reported. The gene product of neuregulin 1 is glial growth factor 2, suggesting a deficiency of glial growth in schizophrenia. In regard to the rhesus factor, . . . [Full Text of this Article]

AUTHOR INFORMATION
Hans W. Moises, MD; Irving I. Gottesman, PhD, HonFRCPsych

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