Natural medicines and their underlying mechanisms of prevention and recovery from amyloid b-induced axonal degeneration in alzheimer’s disease

Tomoharu Kuboyama, Ximeng Yang, Chihiro Tohda*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

7 Scopus citations

Abstract

In Alzheimer’s disease (AD), amyloid β (Aβ) induces axonal degeneration, neuronal network disruption, and memory impairment. Although many candidate drugs to reduce Aβ have been clinically investigated, they failed to recover the memory function in AD patients. Reportedly, Aβ deposition occurred before the onset of AD. Once neuronal networks were disrupted by Aβ, they could hardly be recovered. Therefore, we speculated that only removal of Aβ was not enough for AD therapy, and prevention and recovery from neuronal network disruption were also needed. This review describes the challenges related to the condition of axons for AD therapy. We established novel in vitro models of Aβ-induced axonal degeneration. Using these models, we found that several traditional medicines and their constituents prevented or helped recover from Aβ-induced axonal degeneration. These drugs also prevented or helped recover from memory impairment in in vivo models of AD. One of these drugs ameliorated memory decline in AD patients in a clinical study. These results indicate that prevention and recovery from axonal degeneration are possible strategies for AD therapy.

Original languageEnglish
Article number4665
Pages (from-to)1-14
Number of pages14
JournalInternational Journal of Molecular Sciences
Volume21
Issue number13
DOIs
StatePublished - 2020/07/01

Keywords

  • Amyloid β
  • Axon
  • Diosgenin
  • Kihito
  • Naringenin
  • Polygalae Radix
  • Traditional medicines

ASJC Scopus subject areas

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

Fingerprint

Dive into the research topics of 'Natural medicines and their underlying mechanisms of prevention and recovery from amyloid b-induced axonal degeneration in alzheimer’s disease'. Together they form a unique fingerprint.

Cite this