Therefore, together with our present results, we propose that, in a pathological condition like AD, oligomeric Aβ firstly triggers a rapid and potent inflammation and subsequently fibrillar Aβ sustains a chronic inflammatory environment, which suppresses the activation of phagocytic machinery, thereby affecting the ability of microglia to handle potentially toxic compounds, inhibiting clearance of fAβ and plaques, inducing a secondary immune response, and in turn aggravating brain inflammation. This evidence concerns the gene FANCB and Alzheimer disease.