The increased expression of B1R in reactive astrocytes surrounding Aβ plaques in the hippocampus of 10-month-old APP mice (J20 line), and the ability of B1R antagonism to reduce amyloidosis and cerebrovascular and memory deficits, serve as evidence for the harmful role of inducible B1R in AD neuroinflammation [30]. This evidence concerns the gene BDKRB1 and Alzheimer disease.