151. Distribution of the B33 CTG repeat polymorphism in a subtype of schizophrenia
- Author
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D. Bengel, Gerald Stöber, U. Balling, Cristopher A. Ross, Klaus-Peter Lesch, Ernst Franzek, Gerd Jungkunz, Shihua Li, Armin Heils, Peter Riederer, and Helmut Beckmann
- Subjects
Adult ,Male ,congenital, hereditary, and neonatal diseases and abnormalities ,Locus (genetics) ,Trinucleotide Repeats ,medicine ,Humans ,Pharmacology (medical) ,Genetic Predisposition to Disease ,Genetic Testing ,Allele ,Gene ,Biological Psychiatry ,Genetic testing ,Aged ,Genes, Dominant ,Genetics ,Ctg repeat ,Polymorphism, Genetic ,medicine.diagnostic_test ,Schizophrenia, Catatonic ,Chromosome Mapping ,General Medicine ,Middle Aged ,Psychiatry and Mental health ,Chromosome 3 ,Periodic catatonia ,Female ,Chromosomes, Human, Pair 3 ,Psychology ,Trinucleotide repeat expansion - Abstract
Clinical evidence for a dominant mode of inheritance and anticipation in periodic catatonia, a distinct subtype of schizophrenia, suggests that trinucleotide repeat expansions may be involved in the aetiology of this disorder. Since genes with triplet repeats are putative canditates for causing schizophrenia, we have analysed the polymorphic B33 CTG repeat locus on chromosome 3 in 45 patients with periodic catatonia and 43 control subjects. The B33 CTG repeat locus was highly polymorphic, but all alleles in both the patient and control groups had repeat lengths within the normal range. We conclude that susceptibility to periodic catatonia is not influenced by variation at the B33 CTG repeat locus. Nevertheless, that periodic catatonia displays dominant inheritance and anticipation, characteristic of genetic disorders involving trinucleotide repeats, justifies further screening for triplet repeat expansions in this illness.
- Published
- 1998