Calycosin ameliorates advanced glycation end product-induced neurodegenerative changes in cellular and rat models of diabetes-related Alzheimer's disease

Growing pieces of evidence suggest that Alzheimer's disease (AD) is interlinked with Type 2 diabetes mellitus (DM), which has been described as type 3 DM. In this study, we investigate the neuronal insult attributable to advanced glycation end products (AGEs) as the models of DM-related AD to understand the effects exerted by calycosin on neurodegenerative changes both in vivo and in vitro studies and also studied the associated molecular mechanisms. The results reported herein revealed that the viability of the PC12 cells induced by AGEs increased when treated with calycosin. It was also observed that the learning and memory abilities of AGE-induced DMrelated AD rats improved under these conditions. Analysis of the reported results indicates that calycosin can effectively down-regulate the activity of GSK-3 ss to result in the reversal of the process of tau hyperphosphorylation, inhibit the expression of RAGE and BACE-1 proteins, resulting in a decrease in the production of ss-amyloid and regulate the PGC-1a/TFAM signaling pathway to repair mitochondrial dysfunction. It can be inferred that calycosin can potentially exhibit important therapeutic properties that can be exploited during the treatment of AD, especially DM-related AD.

Automated summary

Growing evidence suggests that calycosin may have therapeutic effects on Alzheimer's disease, especially in Alzheimer's disease related to diabetes. Experimental results show that calycosin can promote neuronal survival, improve learning and memory abilities, down-regulate certain disease-related protein activities, reduce the production of amyloid protein, and repair mitochondrial dysfunction.