ApoE transports amylin from blood to brain influencing brain β‐amyloid level

Human amylin forms parenchymal complexes with apoE, exacerbating Aβ pathology, especially in apoE4⁺ mice. In the presence of non-amyloidogenic (mouse) amylin, apoE4 does not lead to Aβ or amylin accumulation. The lack of amylin and Aβ in EKO-HIP brains implicates apoE as a molecular carrier for both proteins at the blood-brain barrier. Immunoprecipitation results suggest differential strength of apoE-amylin interactions as a result of apoE isoform. Future studies investigating the specific mechanisms regulating amylin-apoE-Aβ interactions are warranted.