Amyloid beta-protein1-42 increases cAMP and apolipoprotein E levels which are inhibited by β1 and β2-adrenergic receptor antagonists in mouse primary astrocytes

U. Igbavboa, L. N. Johnson-Anuna, X. Rossello, T. A. Butterick, G. Y. Sun, W. Gibson Wood

Research output: Contribution to journalArticlepeer-review

26 Scopus citations


Amyloid beta-protein (Aβ) increases apolipoprotein E (apoE) levels in astrocytes which could alter lipid trafficking. The mechanism for the Aβ-induced increase in apoE levels is not well understood. It is well established that stimulation of β-adrenergic receptors (βARs) increases cAMP levels. Elevation of cAMP levels increases apoE abundance. The current study determined if Aβ1-42 stimulation of cAMP and apoE levels could be inhibited by βAR antagonists in astrocytes. We demonstrate that Aβ1-42 but not the reverse protein Aβ42-1 or Aβ1-40 stimulated cAMP formation and this stimulation was inhibited by selective βAR antagonists in mouse primary cortical astrocytes. Aβ1-42 significantly increased apoE levels which were significantly inhibited by the βAR selective antagonists with the greatest inhibition observed with the β2 antagonist. Separate lines of evidence have suggested that agonist-induced stimulation of βARs and increases in apoE abundance may serve a neuroprotective role in astrocytes. Our results indicate a potential interaction between βARs and apoE which may contribute to reducing Aβ1-42 neurotoxicity.

Original languageEnglish (US)
Pages (from-to)655-660
Number of pages6
Issue number3
StatePublished - Oct 27 2006

Bibliographical note

Funding Information:
This work was supported by grants from the National Institutes of Health AG-23524, AG-18357 and resources/facilities of the Minneapolis VA Medical Center.

Copyright 2008 Elsevier B.V., All rights reserved.


  • Alzheimer's disease
  • amyloid beta-protein
  • apolipoprotein E
  • astrocytes
  • beta-adrenergic receptors
  • cAMP


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