Effects of amyloid β-protein on hippocampal long-term potentiation.
- Author:
Jun-Fang ZHANG
1
;
Dong YANG
;
Jin-Shun QI
Author Information
1. Department of Physiology, Key Laboratory for Cellular Physiology of Ministry of Education, Shanxi Medical University, Taiyuan 030001, China.
- Publication Type:Journal Article
- MeSH:
Alzheimer Disease;
physiopathology;
Amyloid beta-Peptides;
physiology;
Animals;
Hippocampus;
physiology;
Humans;
Learning Disorders;
physiopathology;
Long-Term Potentiation;
physiology;
Memory Disorders;
physiopathology;
Neuronal Plasticity;
Synapses;
physiology
- From:
Acta Physiologica Sinica
2010;62(6):479-488
- CountryChina
- Language:Chinese
-
Abstract:
The accumulation of amyloid β-protein (Aβ) plaques is identified as a major pathological feature of Alzheimer's disease (AD). Recent studies show that soluble species of Aβ are involved in the early memory dysfunction long before neurodegenerative changes. However, the mechanism underlying the neurotoxicity of soluble Aβ is still unclear. Long-term potentiation (LTP) has been thought as an important cellular model of synaptic plasticity for many years. The studies on the hippocampal LTP and Aβ, especially those using AD transgenic models, provided more evidence for the Aβ-induced dysfunction of learning and memory. Based on the recent researches on AD, this article reviewed the effects of Aβ, especially soluble Aβ and its active fragments, on the hippocampal LTP. The possible mechanisms by which Aβ impairs hippocampal LTP are also discussed.
