Abstract
The aggregation of α-synuclein is one on the key pathogenic events in Parkinson’s disease. In the present study, we investigated the inhibitory capacities of stilbenes against α-synuclein aggregation and toxicity. Thioflavin T fluorescence, transmission electronic microscopy, and SDS-PAGE analysis were performed to investigate the inhibitory effects of three stilbenes against α-synuclein aggregation: piceatannol, ampelopsin A, and isohopeaphenol. Lipid vesicle permeabilization assays were performed to screen stilbenes for protection against membrane damage induced by aggregated α-synuclein. The viability of PC12 cells was examined using an MTT assay to assess the preventive effects of stilbenes against α-synuclein-induced toxicity. Piceatannol inhibited the formation of α synuclein fibrils and was able to destabilize preformed filaments. It seems to induce the formation of small soluble complexes protecting membranes against α-synuclein-induced damage. Finally, piceatannol protected cells against α-synuclein-induced toxicity. The oligomers tested (ampelopsin A and hopeaphenol) were less active.
Highlights
Parkinson’s disease (PD) is the second most encountered neurodegenerative disorder afterAlzheimer’s disease [1]
Finding molecules to prevent the aggregation of α-synuclein could be a therapeutic goal in PD and, and a tetramer—were tested for their capacity to inhibit α‐
A tetramer—were tested for their capacity to inhibit α-synuclein fibril formation
Summary
Parkinson’s disease (PD) is the second most encountered neurodegenerative disorder afterAlzheimer’s disease [1]. One of the major hallmarks of PD and some other related disorders is the presence of intracellular inclusions known as Lewy bodies that develop inside nerve cells. They are mainly constituted of α-synuclein fibrils [2,3]. While deposits of α-synuclein fibrils in Lewy bodies are a ubiquitous pathological feature of PD [2], growing evidence has shown that the most toxic species are the soluble α-synuclein oligomeric intermediates [7,8] These species could target biological membranes, possibly forming structures with pore-like morphologies that may induce toxicity by the disruption of the cellular membranes [9,10]
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