Alzheimer disease makes new blood contacts

Abstract

In this issue of Blood, Chen and colleagues demonstrate an unanticipated role for the contact system in a murine model of Alzheimer disease (AD). The study bolsters the key role of vascular dysfunction in AD by identifying factor XII (FXII) activation as a new molecular player in AD pathogenesis through mechanisms linked to cerebral fibrin deposition, neuroinflammation, and neuronal damage.