ApoER2-Dab1 disruption as the origin of pTau-related neurodegeneration in sporadic Alzheimer's disease.
Christopher E RamsdenDaisy ZamoraMark S HorowitzJahandar JahanipourGregory S KeyesXiufeng LiHelen C MurrayMaurice A CurtisRichard L M FaullAndrea SedlockDragan MaricPublished in: medRxiv : the preprint server for health sciences (2023)
Findings support the RAAAD-P-LTP hypothesis, a unifying model that implicates dendritic ApoER2-Dab1 disruption as the major driver of both pTau accumulation and neurodegeneration in sAD. This model provides a new conceptual framework to explain why specific neurons degenerate and identifies RAAAD-P-LTP pathway components as potential mechanism-based biomarkers and therapeutic targets for sAD.