HIV-1 Tat Protein Promotes Amyloid beta Generation and Tau Phosphorylation in Rat Hippocampal Slices.
10.4167/jbv.2014.44.1.102
- Author:
Eun Ok LEE
1
;
Kyoung A JHANG
;
Ye Won AN
;
Woong JU
;
Young Hae CHONG
Author Information
1. Department of Microbiology, School of Medicine, Ewha Medical Research Institute, Ewha Womans University, Seoul, Korea. younghae@ewha.ac.kr
- Publication Type:Original Article
- Keywords:
HIV-1-associated neurocognitive disorder;
HIV-1 Tat;
pTau;
Abeta;
Hippocampus;
Alzheimer's disease
- MeSH:
Alzheimer Disease;
Amyloid*;
Animals;
Brain;
Dementia;
Gene Products, tat*;
Hippocampus;
HIV-1*;
Humans;
Immunoblotting;
Pathology;
Phosphorylation*;
Rats*
- From:Journal of Bacteriology and Virology
2014;44(1):102-107
- CountryRepublic of Korea
- Language:English
-
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.
