Effect of COMT Val(158)Met genotype on nicotine withdrawal-related cognitive dysfunction in smokers with and without schizophrenia

• Type of Material: Article
• Authors: Victoria C. Wing, University of Toronto; Yilang Tang, Emory University; Kristi A. Sacco, Yale University; Joseph Cubells, Emory University; Tony P. George, University of Toronto
• Language: English
• Date: 2013-11
• Publisher: Elsevier
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © 2013 Elsevier B.V. Published by Elsevier Inc. All rights reserved.
• License: Creative Commons Attribution 4.0 International
• Final Published Version (URL): http://dx.doi.org/10.1016/j.schres.2013.09.005
• Title of Journal or Parent Work: Schizophrenia Research
• ISSN: 0920-9964
• Volume: 150
• Issue: 2-3
• Start Page: 602
• End Page: 603
• Grant/Funding Information: This work was conducted at Yale University, New Haven, CT, USA, and funded by grants R01-DA-14039, R01-DA-13672 and K02-DA-16611 (to TPG) and K02-DA-5766 (to JFC) from the National Institute on Drug Abuse (NIDA), a National Alliance for Research of Schizophrenia and Depression Independent Investigator Award (to TPG), and the Chair in Addiction Psychiatry at the University of Toronto (TPG).
• Keywords: PSYCHIATRY, SSCI; PSYCHIATRY, SCI; Psychiatry; SMOKING; Science & Technology; FUNCTIONAL POLYMORPHISM; Life Sciences & Biomedicine; BRAIN
• Research Categories: Biology, Neuroscience; Psychology, Behavioral; Biology, Genetics

Abstract

Cigarette smokers with schizophrenia exhibit more severe cognitive dysfunction during smoking abstinence than control smokers, and cognitive deficits are associated with higher rates of smoking cessation failure (Dolan et al., 2004; Wing et al., 2012). The pro-cognitive effects of nicotine may result from enhanced dopamine (DA) release in the prefrontal cortex (PFC). Catechol-O-methyltransferase (COMT) is the primary enzyme responsible for DA metabolism in cortical brain regions. Allelic variation at a single nucleotide polymorphism (SNP) in the COMT gene at position 158 in the membrane-bound form (rs4680 or Val158met) strongly influences the level of COMT activity.