The Association between COMT, BDNF, and NRG1 and Premorbid Social Functioning in Patients with Psychosis, Their Relatives, and Controls. (1st July 2012)

• Record Type: Journal Article
• Authors: Walshe, Muriel; Vassos, Evangelos; Picchioni, Marco; Shaikh, Madiha; Toulopoulou, Timothea; Collier, David; McDonald, Colm; Murray, Robin; Bramon, Elvira
• Other Names: Evers Andrea Academic Editor.; Niznikiewicz Margaret A. Academic Editor.; Toni Cristina Academic Editor.
• Is Part Of: Scientifica. Volume 2012(2012)
• Publication Date: 2012-07-01
• Subjects: Life sciences -- Periodicals; Biology -- Periodicals; Medicine -- Periodicals; Biological Science Disciplines; Medicine; Biology; Life sciences; Medicine; Periodicals; Electronic journals; Periodicals; 500
• DOI: 10.6064/2012/560514
• Languages: English
• ISSNs: 2090-908X

Abstract

Abstract : We investigated the influences of putative candidate genes for psychosis on premorbid social adjustment and on premorbid schizoid-schizotypal traits. A family-based sample was used including 177 patients with schizophrenia or bipolar I disorder with a history of psychotic symptoms, 86 of their unaffected relatives, and 116 unrelated healthy controls. Association analyses on the combined sample were conducted using the Statistical Analysis for Genetic Epidemiology software (SAGE) and adjusting for age, sex, clinical group, and the family-based nature of the data. The COMT Val 158 Met and BDNF Val 66 Met polymorphisms showed no evidence of association with either phenotype. The SNP rs221533 of the NRG1 gene was significantly associated with premorbid adjustment in adolescence with TT homozygous subjects having a poorer performance than C allele carriers. In the context of neurodevelopmental disorders such as schizophrenia and other psychoses, this finding is plausible; however, it is preliminary and requires replication in an independent sample. In a broader sense, the use of intermediate quantitative phenotypes such as the ones presented in this study may be of help to understand the mechanism of action of genetic risk factors.