PMID- 16897602 OWN - NLM STAT- MEDLINE DCOM- 20070613 LR - 20181113 IS - 0300-9564 (Print) IS - 0300-9564 (Linking) VI - 114 IP - 2 DP - 2007 Feb TI - Interaction between catechol-O-methyltransferase (COMT) Val108/158Met and brain-derived neurotrophic factor (BDNF) Val66Met polymorphisms in age at onset and clinical symptoms in schizophrenia. PG - 255-9 AB - Catechol-O-methyltransferase (COMT) gene is one of the candidate genes for schizophrenia because it codes an enzyme that participates in the metabolic inactivation of dopamine and noradrenaline and a limiting factor of dopamine metabolism in the prefrontal cortex. COMT gene lies on chromosome 22q11.2, which has been associated with schizophrenia susceptibility. A single-nucleotide polymorphism of COMT gene at position 108/158 results in an amino acid substitution from valine (val) to methionine (met), which modifies its enzymatic activity and may change the brain morphology and expressional behaviors. On the other hand, brain-derived neurotrophic factor (BDNF) plays a critical role in the development of mesolimbic dopaminergic- related systems. BDNF also contains a functional single-nucleotide polymorphism at codon 66 (Val66Met) of its prodomain and this polymorphism is responsible for schizophrenia susceptibility. In this study, we first investigated the relationship between COMT Val108/158Met polymorphism and age at onset as well as levels of clinical symptoms in 158 of chronic schizophrenia inpatients and then we investigated the gene-by-gene interaction between COMT Val108/158Met polymorphism and BDNF Val66Met polymorphism with age- and sex-matched control subjects (n = 318). We concluded that the COMT Val108/158Met polymorphism was not related to either the onset at age or the levels of clinical symptoms after long-term antipsychotic treatment in schizophrenia. FAU - Numata, S AU - Numata S AD - Department of Psychiatry, Course of Integrated Brain Sciences, Medical Informatics, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, Japan. FAU - Ueno, S AU - Ueno S FAU - Iga, J AU - Iga J FAU - Yamauchi, K AU - Yamauchi K FAU - Hongwei, S AU - Hongwei S FAU - Kinouchi, S AU - Kinouchi S FAU - Shibuya-Tayoshi, S AU - Shibuya-Tayoshi S FAU - Tayoshi, S AU - Tayoshi S FAU - Aki, H AU - Aki H FAU - Sumitani, S AU - Sumitani S FAU - Itakura, M AU - Itakura M FAU - Ohmori, T AU - Ohmori T LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20060808 PL - Austria TA - J Neural Transm (Vienna) JT - Journal of neural transmission (Vienna, Austria : 1996) JID - 9702341 RN - 0 (Brain-Derived Neurotrophic Factor) RN - EC 2.1.1.6 (Catechol O-Methyltransferase) SB - IM MH - Adult MH - Age of Onset MH - Brain-Derived Neurotrophic Factor/*genetics MH - Catechol O-Methyltransferase/*genetics MH - Female MH - Genetic Predisposition to Disease MH - Humans MH - Male MH - Middle Aged MH - Polymerase Chain Reaction MH - *Polymorphism, Single Nucleotide MH - Schizophrenia/*epidemiology/*genetics EDAT- 2006/08/10 09:00 MHDA- 2007/06/15 09:00 CRDT- 2006/08/10 09:00 PHST- 2006/04/27 00:00 [received] PHST- 2006/06/04 00:00 [accepted] PHST- 2006/08/10 09:00 [pubmed] PHST- 2007/06/15 09:00 [medline] PHST- 2006/08/10 09:00 [entrez] AID - 10.1007/s00702-006-0543-1 [doi] PST - ppublish SO - J Neural Transm (Vienna). 2007 Feb;114(2):255-9. doi: 10.1007/s00702-006-0543-1. Epub 2006 Aug 8.