Progress in understanding basal Ganglia dysfunction as a common target for methamphetamine abuse and HIV-1 neurodegeneration

Shaji Theodore, Wayne A. Cass, Avindra Nath, William F. Maragos

Research output: Contribution to journalReview articlepeer-review

30 Scopus citations

Abstract

HIV-1 infection with concurrent methamphetamine (MA) abuse results in exacerbated neurodegenerative changes and rapid progression of a form of sub-cortical dementia termed HIV-1 associated dementia (HAD). A notable feature of HAD is the involvement of the dopaminergic system manifested as parkinsonian like movement abnormalities. The HIV-1 transactivator of transcription (Tat) protein is very often used in experimental studies trying to understand neurotoxic consequences of HIV-1 infection, since the pathophysiological changes induced by Tat mirrors, in part, the means by which HIV-1 infection of the nervous system results in neuronal damage. Understanding the interaction of Tat and MA in the basal ganglia and the resultant injury to the dopaminergic system in rodent models as well as cell culture will shed light on the dopaminergic pathology occurring in HIV-1 infected-MA abusers. The aim of this review is to update the reader on the current knowledge of MA and HIV-1 neurotoxicity, specifically Tat, and discuss the progress in understanding how MA synergizes with the HIV-1 transactivator protein Tat to damage the basal ganglia.

Original languageEnglish (US)
Pages (from-to)301-313
Number of pages13
JournalCurrent HIV research
Volume5
Issue number3
DOIs
StatePublished - May 2007
Externally publishedYes

Keywords

  • AIDS
  • Cytokines
  • Dopamine
  • Drug abuse
  • Glia
  • Neurodegeneration
  • Striatum

ASJC Scopus subject areas

  • Infectious Diseases
  • Virology

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