Memory loss caused by beta-amyloid protein is rescued by a beta(3)-adrenoceptor agonist

作者：Gibbs Marie E^*; Maksel Danuta; Gibbs Zoe; Hou Xu; Summers Roger J; Small David H

来源：Neurobiology of Aging, 2010, 31(4): 614-624.

DOI：10.1016/j.neurobiolaging.2008.05.018

• Chick
• Amyloid
• Abeta
• Dementia
• Memory
• Alzheimer's disease
• Neurotoxicity
• Passive avoidance

Accumulation of the neurotoxic beta-amyloid protein (A beta) in the brain is a key step in the pathogenesis of Alzheimer's disease (AD) Although transgenic mouse models of AD have been developed, there is a clear need for a validated animal model of A beta-induced amnesia which can be used for toxicity testing and drug development Intracranial injections of A beta(1-42) impaired memory in a single trial discriminative avoidance learning task in chicks Memory inhibition was closely associated with the state of aggregation of the A beta peptide, and a scrambled-sequence of A beta(1-42) peptide failed to impair memory A beta had little effect on labile (short-term and intermediate) memory, but blocked consolidation of memory into long-term storage mimicking the type of anterograde amnesia that occurs in early AD Since noradrenaline exerts a modulatory influence on labile memory in the chick, we examined the effects of two beta-adrenoceptor (AR) agonists on A beta-induced amnesia A beta(3)-AR agonist (CL316243), but not a beta(2)-AR agonist, rescued A beta-induced memory loss, suggesting the need for further studies on the role of beta(3)-ARs in AD.

• 出版日期2010-4