Factor XII deletion mitigates cerebral microbleed load but not hemodynamic dysfunction in the arcAβ mice

Cerebrovascular dysfunction and a prothrombotic state have been found in patients with Alzheimer’s disease (AD). The factor XII (FXII)-driven activated contact system has been implicated in the vascular pathology and inflammation in AD patients and AD mouse models. Here we investigated the effect of genetic deletion of FXII on AD-related vascular dysfunction using magnetic resonance imaging (MRI). AD mouse line ArcAβ, arcAβ/FXII-/-, FXII-/- and non-transgenic littermates  of 17 months of age (n = 40) were assessed for 1) cerebral microbleeds (CMB) load using susceptibility weighted imaging (SWI) MRI, 2) cerebral blood flow (CBF) using arterial spin labeling, and 3) vascular reactivity by estimating changes in cerebral blood volume (∆CBV) during hypercapnic stimulus using acetazolamide.