Molecular Mechanisms of Amyloid Oligomers Toxicity

被引:316
作者
Kayed, Rakez [1 ]
Lasagna-Reeves, Cristian A. [1 ]
机构
[1] Univ Texas Med Branch, Dept Neurol, George P & Cynthia Woods Mitchell Ctr Neurodegene, Galveston, TX 77555 USA
关键词
Alzheimer's disease; amyloid; amyloid oligomers; amyloid toxicity; P75 NEUROTROPHIN RECEPTOR; A-BETA OLIGOMERS; INTRANEURONAL A-BETA-42 ACCUMULATION; NICOTINIC ACETYLCHOLINE-RECEPTOR; ALZHEIMERS-DISEASE PATHOLOGY; ATOMIC-FORCE MICROSCOPY; HUMAN CORTICAL-NEURONS; BLOOD-BRAIN-BARRIER; PRECURSOR PROTEIN; TRANSGENIC MICE;
D O I
10.3233/JAD-2012-129001
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Amyloid oligomers have emerged as the most toxic species of amyloid-beta (A beta). This hypothesis might explain the lack of correlation between amyloid plaques and memory impairment or cellular dysfunction. However, despite the numerous published research articles supporting the critical role A beta oligomers in synaptic dysfunction and cell death, the exact definition and mechanism of amyloid oligomers formation and toxicity still elusive. Here we review the evidence supporting the many molecular mechanisms proposed for amyloid oligomers toxicity and suggest that the complexity and dynamic nature of amyloid oligomers may be responsible for the discrepancy among these mechanisms and the proposed cellular targets for amyloid oligomers.
引用
收藏
页码:S67 / S78
页数:12
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