APOB and hyperinsulinemic hypoglycemia, familial, 4: Using the mucopolysaccharidosis type IIIA (MPS-IIIA) murine model, a neurological MPS caused by the N-sulfoglucosamine sulfohydrolase deficiency (Table 1), studies on a chimeric sulphamidase, containing a signal peptide from Apolipoprotein B (ApoB-BD), showed a highly secreted iduronate-2-sulphatase (IDS) and efficient BBB transcytosis and restoration of sulphamidase activity in the brain of treated mice (Sorrentino et al., 2013).