Deletion of PLCB1 gene in schizophrenia-affected patients

J Cell Mol Med. 2012 Apr;16(4):844-51. doi: 10.1111/j.1582-4934.2011.01363.x.

Abstract

A prevalence of 1% in the general population and approximately 50% concordance rate in monozygotic twins was reported for schizophrenia, suggesting that genetic predisposition affecting neurodevelopmental processes might combine with environmental risk factors. A multitude of pathways seems to be involved in the aetiology and/or pathogenesis of schizophrenia, including dopaminergic, serotoninergic, muscarinic and glutamatergic signalling. The phosphoinositide signal transduction system and related phosphoinositide-specific phospholipase C (PI-PLC) enzymes seem to represent a point of convergence in these networking pathways during the development of selected brain regions. The existence of a susceptibility locus on the short arm of chromosome 20 moved us to analyse PLCB1, the gene codifying for PI-PLC β1 enzyme, which maps on 20p12. By using interphase fluorescent in situ hybridization methodology, we found deletions of PLCB1 in orbito-frontal cortex samples of schizophrenia-affected patients.

MeSH terms

  • Adolescent
  • Adult
  • Chromosomes, Human, Pair 20
  • Female
  • Gene Deletion*
  • Humans
  • In Situ Hybridization, Fluorescence
  • Male
  • Phospholipase C beta / genetics*
  • Schizophrenia / genetics*
  • Young Adult

Substances

  • PLCB1 protein, human
  • Phospholipase C beta