ELSEVIER Psychiatry Research 62 (1996) 221-226 PSYCHIATRY RESEARCH Association study between schizophrenia and monoamine oxidase A and B DNA polymorphisms Beatrice Corona’b, Dominique Campion* a, Florence Thibaut a, Sonia Dollfus”, Philippe Preterrea, Sophie Langlois”, Thierry Vasse”, Viviane Moreaub, Cosette Martinb, FranCoise Charbonnierb, Claudine Laurentc, Jacques Mallet’, Michel Petita, Thierry Frebourgb aGroupe de Recherche sur la Schizophrt%ie. UniversitP de Rouen. Centre Hospitalier Spkialise du Rouvray, 4 rue Paul Eluard, 76300 Sotteville Les Rouen, France b,kboratoire de G&Ptique Mobkuiaire. Centre Hospitalo- Vniversitaire de Rouen, 76031 Rouen, France CLaboratoire de Gknetique Mokculaire de la Neurotransmission (CNRS UMR-C 9923). Gif sur Yvette, France Received 18 October 1995; revised 6 February 1996;accepted 20 February 1996 Monoamine oxidases (MAO) A and B, which are encoded by two distinct genes located on the human X chromo- some, are both involved in the oxidative metabolism of dopamine. Decreased levels of platelet MAO-B activity has been reported in patients with schizophrenia and genetic variation in MAO activity had been proposed as a significant factor in the etiology of this disease. We carried out an association study using two intragenic polymorphisms within the MAO-A and MAO-B genes in 110 schizophrenic patients and 87 control subjects. For each polymorphic marker, no significant difference in allelic frequencies was observed between patients and controls. Nevertheless, a trend toward an association between allele 1 of the MAO-B gene and paranoid schizophrenia was found. Our results do not support the hypothesis that inherited variants of MAO genes might play a major role in a genetic predisposition to schizophrenia. Since several previous reports found a low MAO-B platelet activity in patients with paranoid schizophrenia, the identification of polymorphisms related to enzyme activity would be useful. Keywok Schizophrenia; Monoamine oxidases; Dopamine; Candidate gene 1. Introduction Family, twin and adoption studies suggest that genetic factors are likely to play a role in the etiol- ogy of schizophrenia (Gottesman and Shields, l Corresponding author, Tel.: +33 35 64 33 33; Fax: +33 35 64 34 31. 1982). Pharmacological studies have indicated that a dysfunction of dopaminergic systems could be the basis of schizophrenia (for review, see Davis et al., 1991) and genes involved in dopaminergic transmission are therefore good candidate genes for the predisposition to this disease. Nevertheless, linkage and association studies have failed so far to implicate most of these genes in the etiology of 0165-1781/96/$15.000 1996Elsevier Science Ireland Ltd. All rights reserved PII: SO165-1781(96)02933-Z