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March 1992

Exclusion of Linkage Between the Serotonin2 Receptor and Schizophrenia in a Large Swedish Kindred

Author Affiliations

From the Department of Genetics (Drs Hallmayer and CavalliSforza), Stanford (Calif) University School of Medicine; the Department of Psychiatry, University of Toronto (Ontario) (Dr Kennedy); the Department of Psychiatry, Karolinska Institute, Stockholm, Sweden (Dr Wetterberg and Ms Sjögren); and the Department of Genetics, Yale University School of Medicine, New Haven, Conn (Dr Kidd). Dr Kennedy is felllow of the National Alliance for Research in Schizophrenia and Depression.

Arch Gen Psychiatry. 1992;49(3):216-219. doi:10.1001/archpsyc.1992.01820030048006

• Family, twin, and adoption studies suggest that genetic factors play an important role in the etiology of schizophrenia. Detection of single gene(s) involved in a higher susceptibility to a hereditary disease is possible with linkage analysis. The effects of serotonin2-receptor antagonists on symptoms of schizophrenia suggest that a mutation in the gene coding for this receptor subtype might be involved in the pathophysiology of this disease. Recently a copy DNA encoding the serotonin 5-HT2 receptor has been isolated and with a human 5-HT2 receptor copy DNA probe the HTR2 lo$ cus has been mapped to chromosome 13. Using multipoint linkage analysis between schizophrenia and genetic markers spanning the region of the HTR2 locus, we were able to exclude linkage between this candidate gene and schizophrenia in a Swedish kindred. Given this result, we conclude that the serotonin 5-HT2 receptor gene itself is not a major susceptibility gene for schizophrenia in this family.