The herein-reported lack of changes in microglia of APPPS1.Il12b−/− versus APPPS1 mice in light of the pronounced loss of mature oligodendrocytes and impaired myelin integrity may, thus, indicate that the reduction of amyloid upon IL-12 deficiency is rather a result of the inhibition of the AD-specific IL-12-dependent disintegration of myelin (driving enhanced Aβ deposition) than a consequence of an increase in microglial phagocytosis. This evidence concerns the gene IL12B and Alzheimer disease.