Abstract
It has been recently suggested that resveratrol can be effective in slowing down Alzheimer's disease (AD) development. As reported in many biochemical studies, resveratrol seems to exert its neuro-protective role through inhibition of β-amyloid aggregation (Aβ), by scavenging oxidants and exerting anti-inflammatory activities. In this paper, we demonstrate that resveratrol is cytoprotective in human neuroblastoma cells exposed to Aβ and or to Aβ-metal complex. Our findings suggest that resveratrol acts not through anti-aggregative pathways but mainly via its scavenging properties.
Highlights
IntroductionThe underlying causes of Alzheimer’s disease (AD) are still debated, two pathological hallmarks have been identified: senile plaques (SPs) and neurofibrillary tangles (NTFs)
Alzheimer’s disease (AD) is one of the most common form of dementia worldwide
It has been reported that resveratrol can extend the lifespan in several organisms [31,32,33] and the compound has gathered great interest as anti-aging molecule
Summary
The underlying causes of AD are still debated, two pathological hallmarks have been identified: senile plaques (SPs) and neurofibrillary tangles (NTFs). The latter are formed by hyperphosphorilation and abnormal deposition of tau (t) protein. SPs consist of deposits of b-amyloid protein (Ab) mainly. Ab derives from proteolitical cleavage of the amyloid precursor protein (APP) by three enzymes: a-, b- and c-secretase. When APP is metabolized by b- and c-secretase, Ab1–40 and the more toxic form Ab1–42 are produced; a phenomenon that is known as the ‘‘amyloidogenic pathway’’ [1]. Even though SPs are the most evident AD hallmark, recent reports highlight that Ab oligomers, because of their potent synaptotoxicity, play a crucial role in AD onset and development [3,4,5]
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