Even though the exact underlying pathogenesis mechanisms are not clear, it is possible that cocaine use may cause complex dopaminergic and mitochondrial dysfunction as well as increase the intracellular aggregation of α-synuclein and tau proteins, which, respectively, lead to synucleinopathies and tauopathies, and this, in turn, would activate a cascade of pro-inflammatory elements that would cause neuroinflammation and neurodegeneration. Here, SNCA is linked to synucleinopathy.