Journal
MOLECULES
Volume 22, Issue 8, Pages -Publisher
MDPI AG
DOI: 10.3390/molecules22081293
Keywords
alpha-synuclein; trehalose; transduced PC12 cell; Parkinson's disease
Funding
- National Natural Science Foundation of China [21374022, 81572713]
- Shanghai Natural Science Foundation [14ZR1401500]
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Fibrillar accumulation of A53T mutant alpha-synuclein (A53T-AS) in Lewy bodies is a symptom of Parkinsonism. Inhibitions of the overexpression and fibrillar aggregation of alpha-synuclein (AS) in vivo could be a promising strategy for treating Parkinson's disease (PD). In this study, at concentrations lower than 1 mM, trehalose decreased the A53T-AS expression level in transduced PC12 cells. Although H2O2 and aluminum ions increased the expression level and neurotoxicity of A53T-AS in cells, proper trehalose concentrations inhibited the event. These studies adequately prove that trehalose at an appropriate dose would be potentially useful for PD treatment.
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