Pathologically, PD-GBA cases are characterized by limbic or neocortical Lewy body deposition (48), and colocalization of glucocerebrosidase with Lewy bodies in these GBA mutation carriers has been demonstrated (49), supporting the theory that mutant glucocerebrosidase may contribute directly to increased α-synuclein aggregation (50, 51). The gene discussed is SNCA; the disease is Parkinson disease.