Introduction

Parkinson’s disease (PD) is a neurodegenerative disease caused by the progressive loss of midbrain dopaminergic neurons (mDAn). Genetic mutations affecting mDA neurons account for up to 15% of PD onsets, providing a valuable tool for studying basic pathophysiological mechanisms of the disease. One of the most relevant mutations is the A53T mutation in the SNCA gene, which causes the production of a misfolded form of alpha synuclein (αSyn), resulting in αSyn accumulation. It has been reported that PD patient neurons display a ~20% reduction of mitochondrial complex I activity. Rotenone is known to reduce mitochondrial complex I activity. Therefore testing Rotenone administration in vitro could mimic PD effect on mDAn mitochondria functionality.