The association between Aβ and CysC was shown to prevent Aβ accumulation and fibrillogenesis in experimental systems, arguing that CysC plays a protective role in the pathogenesis of AD in humans and explains why a decrease in CysC concentration caused by the CST3 polymorphism or by specific presenilin 2 mutations, can lead to the development of the disease. Here, CST3 is linked to Alzheimer disease.