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lüll HIV-1 neuropathogenesis: glial mechanisms revealed through substance abuse Hauser KF; El-Hage N; Stiene-Martin A; Maragos WF; Nath A; Persidsky Y; Volsky DJ; Knapp PEJ Neurochem 2007[Feb]; 100 (3): 567-86Neuronal dysfunction and degeneration are ultimately responsible for the neurocognitive impairment and dementia manifest in neuroAIDS. Despite overt neuronal pathology, HIV-1 does not directly infect neurons; rather, neuronal dysfunction or death is largely an indirect consequence of disrupted glial function and the cellular and viral toxins released by infected glia. A role for glia in HIV-1 neuropathogenesis is revealed in experimental and clinical studies examining substance abuse-HIV-1 interactions. Current evidence suggests that glia are direct targets of substance abuse and that glia contribute markedly to the accelerated neurodegeneration seen with substance abuse in HIV-1 infected individuals. Moreover, maladaptive neuroplastic responses to chronic drug abuse might create a latent susceptibility to CNS disorders such as HIV-1. In this review, we consider astroglial and microglial interactions and dysfunction in the pathogenesis of HIV-1 infection and examine how drug actions in glia contribute to neuroAIDS.|AIDS Dementia Complex/complications/pathology/*physiopathology[MESH]|Animals[MESH]|Brain/pathology/*physiopathology/virology[MESH]|Causality[MESH]|Cell Communication/drug effects/physiology[MESH]|HIV-1/immunology/*metabolism[MESH]|Humans[MESH]|Nerve Degeneration/pathology/*physiopathology/virology[MESH]|Neuroglia/*metabolism/pathology/virology[MESH]|Psychotropic Drugs/adverse effects[MESH]|Substance-Related Disorders/complications/pathology/*physiopathology[MESH] |