Furthermore, chronically high levels of Aβ have been shown to cause immune tolerance or hypo-responsiveness to Aβ epitopes in APP-transgenic mice (58) and given the early presence of cerebral amyloid angiopathy (CAA) in our model (59), it is possible that Aβ species, including oligomeric forms, might drain constantly into the periphery inducing long-term immune exhaustion. This evidence concerns the gene APP and cerebral amyloid angiopathy.