Nature Neuroscience7, 575 - 580 (2004)
Published online: 25 May 2004; | doi:10.1038/nn1258
Neuregulin 1-erbB signaling and the molecular/cellular basis of schizophrenia
Gabriel Corfas1, Kristine Roy1
& Joseph D Buxbaum2
1
Gabriel Corfas and Kristine Roy are in the Division of Neuroscience, Children's Hospital, and Department of Neurology, Harvard Medical School, Boston, Massachusetts 02115, USA.
2
Joseph D. Buxbaum is in the Departments of Psychiatry and Neurobiology, Mount Sinai School of Medicine, New York, New York 10029, USA.
Schizophrenia is a devastating psychiatric disease that affects 0.5−1% of the world's adult population. The hypothesis that this disease is a developmental disorder of the nervous system with late onset of its characteristic symptoms has been gaining acceptance in past years. However, the anatomical, cellular and molecular bases of schizophrenia remain unclear. Numerous studies point to alterations in different aspects of brain development as possible causes of schizophrenia, including defects in neuronal migration, neurotransmitter receptor expression and myelination. Recently, the gene that encodes neuregulin-1 (NRG1) has been identified as a potential susceptibility gene for schizophrenia, and defects in the expression of erbB3, one of the NRG1 receptors, have been shown to occur in the prefrontal cortex of schizophrenic patients, suggesting that NRG1-erbB signaling is involved in the pathogenesis of schizophrenia. These findings open new approaches to defining the molecular and cellular basis of schizophrenia in more mechanistic terms.
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