Department of Neurology and Neurobiology of Aging, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan.
J Neurochem. 2011 Apr;117(1):19-28. doi: 10.1111/j.1471-4159.2011.07187.x. Epub 2011 Feb 9.
The pathogenesis of Alzheimer's disease involves the progressive accumulation of amyloid β-protein (Aβ). Recent studies using synthetic Aβ peptides, a cell culture model, Aβ precursor protein transgenic mice models suggest that pre-fibrillar forms of Aβ are more deleterious than extracellular fibril forms. Recent findings obtained using synthetic Aβ peptides and human samples indicated that low-n oligomers (from dimers to octamers) may be proximate toxins for neuron and synapse. Here, we review the recent studies on the soluble oligomers, especially low-n oligomers in Alzheimer's disease.
阿尔茨海默病的发病机制涉及淀粉样β-蛋白（Aβ）的进行性积累。最近使用合成 Aβ 肽、细胞培养模型、Aβ 前体蛋白转基因小鼠模型的研究表明，Aβ 的预纤维形式比细胞外纤维形式更具危害性。最近使用合成 Aβ 肽和人类样本获得的发现表明，低聚物（从二聚体到八聚体）可能是神经元和突触的近毒物质。在这里，我们回顾了最近关于可溶性低聚物，特别是阿尔茨海默病中低聚物的研究。
