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From Hawaii AIDS Clinical Research Program (V.G.V., S.R.-K., W.A., B.T.S., G.W., J.H.K., C.M.S.), John A. Burns School of Medicine, University of Hawaii, Honolulu, University of North Carolina (K.R.R.), Chapel Hill, NC, Division of Behavioral Neuroscience (R.H.P.), Department of Psychology, University of Missouri, St. Louis, and School of Medicine (J.C.M.A.), Johns Hopkins University, School of Medicine, Baltimore, MD; and Divisions of Neurology (P.S., S.N.) and Infectious Diseases (S.T.), Department of Medicine, and Office of Special Projects (S.T.C.), Phramongkutklao Hospital, Department of Retrovirology (S.R.-K., M.S.d.S., J.H.K.), Armed Forces Research Institute of the Medical Sciences, Faculty of Tropical Medicine (G.W.), Mahidol University, and Division of Research (T.C.), Royal Thai Army, Armed Forces Research Institute of the Medical Sciences, Royal Thai Army Medical Department, Bangkok, Thailand.
Address correspondence and reprint requests to Dr Valcour, Office of Neurology and Aging Research, Sinclair 202, Leahi Hospital, 3675 Kilauea Avenue, Honolulu, HI 96816; e-mail: Vvalcour{at}hawaii.edu
HIV-associated dementia (HAD) is not firmly established in patients with circulating recombinant form (CRF) 01_AE HIV-1. In this study, we compared neuropsychological performance among 15 Thai individuals with HAD, 15 Thai individuals without HAD, and 30 HIV-negative control subjects. HIV-1 participants were highly active anti-retroviral therapy naive and matched by age, education, and CD4 count. Neuropsychological testing abnormalities were identified in most cognitive domains among HAD vs HIV-negative participants, confirming the presence of HAD in CRF01_AE.
Disclosure: The authors report no conflicts of interest.
Received May 8, 2006. Accepted in final form October 19, 2006.
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