New treatment for alzheimer's disease, kamikihito, reverses amyloid- β -induced progression of tau phosphorylation and axonal atrophy

Hidetoshi Watari, Yutaka Shimada, Chihiro Tohda*

*この論文の責任著者

研究成果: ジャーナルへの寄稿学術論文査読

22 被引用数 (Scopus)

抄録

Aims. We previously reported that kamikihito (KKT), a traditional Japanese medicine, improved memory impairment and reversed the degeneration of axons in the 5XFAD mouse model of Alzheimer's disease (AD). However, the mechanism underlying the effects of KKT remained unknown. The aim of the present study was to investigate the mechanism by which KKT reverses the progression of axonal degeneration. Methods. Primary cultured cortical neurons were treated with amyloid beta (Aβ) fragment comprising amino acid residues (25-35) (10 M) in an in vitro AD model. KKT (10 g/mL) was administered to the cells before or after Aβ treatment. The effects of KKT on Aβ-induced tau phosphorylation, axonal atrophy, and protein phosphatase 2A (PP2A) activity were investigated. We also performed an in vivo assay in which KKT (500 mg/kg/day) was administered to 5XFAD mice once a day for 15 days. Cerebral cortex homogenates were used to measure PP2A activity. Results. KKT improved Aβ-induced tau phosphorylation and axonal atrophy after they had already progressed. In addition, KKT increased PP2A activity in vitro and in vivo. Conclusions. KKT reversed the progression of Aβ-induced axonal degeneration. KKT reversed axonal degeneration at least in part through its role as an exogenous PP2A stimulator.

本文言語英語
論文番号706487
ジャーナルEvidence-based Complementary and Alternative Medicine
2014
DOI
出版ステータス出版済み - 2014

ASJC Scopus 主題領域

  • 補完代替医療

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