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Journal of Biomedicine and Biotechnology
Volume 2006, Article ID 65741, 10 pages
Review Article

HIV Neurotoxicity: Potential Therapeutic Interventions

Department of Pharmacology and Physiology and Department of Forensic Sciences, Center for Health Sciences, Oklahoma State University, Tulsa, OK 74107-1898, USA

Received 1 December 2005; Revised 21 February 2006; Accepted 27 February 2006

Copyright © 2006 David R. Wallace. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Individuals suffering from human immunodeficiency virus type 1 (HIV-1) infection suffer from a wide range of neurological deficits. The most pronounced are the motor and cognitive deficits observed in many patients in the latter stages of HIV infection. Gross postmortem inspection shows cortical atrophy and widespread neuronal loss. One of the more debilitating of the HIV-related syndromes is AIDS-related dementia, or HAD. Complete understanding of HIV neurotoxicity has been elusive. Both direct and indirect toxic mechanisms have been implicated in the neurotoxicity of the HIV proteins, Tat and gp120. The glutamatergic system, nitric oxide, calcium, oxidative stress, apoptosis, and microglia have all been implicated in the pathogenesis of HIV-related neuronal degeneration. The aim of this review is to summarize the most recent work and provide an overview to the current theories of HIV-related neurotoxicity and potential avenues of therapeutic interventions to prevent the neuronal loss and motor/cognitive deficits previously described.