Experimental and Molecular Medicine (Mar 2023)

Levosimendan inhibits disulfide tau oligomerization and ameliorates tau pathology in TauP301L-BiFC mice

  • Sungsu Lim,
  • Seulgi Shin,
  • Yoonsik Sung,
  • Ha Eun Lee,
  • Kyu Hyeon Kim,
  • Ji Yeon Song,
  • Gwan-Ho Lee,
  • Hira Aziz,
  • Nataliia Lukianenko,
  • Dong Min Kang,
  • Nicolette Boesen,
  • Hyeanjeong Jeong,
  • Aizhan Abdildinova,
  • Junghee Lee,
  • Byung-Yong Yu,
  • Sang Min Lim,
  • Jun-Seok Lee,
  • Hoon Ryu,
  • Ae Nim Pae,
  • Yun Kyung Kim

DOI
https://doi.org/10.1038/s12276-023-00959-5
Journal volume & issue
Vol. 55, no. 3
pp. 612 – 627

Abstract

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Alzheimer’s disease: A tool for preventing toxic tangles The discovery that an already approved drug can disrupt tau protein aggregation in cultured cells and live mice could guide the development of new therapies for Alzheimer’s. Tau plays an important role in organizing the internal structure of neurons, but in neurodegenerative disease is seen to form abnormal assemblies that are toxic to cells. Researchers led by Ae Nim Pae and Yun Kyung Kim at the Korea Institute of Science and Technology, Seoul, South Korea have devised an assay that allowed them to identify agents that actively interfere with this process. Levosimendan, a drug approved for heart failure, broke up tau aggregates in cell culture and reduced cognitive symptoms in a mouse model of tau-induced neurodegeneration. Further investigation of levosimendan’s mode of action could yield interventions that slow or prevent Alzheimer’s progression.