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1
Amyloid-β protein oligomerization and the importance of tetramers and dodecamers in the aetiology of Alzheimer's disease.淀粉样β蛋白寡聚化以及四聚体和十二聚体在阿尔茨海默病发病机制中的重要性。
Nat Chem. 2009 Jul;1(4):326-31. doi: 10.1038/nchem.247.
2
Beta-amyloid monomers are neuroprotective.β-淀粉样蛋白单体具有神经保护作用。
J Neurosci. 2009 Aug 26;29(34):10582-7. doi: 10.1523/JNEUROSCI.1736-09.2009.
3
Intraneuronal beta-amyloid accumulation in the amygdala enhances fear and anxiety in Alzheimer's disease transgenic mice.杏仁核内的神经元β-淀粉样蛋白积累增强了阿尔茨海默病转基因小鼠的恐惧和焦虑。
Biol Psychiatry. 2010 Mar 15;67(6):513-21. doi: 10.1016/j.biopsych.2009.06.015. Epub 2009 Aug 7.
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Soluble oligomers of amyloid Beta protein facilitate hippocampal long-term depression by disrupting neuronal glutamate uptake.β-淀粉样蛋白的可溶性寡聚体通过破坏神经元谷氨酸摄取来促进海马体长期抑制。
Neuron. 2009 Jun 25;62(6):788-801. doi: 10.1016/j.neuron.2009.05.012.
5
Role of amyloid-beta glycine 33 in oligomerization, toxicity, and neuronal plasticity.淀粉样β蛋白甘氨酸33在寡聚化、毒性和神经元可塑性中的作用。
J Neurosci. 2009 Jun 10;29(23):7582-90. doi: 10.1523/JNEUROSCI.1336-09.2009.
6
Amyloid beta protein: Abeta40 inhibits Abeta42 oligomerization.淀粉样β蛋白:β淀粉样蛋白40抑制β淀粉样蛋白42寡聚化。
J Am Chem Soc. 2009 May 13;131(18):6316-7. doi: 10.1021/ja8092604.
7
Amyloid beta mediates memory formation.β淀粉样蛋白介导记忆形成。
Learn Mem. 2009 Mar 24;16(4):267-72. doi: 10.1101/lm.1310209. Print 2009 Apr.
8
Cellular prion protein mediates impairment of synaptic plasticity by amyloid-beta oligomers.细胞朊蛋白介导β-淀粉样寡聚体对突触可塑性的损害。
Nature. 2009 Feb 26;457(7233):1128-32. doi: 10.1038/nature07761.
9
Picomolar amyloid-beta positively modulates synaptic plasticity and memory in hippocampus.皮摩尔浓度的β-淀粉样蛋白正向调节海马体中的突触可塑性和记忆。
J Neurosci. 2008 Dec 31;28(53):14537-45. doi: 10.1523/JNEUROSCI.2692-08.2008.
10
Frequent amyloid deposition without significant cognitive impairment among the elderly.老年人中频繁出现淀粉样蛋白沉积但无明显认知障碍。
Arch Neurol. 2008 Nov;65(11):1509-17. doi: 10.1001/archneur.65.11.1509.

β-淀粉样寡聚体:在阿尔茨海默病中作为关键神经毒素的可能作用。

Amyloid-beta oligomers: possible roles as key neurotoxins in Alzheimer's Disease.

作者信息

Lublin Alex L, Gandy Sam

机构信息

Department of Neurology, Mount Sinai Alzheimer's Disease Research Center, Mount Sinai School of Medicine, New York, NY, USA.

出版信息

Mt Sinai J Med. 2010 Jan-Feb;77(1):43-9. doi: 10.1002/msj.20160.

DOI:10.1002/msj.20160
PMID:20101723
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3306842/
Abstract

Alzheimer's disease is the most common form of senile dementia. Although the amyloid-beta peptide was identified in 1984 as the major constituent of the senile plaques that characterize the disease, accumulating evidence indicates that the plaque density does not correspond well to the concurrent disease state. In order to resolve this disconnect, a number of recent studies have shifted away from the senile plaque and classical fibrillar forms of amyloid toward a less well structured species as the proximate neurotoxic factor underlying cognitive failure in Alzheimer's disease: soluble amyloid-beta peptide oligomer (also known as the amyloid-beta peptide-derived diffusible ligand). Paradoxically, several studies in the last 2 years have shown that picomolar levels of amyloid-beta peptide have neutral activity or perhaps even an essential role in learning and memory. Here we highlight some of the key observations underlying the growing focus on the amyloid-beta peptide oligomer.

摘要

阿尔茨海默病是最常见的老年痴呆形式。尽管β-淀粉样肽在1984年被确定为该疾病特征性老年斑的主要成分,但越来越多的证据表明,斑块密度与同时存在的疾病状态并不十分相符。为了解决这一脱节问题,最近的一些研究已从老年斑和经典的淀粉样纤维形式转向一种结构较不完善的物质,将其视为阿尔茨海默病认知功能衰退的直接神经毒性因子:可溶性β-淀粉样肽寡聚体(也称为β-淀粉样肽衍生的可扩散配体)。矛盾的是,过去两年的几项研究表明,皮摩尔水平的β-淀粉样肽具有中性活性,甚至可能在学习和记忆中起重要作用。在此,我们重点介绍一些使人们越来越关注β-淀粉样肽寡聚体的关键观察结果。

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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99a7/3306842/494375649852/nihms359076f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99a7/3306842/c9914fd93ba3/nihms359076f2.jpg
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