Cordycepin, a bioactive compound from Cordyceps spp., moderates Alzheimer’s disease-associated pathology via anti-oxidative stress and autophagy activation

Abstract

Alzheimer’s causes cognitive dysfunction. This study investigated the neuro-promoting effects of cordycepin on amyloid-beta precursor protein (APP) synthesis in human neuroblastoma SH-SY5Y cells. Cordycepin was found to boost SH-SY5Y cell proliferation and decreased AD pathology. APP, PS1, and PS2 were downregulated whereas ADAM10 and SIRT1 were upregulated by cordycepin. Cordycepin also reduced APP secretion in a dose-dependent manner. Cordycepin alleviated oxidative stress by the upregulation of GPX and SOD, as well as autophagy genes (LC3, ATG5, and ATG12). Cordycepin activity was also found to be SIRT1-dependent. Therefore, cordycepin may relieve the neuronal degeneration caused by APP overproduction, and oxidative stress.

Keywords:

• Cordycepin
• Alzheimer’s disease
• oxidative stress
• autophagy
• SIRT1

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

This work was financially supported by Suranaree University of Technology (SUT) Research and Development Fund, Thailand Science, Research, and Innovation (TSRI), and National Science, Research, and Innovation Fund (NSRF) [project code 90464].