To target the role of lysosomes in Aβ42 detoxification as a putative therapeutic approach, we used Z-Phe-Ala-diazomethylketone (PADK; 18 mg/kg/day, 11 days; intraperitoneally (i.p.)) to increase CatB, a cathepsin family member that proteolytically cleaves Aβ42 into less amyloidogenic peptides [13,34] and produces the shorter Aβ38 shown to correspond with Aβ42 clearance in AD transgenic mice [14]. This evidence concerns the gene TYRP1 and Alzheimer disease.