NeuroAIDS, Drug Abuse, and Inflammation: Building a Collaborative Research Agenda

Welcome

The National Institute on Drug Abuse, National Institutes of Health, is pleased to have sponsored this workshop.

The goal of this focused, discussion-based workshop was to identify specific gaps in knowledge that can be addressed with collaborative, multidisciplinary research efforts. By bringing in researchers from three discrete areas (HIV/neuroAIDS, glial inflammation, and drug abuse pharmacology), as well as from combinations of these areas, many questions that are relevant to this goal were addressed. This workshop encouraged interaction and potential collaboration between researchers in the area of HIV/neuroAIDS, glial inflammation, neurobiology and drug abuse pharmacology. The format of the meeting resembled a large panel discussion with invited participants engaged in discussion, and included breakout sessions to discuss priorities for future research.

The workshop addressed the neurobiological interactions between drugs of abuse and HIV infection in the brain. Although Highly Active Antiretroviral Therapy (HAART) has dramatically improved survival and quality of life for HIV-infected patients, and has partially reduced the incidence of HIV-associated neurological complications, the prevalence of HIV-associated neurologic complications is actually increasing. Current understanding of the neurological complications of AIDS is restricted mainly to HIV-associated dementia, a late stage of disease involving neuronal toxicity and degeneration. Although this consequence is believed to be mediated by a complex cascade of events involving HIV-induced glial activation and release of inflammatory and neurotoxic molecules, mechanistic connections between these chronic host responses and progressive neurobiological impairment are not well understood. In addition, despite emerging evidence of a connection between drug use and pathogenesis and/or progression of neurodegeneration in the context of HAART, there is limited understanding of the biologic basis for such interactions. Recent observations support the idea that HIV-infected drug abusers have more severe encephalitis at autopsy, and may experience an accelerated progression of neuroAIDS. It is possible that drugs of abuse cause destabilization of neuronal circuits and glia that may cause some cell populations in the brain to be more sensitive to neurotoxic HIV proteins or inflammatory products of infected and/or activated glia.

This workshop was a joint effort between the AIDS Research Program (Contact: Lynda Erinoff, Ph.D.) and the Division of Basic Neuroscience and Behavioral Research (Contact: Diane Lawrence, Ph.D. ) at NIDA.