Ultimately Aβ oligomers are deposited as extracellular plaques in the brain, a hallmark of AD, which contribute to neuroinflammation and neuronal death.21 The main Aβ species generated excessively in AD is Aβ1–42, which is a small ∼4.5 kDa peptide produced by the cleavage of amyloid precursor protein on neuronal membranes by β- and γ-secretases.22,23 Removal of Aβ from the extracellular space by phagocytosis into microglia and astrocytes, as well as by clearance across endothelial cells into the blood or lymph vessels, is thought to limit the build-up of the extracellular Aβ concentration. Here, PPIB is linked to Alzheimer disease.