It has been hypothesized that pathological alpha-synuclein accumulation leads to sequestration in aggregates, with the consequent depletion of the pool and the loss of function associated with normal physiological alpha-synuclein, contributing to alterations in neurotransmission that are associated with the progression of synucleinopathies [22,23,24,25]. This evidence concerns the gene SNCA and synucleinopathy.