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The aggregation of amyloid-β (Aβ) caused primarily by misfolding of the peptide is one of the most predominant pathogenic hallmarks for Alzheimer’s disease (AD). Curcumin, a multifunctional phytopolyphenol by virtue of its antioxidant properties, is effective in ameliorating the oxidative stress caused by free radicals. In presence of free radicals and reactive oxygen species, the structural transition of the Aβ peptide is favored toward more beta sheet-rich conformations that in turn initiate the aggregation of the peptide. The insoluble aggregates form the amyloid plaques in brain causing memory loss, cognitive deficit, and eventually neuronal death in AD. Curcumin can potentially arrest the amyloid aggregation at various stages. As the abundance of metal ions like Zn 2+ and Cu 2+ in the cellular microenvironment also aggravates the structural transition of Aβ peptide, therefore, the metal ion chelation properties of curcumin could also be implicated in its beneficial role to prevent amyloidosis. |
