HIV-1 Tat Protein Promotes Amyloid beta Generation and Tau Phosphorylation in Rat Hippocampal Slices
Journal of Bacteriology and Virology
;
: 102-107, 2014.
Article
in English
| WPRIM
| ID: wpr-112740
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.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Pathology
/
Phosphorylation
/
Brain
/
Immunoblotting
/
Gene Products, tat
/
HIV-1
/
Dementia
/
Alzheimer Disease
/
Hippocampus
/
Amyloid
Limits:
Animals
/
Humans
Language:
English
Journal:
Journal of Bacteriology and Virology
Year:
2014
Type:
Article
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