Figure 1.

Hypothetical schematic representation of the two possible series of molecular events intervening either between synaptic α-synuclein deposition and the induction of mitochondrial dysfunction (a) or between mitochondrial functional deficits and accumulation of α-synuclein at the synapse (b). Please note that in both of the two situations, Ca²⁺ rise and production of oxidative stress mediators are pivotally involved in the interconnection between mitochondrial impairment and α-synuclein synaptic pathology.