Journal Browser Advanced Search Help
Journal Browser Advanced search HELP
J Bacteriol Virol. 2014 Mar;44(1):102-107. English. Original Article. https://doi.org/10.4167/jbv.2014.44.1.102
Lee EO , Jhang KA , An YW , Ju W , Chong YH .
Department of Microbiology, School of Medicine, Ewha Medical Research Institute, Ewha Womans University, Seoul, Korea. younghae@ewha.ac.kr
Department of Obstetrics and Gynecology, School of Medicine, Ewha Womans University Mokdong Hospital, Ewha Womans University, Seoul, Korea.
Abstract

HIV-1 Tat protein has been implicated as a causative agent in the pathogenesis of HIV-1-associated neurocognitive disorder (HAND) and Alzheimer's disease (AD)-like pathology in HIV-1 infected patients. Here, we provide insights into the potential roles of extracellular HIV-1 Tat protein in amyloid beta (Abeta) generation and Tau phosphorylation, two major neuropathological features of AD. Exposure of the rat hippocampal slices to the full-length HIV-1 Tat protein (Tat1-86) for 3 days led to the increased levels of Abeta precursor protein (APP) accumulation, which accompanied by Abeta generation in the hippocampus, the brain region most commonly damaged in HIV-1-associated dementia (HAD). Moreover, extracellular HIV-1 Tat significantly stimulated the level of phosphrylated Tau (pTau) identified using immunoblotting with AT8 antibody, which recognizes abnormally hyperphosphorylated Tau. Collectively, our data suggest that HIV-1 Tat plays important roles in increasing the levels of APP accumulation, Abeta generation and Tau phosphorylation in the hippocampus, and thereby might contribute to the development of AD-like pathology in HIV-1-infected patients.

Copyright © 2019. Korean Association of Medical Journal Editors.