Ever since α-synuclein (αS) was identified to be a primary component of Lewy bodies and Lewy neurites (1) in synucleinopathies, such as Parkinson’s disease (PD), dementia with Lewy Bodies (DLB) and multiple-system atrophy (MSA), the endeavors of many laboratories have coalesced around elucidating αS native structure, physiological function, aggregation propensity and cell toxicity. This evidence concerns the gene SNCG and Lewy body dementia.