1,8-Cineole Ameliorates Advanced Glycation End Products-Induced Alzheimer's Disease-like Pathology In Vitro and In Vivo

Advanced glycation end products (AGEs) are stable products produced by the reaction of macromolecules such as proteins, lipids or nucleic acids with glucose or other reducing monosaccharides, which can be identified by immunohistochemistry in the senile plaques and neurofibrillary tangles of Alzheimer's disease (AD) patients. Growing evidence suggests that AGEs are important risk factors for the development and progression of AD. 1,8-cineole (CIN) is a monoterpenoid compound which exists in many plant essential oils and has been proven to have neuroprotective activity, but its specific effect and molecular mechanisms are not clear. In this study, AGEs-induced neuronal injury and intracerebroventricular-AGE animals as the possible models for AD were employed to investigate the effects of CIN on AD pathology as well as the molecular mechanisms involved both in vivo and in vitro. Our study demonstrated that CIN could ameliorate tau phosphorylation by down-regulating the activity of GSK-3 beta and reducing A beta production by inhibiting the activity of BACE-1 both in vivo and in vitro. It is suggested that CIN has certain therapeutic value in the treatment of AD.

Automated summary

Advanced glycation end products (AGEs) are important risk factors for the development and progression of Alzheimer's disease (AD). 1,8-cineole (CIN) can ameliorate tau phosphorylation and reduce Aβ production by inhibiting the activity of GSK-3β and BACE-1, highlighting its therapeutic potential for AD.