Parkinson’s disease (PD) is characterized by the selective degeneration of dopaminergic neurons in the substantia nigra, yet its underlying molecular mechanism remains unclear. Excessive dopamine oxidation is a pathological hallmark observed in various forms of PD. Mutations in PD-associated genes, such as DJ-1, underscore the critical role of mitochondrial bioenergetics in PD pathogenesis, potentially causing mitochondrial oxidant stress and increased dopamine oxidation. Given that DJ-1 KO and LoF mutations in the gene are associated with Parkinsonism, the molecular mechanism of DJ-1's involvement is being investigated in DJ-1 KO hiPSC-derived dopaminergic neurons. DJ-1 KO neurons exhibit a number of morphological and functional defects at the synapse, which could either be driven directly by DJ-1's interaction with synaptic proteins or, indirectly, by the effects of its loss on mitochondrial metabolism. In order to validate either of these hypothesis and map the physiological interactions of DJ-1, disrupted upon its KO, we have performed IP-MS experiments using endogenous untagged DJ-1 as the bait, with a particular interest towards its synaptic interactome in dopaminergic neurons.