However, our evaluation of the cytotoxic effects of amyloid degradation products formed from various proteins (lysozyme, beta-2-microglobulin, and abeta peptide (1-42), associated with lysozyme and hemodialysis amyloidosis as well as Alzheimer’s disease, respectively) suggests that CTSB can degrade amyloid fibrils without forming low-molecular-weight products with higher cytotoxicity (Fig. 5). This evidence concerns the gene CTSB and early-onset autosomal dominant Alzheimer disease.