| Institution: | (1) Department of Behavioral Sciences, University of Kentucky, Lexington, Kentucky, USA;(2) Department of Neurology, Johns Hopkins University, Baltimore, MD, USA;(3) Department of Anatomy and Neurobiology, University of Kentucky, Lexington, Kentucky, USA;(4) Behavioral Neuroscience Program, Department of Psychology, University of South Carolina, Columbia, SC, USA |
| Abstract: | Background HIV Associated Dementia (HAD) is a common complication of human immunodeficiency virus (HIV) infection that erodes the quality
of life for patients and burdens health care providers. Intravenous drug use is a major route of HIV transmission, and drug
use is associated with increased HAD. Specific proteins released as a consequence of HIV infection (e.g., gp120, the HIV envelope
protein and Tat, the nuclear transactivating protein) have been implicated in the pathogenesis of HAD. In primary cultures
of human fetal brain tissue, subtoxic doses of gp120 and Tat are capable of interacting with a physiologically relevant dose
of cocaine, to produce a significant synergistic neurotoxicity. Using this model system, the neuroprotective potential of
gonadal steroids was investigated. |
