Aβ Damages Learning and Memory in Alzheimer's Disease Rats with Kidney-Yang Deficiency. (8th May 2012)

• Record Type: Journal Article
• Authors: Qi, Dongmei; Qiao, Yongfa; Zhang, Xin; Yu, Huijuan; Cheng, Bin; Qiao, Haifa
• Other Names: Su Shi-Bing Academic Editor.
• Is Part Of: Evidence-based complementary and alternative medicine. Volume 2012(2012)
• Publication Date: 2012-05-08
• Subjects: Alternative medicine -- Periodicals; 615.505
• DOI: 10.1155/2012/132829
• Languages: English
• ISSNs: 1741-427X

Abstract

Abstract : 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 A β 40 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 A β 40 and 42 was not caused via NMDA receptor internalization induced by A β 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 A β increase and the decrease of β 2 receptor function in glia.