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Evidence-Based Complementary and Alternative Medicine
Volume 2012, Article ID 132829, 9 pages
Research Article

Aβ Damages Learning and Memory in Alzheimer’s Disease Rats with Kidney-Yang Deficiency

1Neuroscience Program, Shandong University of Traditional Chinese Medicine, Changqing University Park, Jinan 250355, China
2Qingdao Haici Medical Group, 4 Renmin Road, Qingdao 266033, China
3Institute of Acupuncture and Moxibustion, China Academy of Chinese Medical Sciences, 16 Nanxiaojie, Dongzhimeinei, Beijing 100700, China
4Department of Biomedical Sciences, Florida State University College of Medicine, 1115 West Call Street, Tallahassee, FL 32306, USA

Received 9 January 2012; Accepted 18 February 2012

Academic Editor: Shi-Bing Su

Copyright © 2012 Dongmei Qi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Previous studies demonstrated that Alzheimer’s disease was considered as the consequence produced by deficiency of Kidney essence. However, the mechanism underlying the symptoms also remains elusive. Here we report that spatial learning and memory, escape, and swimming capacities were damaged significantly in Kidney-yang deficiency rats. Indeed, both hippocampal Aβ40 and 42 increases in Kidney-yang deficiency contribute to the learning and memory impairments. Specifically, damage of synaptic plasticity is involved in the learning and memory impairment of Kidney-yang deficiency rats. We determined that the learning and memory damage in Kidney-yang deficiency due to synaptic plasticity impairment and increases of Aβ40 and 42 was not caused via NMDA receptor internalization induced by Aβ increase. β-Adrenergic receptor agonist can rescue the impaired long-term potential (LTP) in Kidney-yang rats. Taken together, our results suggest that spatial learning and memory inhibited in Kidney-yang deficiency might be induced by Aβ increase and the decrease of β2 receptor function in glia.