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Publication Abstract Display
Type: Poster
Title: Methamphetamine use exacerbates HIV-associated neurocognitive impairment in acute and early HIV infection.
Authors: Weber E, Woods SP, Smith D, Morris S, Letendre SL, Grant I, Ellis RJ, Little S, and The TMARC Group
Date: 05-29-2012
Abstract:Methamphetamine (MA) use is a risk factor for HIV infection, and its comorbid presentation is associated with additive structural and functional injury to frontostriatal neural circuitry, including neurocognitive impairment. Yet little is known about the role of MA in the expression of neurocognitive compromise during the acute and early stages of HIV infection (AEH), which is associated with rapid viral replication, increased immune activation, and alterations in brain metabolism. The present study examined the impact of MA use on HIV-associated neurocognitive impairment (HNCI) among 46 antiretroviral-naïve adults with a median duration of infection of 75 [IQR = 25,87] days and current CD4 count of 609 (IQR = 431,717.5). Participants were administered a brief neurocognitive battery adjusted for demographics and assessed executive functions, memory, psychomotor speed, and verbal fluency. Sixty-one percent of the participants evidenced HNCI as determined by global deficit scores (GDS) >0.5. Participants were also administered the Drug Abuse Screening Test (DAST-20) for MA use and the Alcohol Use Disorders Identification Test (AUDIT). Spearmanís rho correlations revealed a moderate relationship (rho = 0.38; p = 0.011) between DAST total and GDS, whereby individuals with greater risk of MA use disorders exhibited lower neurocognitive functioning, particularly in fine motor coordination. Within a small subset of participants who underwent lumbar puncture (n = 14), DAST total was correlated at a trend level with viral load in CSF (rho = 0.50; p = 0.067), but not plasma (rho = 0.04; p > 0.10). Alcohol use was not associated with neurocognitive functioning or viral loads (ps > 0.10). These results suggest that MA use may play an important role in the risk of neurocognitive impairment and increased HIV RNA in CSF during AEH. The neural mechanisms of MAís apparent exacerbation of CNS injury in AEH remain to be determined, but may involve dopaminergic systems vulnerable to effects of neuroinflammation, vasculopathy, and/or oxidative stress that have been previously reported in chronically infected MA users.

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