Thiosemicarbazone modification of 3-acetyl coumarin inhibits Aβ peptide aggregation and protect against Aβ-induced cytotoxicity

Aggregation of amyloid-β peptide (Aβ) into amyloid plaques is essential event in Alzheimer's disease (AD) pathogenesis. Inhibition of Aβ aggregation is a promising avenue to explore as therapeutic treatment for AD. Our results indicate that 3-acetyl coumarin thiosemicarbazone inhibits Aβ(1-42) peptide aggregation up to 80% compared to the parent 3-acetyl coumarin which inhibits 49%. Further, 3-acetyl coumarin thiosemicarbazone provides neuroprotection against Aβ-induced cytotoxicity in SH-SY5Y cell line. These findings indicate that thiosemicarbazone modification renders 3-acetyl coumarin significant neuroprotective properties.117