Among these families (24 with facioscapulohumeral disease, 10 with Friedreich's ataxia, and 15 with schizophrenia) the prevalences of TPO Ab and Tg Ab were 27.8% and 26.7%, respectively, in women and 9.2% and 11.7%, respectively, in men.
We conclude that the genetic predisposition to schizophrenia in these pedigrees is not due to aberrations in the DRD2 locus or the porphobilinogen deaminase locus.
We conclude that the genetic predisposition to schizophrenia in these pedigrees is not due to aberrations in the DRD2 locus or the porphobilinogen deaminase locus.
Genetic variants of red-cell acid phosphatase (ACP1), esterase D (ESD), transferrin (TF) and the group-specific component (GC) were investigated in schizophrenic patients with and without a family history of both schizophrenia and other psychiatric disorders.
To evaluate whether the susceptibility gene on 5q11-13 is a common cause of schizophrenia in other populations, we examined five affected North American pedigrees using probes to the D5S39, D5S76 and dihydrofolate reductase loci.
Data were subjected to a logistic analysis in which the dependent variable was the presence of schizophrenia spectrum disorders in relatives, and the independent variables were the presence or absence of HLA A1 and CRAG A1 antigens, the sex of the proband, the sex of the relative, the severity of illness in the proband, and the type of relationship.
The authors recommend undertaking multivariate studies of monoamine oxidase, dopamine beta-hydroxylase, and other traits associated with schizophrenia in single, large pedigrees ascertained through schizophrenic probands.
A parallel study in rats showed no effect of haloperidol treatment upon hippocampal synaptophysin messenger RNA, suggesting that neuroleptic treatment does not underlie the reductions found in schizophrenia.