While it is possible that soluble oligomeric protein or other toxic species are still present in these atypical cases, the non-appearance of typical Lewy pathology composed of insoluble fibrillar α-synuclein, or neurofibrillary tangles composed of tau, suggest that inclusion pathology may be a by-product of LRRK2-PD pathogenesis rather than a required element. This evidence concerns the gene LRRK2 and Parkinson disease.