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Abstract

Lewy bodies comprised of aggregated alpha synuclein (αSyn) protein are a pathological hallmark of the Parkinson's disease (PD). Increased oxidative stress, mitochondrial dysfunction and synaptic loss are also features of the PD brain. NRF2 regulates the antioxidant response pathway and has been shown to be neuroprotective in many models of neurodegenerative diseases. Dimethyl fumarate (DMF) is a NRF2 activator that is FDA approved for treatment of multiple sclerosis making it an attractive candidate to be repurpose for use in PD. Here we investigate the antioxidant, mitochondrial and synaptic effects of DMF in neurons isolated from the A53T αSyn mouse model of synucleinopathy.

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