ITGAM and Alzheimer disease: Fibrin–Aβ fibrils are not accessible to breakdown by plasmin, activate FXII, and inhibit microglia/macrophages scavenging through CD11b silencing.26Blockage of fibrin–Aβ interaction (as demonstrated through RU-505) could pave the way to overcome the failures in disease-modifying therapies for neurodegeneration.27Finally, FXIIa, high molecular-weight kininogen, and kallikrein activities, all thrombo-inflammatory mediators, are detected in AD and their effects can be experimentally attenuated by FXII depletion.28