The major pathologies of these dementias arising from secondary protein aggregation [2] are characterized as: amyloidopathies, amyloid plaques accumulating from secreted Amyloid-β peptides cleaved from the transmembrane amyloid precursor protein (APP); tauopathies, accumulation of hyperphosphorylated tau into neuropil threads and/or neurofibrillary tangles [3]; and α-synucleinopathies, accumulation of α-synuclein fibrils into Lewy bodies. Here, SNCA is linked to synucleinopathy.