We first focused on an estimation of enzymatic activities of lysosomal hydrolases encoded by genes causing the mucopolysaccharidosis (IDUA) and sphingolipidoses (GCase, ASMase, GALC, GLA) and additional glycogen storage disorders (glycogenosis) (GAA) in patients with late-onset SCZ. This evidence concerns the gene SMPD1 and sphingolipidosis.