Signaling pathways to neuronal damage and apoptosis in human immunodeficiency virus type 1-associated dementia: Chemokine receptors, excitotoxicity, and beyond.
Dementia can occur as a debilitating consequence of human immunodeficiency virus-1 (HIV-1) infection. The neuropathology incited by HIV infection involves activation of chemokine receptors, inflammatory factors, and N-methyl-D-aspartate (NMDA) receptor-mediated excitotoxicity, all of which can activate several downstream mechanisms. This article discusses recently identified pathways to neuronal damage triggered by HIV-1 and efforts aimed at development of applicable therapeutic intervention.
The Burnham Institute, Center for Neuroscience and Aging Research, La Jolla, California 92037, USA.
Marcus
M
Kaul
Stuart A
SA
Lipton
D015526:AIDS Dementia Complex / Q000276:immunology / Q000473:pathology*; D017209:Apoptosis; D015497:HIV-1; D006801:Humans; D009474:Neurons / Q000473:pathology / Q000821:virology*; D009498:Neurotoxins / Q000276:immunology; D019707:Receptors, Chemokine / Q000276:immunology*; D015398:Signal Transduction / Q000276:immunology*
D009498:Neurotoxins; D019707:Receptors, Chemokine