The clearance of protein aggregates by autophagic or proteasomal degradation, the sequestration of α-synuclein in mature Lewy bodies, and the extrusion of toxic aggregates into the extracellular matrix for uptake by neighboring glia (or removal by glymphatic clearance) all conceivably impact the course of Lewy body disease but are not adequate to fully contain the spread of protein aggregates. This evidence concerns the gene SNCA and Lewy body dementia.