title: Analysis of 14 CAG repeat-containing genes in schizophrenia.
abstract: Recently, it has been suggested that trinucleotide repeat-containing genes may be involved in the etiology of schizophrenia. This study was aimed at investigating putative associations between allelic variants or expansions of CAG repeat-containing genes (CAGrCG) and schizophrenia or its variability with respect to responsiveness to conventional neuroleptics. CAG repeat allelic variants of 14 expressed sequences were compared among three groups of subjects: neuroleptic-responder (R; n = 43) and neuroleptic-nonresponder (NR; n = 63) schizophrenic patients, and a control group (C; n = 122). No CAG expansions, in the range of those observed in neurodegenerative diseases, were identified in these 14 expressed sequences. The sizes of CAG repeat for the hGT1 gene were marginally different among the three groups of subjects (Kruskal-Wallis H (2, 456) = 10.48, Bonferroni corrected P = 0.047). Comparisons among the different groups indicated that neuroleptic responders have shorter alleles compared to controls (Mann-Whitney adjusted Z = -3.23, P = 0.0012). NR patients were not different from controls. These preliminary results suggest that the hGT1 gene, or a gene in its vicinity, may be involved in the etiology of schizophrenia or in modifying the disease phenotype with regard to outcome and/or neuroleptic responsiveness. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 88:694-699, 1999.
authors.affiliation: Montreal General Hospital Research Institute, Montréal, Canada. rjoob e@po-box.mcgill.ca
authors.forename: R
authors.initials: R
authors.lastname: Joober
authors.forename: C
authors.initials: C
authors.lastname: Benkelfat
authors.forename: A
authors.initials: A
authors.lastname: Toulouse
authors.forename: R G
authors.initials: RG
authors.lastname: Lafrenière
authors.forename: S
authors.initials: S
authors.lastname: Lal
authors.forename: S
authors.initials: S
authors.lastname: Ajroud
authors.forename: G
authors.initials: G
authors.lastname: Turecki
authors.forename: D
authors.initials: D
authors.lastname: Bloom
authors.forename: A
authors.initials: A
authors.lastname: Labelle
authors.forename: P
authors.initials: P
authors.lastname: Lalonde
authors.forename: M
authors.initials: M
authors.lastname: Alda
authors.forename: K
authors.initials: K
authors.lastname: Morgan
authors.forename: R
authors.initials: R
authors.lastname: Palmour
authors.forename: G A
authors.initials: GA
authors.lastname: Rouleau
mesh_terms: D000293:Adolescent; D000328:Adult; D000483:Alleles; D000818:Animals; D014150:Antipsychotic Agents / Q000627:therapeutic use; D002886:Chromosomes, Human, Pair 17 / Q000235:genetics; D004252:DNA Mutational Analysis; D016208:Databases, Factual; D020224:Expressed Sequence Tags; D005260:Female; D005787:Gene Frequency / Q000235:genetics; D014644:Genetic Variation / Q000235:genetics; D006801:Humans; D008297:Male; D016555:Matched-Pair Analysis; D051379:Mice; D018994:Myosin Light Chains; D010641:Phenotype; D020161:Physical Chromosome Mapping; D011506:Proteins / Q000235:genetics; D012559:Schizophrenia / Q000188:drug therapy / Q000235:genetics*; D012689:Sequence Homology, Nucleic Acid; D019680:Trinucleotide Repeat Expansion / Q000235:genetics*; D018911:Trinucleotide Repeats / Q000235:genetics*
chemical_list: D014150:Antipsychotic Agents; C000599129:MYL4 protein, human; D018994:Myosin Light Chains; D011506:Proteins