Pan-HDAC inhibitors promote tau aggregation by increasing the level of acetylated TAU

Hyeanjeong Jeong, Seulgi Shin, Jun Seok Lee, Soo Hyun Lee, Ja Hyun Baik, Sungsu Lim, Yun Kyung Kim

Research output: Contribution to journalArticlepeer-review

9 Citations (Scopus)


Epigenetic remodeling via histone acetylation has become a popular therapeutic strategy to treat Alzheimer’s disease (AD). In particular, histone deacetylase (HDAC) inhibitors including M344 and SAHA have been elucidated to be new drug candidates for AD, improving cognitive abilities impaired in AD mouse models. Although emerged as a promising target for AD, most of the HDAC inhibitors are poorly selective and could cause unwanted side effects. Here we show that tau is one of the cytosolic substrates of HDAC and the treatment of HDAC inhibitors such as Scriptaid, M344, BML281, and SAHA could increase the level of acetylated tau, resulting in the activation of tau pathology.

Original languageEnglish
Article number4283
JournalInternational journal of molecular sciences
Issue number17
Publication statusPublished - 2019 Sept 1


  • Alzheimer’s disease
  • Histone deacetylase inhibitor
  • Tau acetylation
  • Tau aggregation

ASJC Scopus subject areas

  • Catalysis
  • Molecular Biology
  • Spectroscopy
  • Computer Science Applications
  • Physical and Theoretical Chemistry
  • Organic Chemistry
  • Inorganic Chemistry


Dive into the research topics of 'Pan-HDAC inhibitors promote tau aggregation by increasing the level of acetylated TAU'. Together they form a unique fingerprint.

Cite this