However, a critical role for kinins in AD cognitive and cerebrovascular deficits has never been confirmed in a clinically relevant transgenic mouse model that recapitulates a wide array of AD landmarks (cerebrovascular, cognitive, neuroinflammation and amyloid pathologies), such as mice that overproduce chronically Aβ peptide through transgene expression of familial AD-related mutated human amyloid precursor protein (hAPP) [21]. This evidence concerns the gene APP and Alzheimer disease.