In a mouse Alzheimer’s disease (AD) model, ablation of CALB1 was found to exacerbate pathogenesis [38], and in both healthy and AD human patient tissues, its downregulation was found to be correlated with that of chitotriosidase (CHIT1) that is involved with AD pathogenesis [39], demonstrating its protective role against neurodegenerative diseases. This evidence concerns the gene CHIT1 and early-onset autosomal dominant Alzheimer disease.