cyanidin-3-o-beta-glucopyranoside and Alzheimer-Disease

Alzheimer's disease (AD) is a neurodegenerative disorder that results in cognitive impairment. It has been proposed that deposits of beta-amyloid (Aβ) form the cores of the plaque and, subsequently, induce the activation of GSK-3β and the hyperphosphorylation of tau, resulting in cognitive impairment. Oxidative stress has been proposed to be an important factor in the pathogenesis of AD. Cyanidin 3-O-glucoside (Cy3G) is a neuroprotective antioxidant. However, the effects of Cy3G on cognition are unclear. In this paper, we show that Cy3G is protective against the Aβ-induced impairment of learning and memory, but has no effect on normal learning and memory. Moreover, we found that Gy3G attenuated the Aβ-induced tau hyperphosphorylation and GSK-3β hyperactivation observed in AD. Taken together, these results demonstrated that Cy3G can rescue the cognitive impairments that are induced by Aβ via the modulation of GSK-3β/tau, suggesting a potential therapeutic role of Cy3G in AD.

Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Anthocyanins; Antioxidants; Cognition Disorders; Glucosides; Glycogen Synthase Kinase 3; Glycogen Synthase Kinase 3 beta; Male; Maze Learning; Peptide Fragments; Phosphorylation; Rats; Rats, Sprague-Dawley; tau Proteins