AI Article Synopsis
- The amyloid-beta (A beta) peptide aggregation is linked to the development of Alzheimer's disease, negatively impacting neuronal health.
- Dietary anthocyanin cyanidin 3-O-glucoside (Cy-3G) has shown potential as a neuroprotective agent by inhibiting A beta1-42 aggregation and preserving neuronal viability in lab tests.
- Cy-3G continues to provide protective effects even when administered after neurotoxic A beta1-42 aggregates have formed.
Article Abstract
The amyloid-beta (A beta) 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 A beta1-42 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 A beta1-42 treatment prevents neuronal viability loss. These protective effects were still evident when Cy-3G treatment was initiated after the appearance of oligomeric A beta1-42 neurotoxicity. Taken together, these results suggest that Cy-3G may protect and rescue the neuronal cells from toxicity induced by A beta1-42.
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| http://dx.doi.org/10.1097/WNR.0b013e32830fe4b8 | DOI Listing |
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