In Alzheimer’s Disease, in which exosomes are loaded with amyloid-β (Aβ) peptides and with molecules involved in its synthesis, degradation and aggregation, exogenous exosomes expressing surface proteins such as the cellular prion protein (PrPc), a receptor for Aβ, can sequester Aβ and counteract its negative effects on plasticity (An et al., 2013). The gene discussed is PRNP; the disease is Alzheimer disease.