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Memory loss caused by -amyloid protein is rescued by a3-adrenoceptor agonist

Citation

Gibbs, ME and Maksel, D and Gibbs, Z and Hou, X and Summers, RJ and Small, DH, Memory loss caused by s-amyloid protein is rescued by as3-adrenoceptor agonist, Neurobiology of Aging, 31, (4) EJ ISSN 0197-4580 (2008) [Refereed Article]

DOI: doi:10.1016/j.neurobiolaging.2008.05.018

Abstract

Accumulation of the neurotoxic β-amyloid protein (Aβ) 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 Aβ-induced amnesia which can be used for toxicity testing and drug development. Intracranial injections of Aβ1-42 impaired memory in a single trial discriminative avoidance learning task in chicks. Memory inhibition was closely associated with the state of aggregation of the Aβ peptide, and a scrambled-sequence of Aβ1-42 peptide failed to impair memory. Aβ 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 β-adrenoceptor (AR) agonists on Aβ-induced amnesia. A β3-AR agonist (CL316243), but not a β2-AR agonist, rescued Aβ-induced memory loss, suggesting the need for further studies on the role of β3-ARs in AD. © 2008 Elsevier Inc.

Item Details

Item Type:Refereed Article
Research Division:Medical and Health Sciences
Research Group:Neurosciences
Research Field:Central Nervous System
Objective Division:Health
Objective Group:Clinical Health (Organs, Diseases and Abnormal Conditions)
Objective Field:Neurodegenerative Disorders Related to Ageing
Author:Small, DH (Professor David Small)
ID Code:55555
Year Published:2008
Web of Science® Times Cited:26
Deposited By:Menzies Institute for Medical Research
Deposited On:2009-03-11
Last Modified:2010-06-04
Downloads:0

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