Long-term depression links amyloid-β to the pathological hyperphosphorylation of tau
Henry B. C. Taylor, Nigel J. Emptage, Alexander Jeans
Abstract
increases glutamate release probability, thus leading to enhanced LTD induction, which in turn drives hyperphosphorylation of tau. Our data identify a mechanistic pathway linking the two critical pathogenic proteins of AD.
Topics & Concepts
HyperphosphorylationGlutamate receptorNMDA receptorNeuroscienceHippocampal formationLong-term depressionAmyloid (mycology)ChemistryTau proteinPathogenesisHippocampusDownregulation and upregulationPathologicalAlzheimer's diseaseCell biologyBiologyAMPA receptorReceptorPhosphorylationDiseaseBiochemistryMedicineInternal medicineImmunologyInorganic chemistryGeneAlzheimer's disease research and treatmentsNeuroscience and Neuropharmacology ResearchMemory and Neural Mechanisms