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• W2058918051 startingPage "75" @default.
• W2058918051 abstract "As many as two-thirds of patients with acquired immunodeficiency syndrome (AIDS) eventually suffer from neurological manifestations, including dysfunction of cognition, movement and sensation. How can human immunodeficiency virus type 1 (HIV-1) result in neuronal damage if neurons themselves are not infected by the virus? In this article Stuart Lipton reviews a series of experiments from several different laboratories that offer related hypotheses accounting for neurotoxicity in the brains of AIDS patients. There is growing support for the existence of HIV- or immune-related toxins that directly or indirectly lead to the injury or demise of neurons via a potentially complex web of interactions between macrophages (or microglia), astrocytes and neurons. However, a final common pathway for neuronal susceptibility appears to be operative, similar to that observed after stroke, trauma and epilepsy. This mechanism involves voltage-dependent Ca2+ channels and NMDA receptor-operated channels, and therefore offers hope for future pharmacological intervention." @default.
• W2058918051 created "2016-06-24" @default.
• W2058918051 creator A5066753734 @default.
• W2058918051 date "1992-01-01" @default.
• W2058918051 modified "2023-09-23" @default.
• W2058918051 title "Models of neuronal injury in AIDS: another role for the NMDA receptor?" @default.
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• W2058918051 doi "https://doi.org/10.1016/0166-2236(92)90013-x" @default.
• W2058918051 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/1373919" @default.
• W2058918051 hasPublicationYear "1992" @default.
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