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

Dayong Wang, Qin Fu, Yuan Zhou, Bing Xu, Qian Shi, Benedict Igwe, Lucas Matt, Johannes W. Hell, Elena V. Wisely, Salvatore Oddo, Yang K. Xiang

Research output: Contribution to journalArticle

51 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)10298-10307
Number of pages10
JournalJournal of Biological Chemistry
Volume288
Issue number15
DOIs
StatePublished - Apr 12 2013
Externally publishedYes

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ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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