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Neuregulin 1: A target for schizophrenia Approximately 1% of the population develops schizophrenia during their lifetime, making this disease more prevalent than Alzheimer's disease, diabetes, or multiple sclerosis. Patients report a variety of symptoms such as hearing internal voices not heard by others, or believing that other people are reading their minds, controlling their thoughts, or plotting to harm them. These symptoms result in fear and withdrawal. In the USA, patients with schizophrenia occupy about 25% of all hospital beds and account for about 20% of all social security disability days. 10% of patients take their own lives. Consequently, 1996 figures suggested that schizophrenia cost the US health care system US $19 billion per year with an additional US $46 billion per year in indirect costs. Improved options for the treatment of schizophrenia are urgently required, however a lack of understanding of the etiology of schizophrenia has made target selection challenging. There is a significant genetic component to schizophrenia and genomic analysis may offer one approach to the identification of new treatment options. DeCODE Genetics have adopted this approach and as a result neuregulin 1 (NRG1) was identified as a candidate gene for schizophrenia. NRG1 is expressed at central nervous system synapses and has a clear role in the expression and activation of neurotransmitter receptors, including glutamate receptors that are implicated in schizophrenia. Mutant mice heterozygous for either NRG1 or its receptor, ErbB4, show a behavioral phenotype that overlaps with mouse models for schizophrenia. Furthermore, NRG1 hypomorphs have fewer functional NMDA receptors than do wild-type mice. Finally DeCODE researchers also report that the behavioral phenotypes of the NRG1 hypomorphs are partially reversible with clozapine, an atypical antipsychotic drug used to treat schizophrenia. NRG1 and its receptor therefore deserve further attention in relation to the treatment of schizophrenia. Entry date September, 2002 Adapted from Stefansson et al, Am J Hum Genet 2002 Jul 23;71(4)
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