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lüll Cell death in HIV dementia Mattson MP; Haughey NJ; Nath ACell Death Differ 2005[Aug]; 12 Suppl 1 (ä): 893-904Many patients infected with human immunodeficiency virus type-1 (HIV-1) suffer cognitive impairment ranging from mild to severe (HIV dementia), which may result from neuronal death in the basal ganglia, cerebral cortex and hippocampus. HIV-1 does not kill neurons by infecting them. Instead, viral proteins released from infected glial cells, macrophages and/or stem cells may directly kill neurons or may increase their vulnerability to other cell death stimuli. By binding to and/or indirectly activating cell surface receptors such as CXCR4 and the N-methyl-D-aspartate receptor, the HIV-1 proteins gp120 and Tat may trigger neuronal apoptosis and excitotoxicity as a result of oxidative stress, perturbed cellular calcium homeostasis and mitochondrial alterations. Membrane lipid metabolism and inflammation may also play important roles in determining whether neurons live or die in HIV-1-infected patients. Drugs and diets that target oxidative stress, excitotoxicity, inflammation and lipid metabolism are in development for the treatment of HIV-1 patients.|*HIV-1/genetics/pathogenicity/physiology[MESH]|AIDS Dementia Complex/drug therapy/genetics/metabolism/*pathology[MESH]|Animals[MESH]|Anti-Retroviral Agents/therapeutic use[MESH]|Apoptosis[MESH]|Brain/metabolism/*pathology/virology[MESH]|Calcium/metabolism[MESH]|Cell Death[MESH]|Gene Products, tat/pharmacology[MESH]|HIV Envelope Protein gp120/pharmacology[MESH]|Humans[MESH]|Inflammation Mediators/metabolism[MESH]|Lipid Metabolism[MESH]|Neuroglia/drug effects/metabolism[MESH]|Neurons/drug effects/metabolism/pathology[MESH]|Oxidative Stress[MESH]|Receptors, Glutamate/metabolism[MESH]|Viral Proteins/pharmacology/toxicity[MESH]|Virus Replication[MESH]|tat Gene Products, Human Immunodeficiency Virus[MESH] |