AGINGCyanidin 3-O-glucopyranoside protects and rescues SH-SY5Y cells against amyloid-beta peptide-induced toxicityTarozzi, Andreaa; Merlicco, Adrianaa; Morroni, Fabianaa; Franco, Francescaa; Cantelli-Forti, Giorgioa; Teti, Gabriellab; Falconi, Mirellab; Hrelia, PatriziaaAuthor Information Departments of aPharmacology bAnatomical Sciences, Alma Mater Studiorum, University of Bologna, Bologna, Italy Correspondence to Assistant Professor Andrea Tarozzi, PhD, Department of Pharmacology, University of Bologna, Via Irnerio 48, Bologna 40126, Italy Tel: +39 051 2091795; fax: +39 051 248862; e-mail: firstname.lastname@example.org Received 12 June 2008; accepted 9 July 2008 NeuroReport: October 8th, 2008 - Volume 19 - Issue 15 - p 1483-1486 doi: 10.1097/WNR.0b013e32830fe4b8 Buy SDC Metrics Abstract The amyloid-β (Aβ) peptide (1–42) aggregation into oligomeric and fibrillar species affects neuronal viability, having a causal role in the development of Alzheimer's disease. Among dietary anthocyanins, cyanidin 3-O-glucoside (Cy-3G) and its metabolites, such as protocatechuic acid (PA), have gained attention as potential neuroprotective agents. In this in-vitro study, we demonstrated that Cy-3G, but not PA, can inhibit Aβ1–42 spontaneous aggregation using thioflavin T fluorescence assay and transmission electron microscopy. Furthermore, treatment of human neuronal SH-SY5Y cells with Cy-3G during oligomeric and fibrillar Aβ1−42 treatment prevents neuronal viability loss. These protective effects were still evident when Cy-3G treatment was initiated after the appearance of oligomeric Aβ1−42 neurotoxicity. Taken together, these results suggest that Cy-3G may protect and rescue the neuronal cells from toxicity induced by Aβ1−42. © 2008 Lippincott Williams & Wilkins, Inc.