Neuroprotective effects of cyanidin 3-O-glucopyranoside on amyloid beta (25–35) oligomer-induced toxicity

Recent studies suggest that the oligomers of short amyloid beta (Aβ) peptides such as Aβ25–35 as well as full-length Aβ peptides (i.e. Aβ1–40 and Aβ1–42 peptides) are responsible for synaptic dysfunction and/or neuronal loss in Alzheimer's disease (AD). Among antioxidant phytochemicals derived from fruit and vegetables, cyanidin 3-O-glucoside (Cy-3G) has recently gained attention for its neuroprotective properties. In this in vitro study, we demonstrated that Cy-3G can inhibit Aβ25–35 spontaneous aggregation into oligomers and their neurotoxicity in human neuronal SH-SY5Y cells. In particular, the pre- and co-treatment of SH-SY5Y cells with Cy-3G reduced the neuronal death, in terms of apoptosis and necrosis, elicited by Aβ25–35 oligomers. Cy-3G also shows the interesting ability to prevent the early events leading to neuronal death such as the Aβ25–35 oligomer binding to plasma membrane and the subsequent membrane integrity loss. Taken together, these findings suggest that Cy-3G may be considered a phytochemical with neuroprotective properties useful in finding potential drug or food supplements for the therapy of AD.