Remarkably, several genes identified in GWAS, including PICALM, known for its involvement in endocytosis facilitating the internalization of cell receptors, have variants that can increase the Aβ accumulation in the brain, exacerbating the AD pathology [161], as shown by triggering clathrin-mediated endocytosis through its interaction with LRP1 [162]. This evidence concerns the gene LRP1 and Alzheimer disease.