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J Bacteriol Virol. 2014 Mar;44(1):102-107. English. Original Article.
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.
Department of Obstetrics and Gynecology, School of Medicine, Ewha Womans University Mokdong Hospital, Ewha Womans University, Seoul, Korea.

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.