It is now well established that there is a subset of LRRK2-associated PD patients who do not display Lewy pathology but may have aggregates of other proteins, such as tau and TDP-43 (Zimprich et al., 2004; Ling et al., 2013; Kalia et al., 2015; Henderson et al., 2019b), suggesting that PD due to LRRK2 dysfunction may occur independently of α-synuclein aggregation. This evidence concerns the gene SNCA and Parkinson disease.