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Assessment of Apoptosis and Neuronal Loss in Animal Models of HIV-1-Associated Neurocognitive Disorders
Book chapter   Peer reviewed

Assessment of Apoptosis and Neuronal Loss in Animal Models of HIV-1-Associated Neurocognitive Disorders

Jean-Pierre Louboutin, Beverly Reyes, Lokesh Agrawal, Elisabeth Van Bockstaele and David S. Strayer
Transmission Electron Microscopy Methods for Understanding the Brain, pp 217-243
23 Feb 2016

Abstract

Caspase gp120 HIV-1 HIV-1-associated neurocognitive disorder Morphometry Neuronal loss Tat Transmission electron microscopy Apoptosis Cell Culture Gene Therapy Immunohistochemistry Oxidative Stress
HIV-1-associated neurocognitive disorder (HAND) is a neurodegenerative disease resulting in various clinical manifestations, characterized by neuroinflammation, oxidative stress, and related events. Neuronal damage in HAND is felt to be mainly indirect: microglial cells infected by HIV-1 increase the production of cytokines and release HIV-1 proteins, the most likely neurotoxins, among which are the envelope proteins gp120 and gp41 and the nonstructural proteins Nef, Rev, Vpr, and Tat. We review and discuss here different methods used in the assessment of apoptosis and neuronal loss in different experimental, acute and chronic, models of HAND. We also briefly consider how these techniques help to evaluate the effects of gene delivery of antioxidant enzymes in animal models of HAND.

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