Issue Archive

[Effects of amyloid β-protein on hippocampal long-term potentiation.] [Ariticle in Chinese]

ZHANG Jun-Fang

Department of Physiology, Key Laboratory for Cellular Physiology of Ministry of Education, Shanxi Medical University, Taiyuan 030001, China

Abstract

The accumulation of amyloid -protein (Aβ) plaques is identified as a major pathological feature of Alzheimer’s disease(AD). Recent studies show that soluble species of Aβare involved in the early memory dysfunction long before neurodegenerativechanges. However, the mechanism underlying the neurotoxicity of soluble Aβis still unclear. Long-term potentiation (LTP) has beenthought as an important cellular model of synaptic plasticity for many years. The studies on the hippocampal LTP and Aβ, especiallythose using AD transgenic models, provided more evidence for the Aβ-induced dysfunction of learning and memory. Based on the recentresearches on AD, this article reviewed the effects of Aβ, especially soluble Aβ and its active fragments, on the hippocampal LTP. Thepossible mechanisms by which Aβimpairs hippocampal LTP are also discussed.

Key words: Alzheimer’s disease; amyloid ;β-protein; long-term potentiation

Received: 2010-08-06　　Accepted: 2010-10-11

Corresponding author: 　　E-mail:

Citing This Article：

ZHANG Jun-Fang. [Effects of amyloid β-protein on hippocampal long-term potentiation.] [Ariticle in Chinese] . Acta Physiol Sin 2010; 62 (6): 479-488 (in Chinese with English abstract).