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  1. Heme oxygenase-1 promoter region (GT)n polymorphism associates with increased neuroimmune activation and risk for encephalitis in HIV infection
  2. Degradation of heme oxygenase-1 by the immunoproteasome in astrocytes: A potential interferon-γ-dependent mechanism contributing to HIV neuropathogenesis
  3. HIV Protease Inhibitors Alter Amyloid Precursor Protein Processing via β-Site Amyloid Precursor Protein Cleaving Enzyme-1 Translational Up-Regulation
  4. The complement system, neuronal injury, and cognitive function in horizontally-acquired HIV-infected youth
  5. Induction of Heme Oxygenase-1 Deficiency and Associated Glutamate-Mediated Neurotoxicity Is a Highly Conserved HIV Phenotype of Chronic Macrophage Infection That Is Resistant to Antiretroviral Therapy
  6. Central and peripheral markers of neurodegeneration and monocyte activation in HIV-associated neurocognitive disorders
  7. Neuropathogenesis of HIV-associated neurocognitive disorders
  8. Heme oxygenase-1 deficiency accompanies neuropathogenesis of HIV-associated neurocognitive disorders
  9. Chronic Inflammation and the Role for Cofactors (Hepatitis C, Drug Abuse, Antiretroviral Drug Toxicity, Aging) in HAND Persistence
  10. Dimethyl Fumarate Modulation of Immune and Antioxidant Responses: Application to HIV Therapy