Three CAG trinucleotide repeats on chromosome 6 (D6S1014, D6S1015, and D6S1058) are not expanded in 30 families with schizophrenia.

Since 1991, more than five neuro-genetic disorders have been recognized to be caused by trinucleotide repeat expansions, and the list of such disease should grow. The diseases are characterized clinically by the phenomenon of anticipation, i.e., worsening of the disease phenotype in successive generations with increasing trinucleotide repeat expansion. The presence of anticipation in familial schizophrenia has been suggested. Several studies have provided supportive evidence that the suceptability locus for schizophrenia is on chromosome 6. Therefore, we analyzed three CAG trinucleotide repeat clones D6S1014, D6S1015, and D6S1058 on chromosome 6, which are polymolphic in 30 families with schizophrenia. No unusually, long alleles that would suggest abnormal expansion of more than 35 trinucleotide repeats were observed for these genes. Also, no statistically significant differences were found between the offspring and parental generations of affected subjects or between the affected and unaffected subjects in families with schizophrenia.