4.5 Article

Blocking β2-adrenergic receptor attenuates acute stress-induced amyloid β peptides production

期刊

BRAIN RESEARCH
卷 1317, 期 -, 页码 305-310

出版社

ELSEVIER SCIENCE BV
DOI: 10.1016/j.brainres.2009.12.087

关键词

Alzheimer's disease; Acute stress; beta 2-adrenergic receptor; Amyloid beta

资金

  1. Shandong Province Nature Science Foundation [Y2007C123]
  2. National Natural Science Foundation of China [30870884]

向作者/读者索取更多资源

Environmental factors play an important role in the Alzheimer's disease (AD) development and stress may accelerate the progression of AD. beta-adrenergic receptors are activated by stress and may influence different aspects of cognitive function. So, it was hypothesized that stress may accelerate the pathological progression of AD by the activation of beta(2)-adrenergic receptor (beta(2)-AR). We have investigated the role of acute stress and activation of beta(2)-AR in amyloid beta (A beta) peptides production in a mouse model of acute restraint stress. Injections of the beta(2)-AR-selective agonist clenbuterol hydrochloride enhanced the production of acute stress-induced A beta peptides production; the beta(2)-AR-selective antagonist ICI 118,551 reduced A beta peptides production. It is suggested that acute stress induces abnormal activation of beta(2)-AR which subsequently enhances A beta peptides (the main neuropathological hallmarks of AD) production possibly resulting in the onset of AD. The findings indicate that new therapeutic strategies designed to blocking beta(2)-AR might be valuable for the prevention and treatment of AD. (C) 2010 Elsevier B.V. All rights reserved.

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