Β2 adrenergic receptor, protein kinase a (PKA) and c-Jun N-terminal kinase (JNK) signaling pathways mediate tau pathology in alzheimer disease models

Abstract

Background: Accumulating evidence indicates that βreceptors (βAR) may be involved in Alzheimer disease (AD) pathology and that amyloid βpeptide (Aβ) may interact with β2AR independently of presynaptic activities. Results: β2AR, PKA, and JNK mediate Aβ-induced phosphorylation of tau in vivo and in vitro. Conclusion: An Aβ-β2AR signaling is involved in tau pathology in AD. Significance: This work indicates a potential mechanism for altering AD pathology by blocking β2ARs. © 2013 by The American Society for Biochemistry and Molecular Biology, Inc.