Recent studies have highlighted that cystatin C shows a controversial influence in the pathology of AD; on the one hand, it appears to control the levels of Aβ that bind directly to Aβ and inhibit its aggregation, but on the other hand, as a substrate for cathepsin B protease, it appears to be competitive for Aβ degradation [142,143,144]. Here, CST3 is linked to Alzheimer disease.