ABSTRACT
The apolipoprotein E (ApoE) genotype has been found to affect the expression of several neuropsychiatric disorders. We determined ApoE genotype frequencies and their relationship to primary negative symptoms in 61 non-deficit and 45 deficit schizophrenic patients, and compared them with 98 control subjects. No difference was observed when genotype or allele frequencies were compared between the three groups. Our data do not support a role for ApoE in the phenotypic expression of schizophrenia.
Subject(s)
Alleles , Apolipoproteins E/metabolism , Schizophrenia/metabolism , Adult , Apolipoproteins E/genetics , Female , Genotype , Humans , Male , Middle Aged , Schizophrenia/geneticsABSTRACT
Given the strong association of the apolipoprotein E (apoE) allele epsilon 4 (epsilon 4) with Alzheimer's disease or cognitive decline in elderly, we tested whether cognitive performance in schizophrenic subjects is associated with an increase in the frequency of the ApoE epsilon 4 allele. Our data indicate that in our sample: (1) there is no association between schizophrenia and the ApoE epsilon 4 allele; and (2) the ApoE epsilon 4 allele is not of major importance with regard to the cognitive decline observed in schizophrenia.
Subject(s)
Alleles , Apolipoproteins E/genetics , Cognition Disorders/genetics , Schizophrenia/genetics , Adult , Case-Control Studies , Chi-Square Distribution , Female , Genetic Markers , Humans , Male , Middle Aged , Schizophrenia/complications , Schizophrenic Psychology , Wechsler ScalesABSTRACT
Monoamine oxidases (MAO) A and B, which are encoded by two distinct genes located on the human X chromosome, 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.
