Nrf2 activation attenuates the early suppression of mitochondrial respiration due to the α-synuclein overexpression.

ABSTRACT:

Background

α-synuclein (SNCA) accumulation in the substantia nigra is one of the characteristic pathologies of Parkinson's disease (PD). A53T missense mutations in the SNCA gene has been proved to enhance the expression of SNCA and accelerate the onset of PD. Mitochondrial dysfunction in SNCA aggregation has been under debate for decades but the causal relationship remains uncertain. At a later stage of PD, the cellular dysfunctions are complicated and multiple factors are tangled. Our aim here is to investigate the mitochondrial functional changes and clarify the main causal mechanism at earlier-stage of PD.

Methods

We used the mutant A53T SNCA-expressed neuro 2a (N2a) cells without detectable cell death to investigate: 1) whether SNCA overexpression impairs the mitochondri

SUBMITTER: Fu MH 

PROVIDER: S-EPMC6138761 | biostudies-literature | 2018 Jun

REPOSITORIES: biostudies-literature