Regarding the effect of AD pathological markers on AQP4, a study with multiple transgenic mouse models of Aβ deposition indicated that the number of astrocyte terminal protrusions and localized AQP4 were significantly reduced in mice that developed cerebral amyloid angiopathy (CAA; associated with the accumulation of Aβ in the brain vasculature, a disease present in the majority of patients with AD) (Wilcock et al., 2009). This evidence concerns the gene AQP4 and cerebral amyloid angiopathy.