Among these, variants affecting CLU (APOJ) or CR1 (complement component 3b/4b receptor 1), being involved in the clearance of Aβ have been associated to AD [72] and heterozygous missense mutations in TREM2 (triggering receptor myeloid 2 cells) have been described to increase by 3-fold the risk of AD [73]. This evidence concerns the gene TREM2 and Alzheimer disease.