Toxic Factors

It has been suggested that viral products, such as envelope protein gp120, may be neurotoxic. For example, gp120 causes cell death in neuronal cultures, and transgenic mice that constitutively overproduce gp120 show neuronal injury, with loss of dendritic spines and synapses. Lipton and colleagues suggested that gp120 may exert its effect by activating N-methyl-D-aspartate (NMDA) receptors, causing influx of calcium. Further evidence of this has been suggested by the fact that memantine, an NMDA antagonist, can block gp120-induced neurotoxicity. Recently, it has also been suggested that gp120 may bind to chemokine receptor sites on neurons, and this process may lead to activation of NMDA receptors and excitotoxicity.

Nonviral toxic products have also been implicated. For example, activated macrophages and astrocytes within the central nervous system are capable of producing increased quantities of quinolinic acid, an excitotoxic molecule. Previous research has found that the amount of quinolinic acid in the cerebrospinal fluid increases with stage of disease and is highest in those with HIV dementia (Fig. 5).

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