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 language||English (US)|
|Number of pages||10|
|Journal||Journal of Biological Chemistry|
|State||Published - Apr 12 2013|
ASJC Scopus subject areas
- Molecular Biology
- Cell Biology