SNCA and lysosomal storage disease: Our findings of aberrant phosphorylated-α-synuclein accumulation in α-Gal A-deficient mouse brain (Figures 5, 6 and 7) suggest that its metabolism relies on, at least in part, functional α-Gal A. Previous studies have indicated the importance of intact ALP function for the efficient degradation of α-synuclein, including several experimental models of lysosomal storage disorders [24, 28–31, 44–47].