Despite the rare occurrence of naturally occurring SNCA mutations in the general population [3], the contribution of α-synuclein to Lewy bodies in both genetically defined and idiopathic Parkinson’s disease, as well as related synucleinopathies such as dementia with Lewy Bodies (DLB) and Multiple Systems Atrophy (MSA), and the extensive validation in in vitro and in vivo model systems, places α-synuclein at the center of these human neurodegenerative diseases. This evidence concerns the gene SNCA and Lewy body dementia.