
COMT Val158Met Polymorphism, Cardiometabolic Risk, and Nadir CD4 Synergistically Increase Risk of Neurocognitive Impairment in Men Living With HIV
Author(s) -
Rowan Saloner,
María Marquine,
Erin E. Sundermann,
Suzi Hong,
J. Allen McCutchan,
Ronald J. Ellis,
Robert K. Heaton,
Igor Grant,
Mariana Cherner
Publication year - 2019
Publication title -
journal of acquired immune deficiency syndromes
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.162
H-Index - 157
eISSN - 1944-7884
pISSN - 1525-4135
DOI - 10.1097/qai.0000000000002083
Subject(s) - neurocognitive , medicine , body mass index , odds ratio , catechol o methyl transferase , cohort , endocrinology , oncology , demography , genotype , genetics , biology , cognition , psychiatry , sociology , gene
The Val allele of the Val158Met single-nucleotide polymorphism of the catechol-o-methyltransferase gene (COMT) results in faster metabolism and reduced bioavailability of dopamine (DA). Among persons living with HIV, Val carriers display neurocognitive deficits relative to Met carriers, presumably due to exacerbation of HIV-related depletion of DA. COMT may also impact neurocognition by modulating cardiometabolic function, which is often dysregulated among persons living with HIV. We examined the interaction of COMT, cardiometabolic risk, and nadir CD4 on neurocognitive impairment (NCI) among HIV+ men.