HIV-1 tat protein promotes amyloid β generation and tau phosphorylation in rat hippocampal slices

Eun Ok Lee, Kyoung A. Jhang, Ye Won An, Woong Ju, Young Hae Chong

Research output: Contribution to journalArticlepeer-review


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 β (Aβ) 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 Aβ precursor protein (APP) accumulation, which accompanied by Aβ 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, Aβ generation and Tau phosphorylation in the hippocampus, and thereby might contribute to the development of AD-like pathology in HIV-1-infected patients.

Original languageEnglish
Pages (from-to)102-107
Number of pages6
JournalJournal of Bacteriology and Virology
Issue number1
StatePublished - Mar 2014


  • Alzheimer's disease
  • Hippocampus
  • Hiv-1 tat
  • Hiv-1-associated neurocognitive disorder
  • Ptau


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