Protective effects of compound FLZ, a novel synthetic analogue of squamosamide, on β-amyloid-induced rat brain mitochondrial dysfunction in vitro

Abstract

Aim:The aim of the present study was to assess the effects of N- [2-(4-hydroxyphenyl)ethyl]-2- (2,5-dimethoxyphenyl)-3-(3-methoxy-4-hydroxyphenyl)

3,6'‐disinapoyl sucrose attenuates Aβ1‐42‐ induced neurotoxicity in Caenorhabditis elegans by enhancing antioxidation and regulating autophagy

“…The pathogenesis of AD is very complex and still not fully understood. Accumulating evidences showed that the misfolding and aggregation of Aβ can induce mitochondrial dysfunction, oxidative stress, neuronal apoptosis, hyperphosphorylated Tau protein and lead to the progressive impairment in memory and cognition, which is involved in the pathogenesis of AD 3‐5 . So, reducing Aβ deposition and neurotoxicity is considered as a significant target for anti‐AD drug research and effective clinical strategy for the prevention and treatment of AD 6,7 …”

“…Accumulating evidences showed that the misfolding and aggregation of Aβ can induce mitochondrial dysfunction, oxidative stress, neuronal apoptosis, hyperphosphorylated Tau protein and lead to the progressive impairment in memory and cognition, which is involved in the pathogenesis of AD. [3][4][5] So, reducing Aβ deposition and neurotoxicity is considered as a significant target for anti-AD drug research and effective clinical strategy for the prevention and treatment of AD. 6,7 Caenorhabditis elegans (C. elegans) is a free-living, non-parasitic nematode, which has been considered as a model organism for the study of ageing and age-related diseases, including AD and Parkinson's disease.…”