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 Kevin Xiang

Research output: Contribution to journalArticle

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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

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ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology
  • Molecular Biology

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