Conclusion

Considerable progress has been made in understanding the mechanisms of toxicity associated with overstimulation of NMDARs that lead to pathological neuronal excitation, excessive Ca2+ influx, free-radical generation, and apoptosis. Increasing evidence indicates that excitotoxicity represents a common final pathway in many neurological disorders, including HIV-associated dementia. NMDAR antagonists can inhibit both in vitro and in vivo the neurotoxicity of glutamate/NMDA and of HIV/gp120. Additionally, chemokine receptors, essential coreceptors of HIV infection, are present in the CNS on neurons, astrocytes, and microglia, and agonists of P-chemokine receptors can, in part, also confer protection against neuronal apoptosis induced by HIV/gp120 or glutamate/NMDA. These findings suggest the possibility of a functional connection between receptors for chemokines and NMDA. Recently, phase III trials with the NMDAR antagonist memantine have demonstrated benefit in a series of neurodegenerative conditions, including Alzheimer's disease and, what is termed in Europe vascular dementia. Moreover, a large, multi center clinical trial of memantine for HIV-associ-ated dementia is currently being analyzed. In the future, clinical studies may lead to therapeutic applications of chemokines for HIV-associated dementia and other neurodegenerative disorders as well.

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