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阿尔茨海默病的转基因小鼠模型:作为治疗干预工具的更好模型的开发。

Transgenic mouse models of Alzheimer disease: developing a better model as a tool for therapeutic interventions.

机构信息

School of Natural Sciences, University of California, Merced, CA 95343, USA.

出版信息

Curr Pharm Des. 2012;18(8):1131-47. doi: 10.2174/138161212799315786.

DOI:10.2174/138161212799315786
PMID:22288400
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4437619/
Abstract

Alzheimer disease (AD) is the leading cause of dementia among elderly. Currently, no effective treatment is available for AD. Analysis of transgenic mouse models of AD has facilitated our understanding of disease mechanisms and provided valuable tools for evaluating potential therapeutic strategies. In this review, we will discuss the strengths and weaknesses of current mouse models of AD and the contribution towards understanding the pathological mechanisms and developing effective therapies.

摘要

阿尔茨海默病(AD)是老年人痴呆症的主要病因。目前,AD 尚无有效的治疗方法。对 AD 转基因小鼠模型的分析促进了我们对疾病机制的理解,并为评估潜在治疗策略提供了有价值的工具。在这篇综述中,我们将讨论当前 AD 小鼠模型的优缺点及其对理解病理机制和开发有效疗法的贡献。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2aab/4437619/1bd1adc56ac0/nihms-688863-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2aab/4437619/1bd1adc56ac0/nihms-688863-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2aab/4437619/1bd1adc56ac0/nihms-688863-f0001.jpg

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本文引用的文献

1
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Neuron. 2010 Oct 6;68(1):19-31. doi: 10.1016/j.neuron.2010.08.023.
2
CX3CR1 deficiency alters microglial activation and reduces beta-amyloid deposition in two Alzheimer's disease mouse models.CX3CR1 缺失改变小胶质细胞激活并减少两种阿尔茨海默病小鼠模型中的 β-淀粉样蛋白沉积。
Am J Pathol. 2010 Nov;177(5):2549-62. doi: 10.2353/ajpath.2010.100265. Epub 2010 Sep 23.
3
Modulation of gamma-secretase reduces beta-amyloid deposition in a transgenic mouse model of Alzheimer's disease.γ-分泌酶的调制可减少阿尔茨海默病转基因小鼠模型中的β-淀粉样蛋白沉积。
Neuron. 2010 Sep 9;67(5):769-80. doi: 10.1016/j.neuron.2010.08.018.
4
Gamma-secretase activating protein is a therapeutic target for Alzheimer's disease.γ-分泌酶激活蛋白是阿尔茨海默病的治疗靶点。
Nature. 2010 Sep 2;467(7311):95-8. doi: 10.1038/nature09325.
5
ATP-binding cassette transporter A1 mediates the beneficial effects of the liver X receptor agonist GW3965 on object recognition memory and amyloid burden in amyloid precursor protein/presenilin 1 mice.三磷酸腺苷结合盒转运体 A1 介导肝 X 受体激动剂 GW3965 对淀粉样前体蛋白/早老素 1 小鼠物体识别记忆和淀粉样蛋白负荷的有益作用。
J Biol Chem. 2010 Oct 29;285(44):34144-54. doi: 10.1074/jbc.M110.108100. Epub 2010 Aug 25.
6
A noncompetitive BACE1 inhibitor TAK-070 ameliorates Abeta pathology and behavioral deficits in a mouse model of Alzheimer's disease.一种非竞争性 BACE1 抑制剂 TAK-070 可改善阿尔茨海默病小鼠模型中的 Abeta 病理和行为缺陷。
J Neurosci. 2010 Aug 18;30(33):11157-66. doi: 10.1523/JNEUROSCI.2884-10.2010.
7
Reduction of amyloid beta-peptide accumulation in Tg2576 transgenic mice by oral vaccination.口服疫苗接种减少 Tg2576 转基因小鼠淀粉样β肽的积累。
Biochem Biophys Res Commun. 2010 Sep 3;399(4):593-9. doi: 10.1016/j.bbrc.2010.07.120. Epub 2010 Aug 1.
8
Dendritic function of tau mediates amyloid-beta toxicity in Alzheimer's disease mouse models.tau 的树突功能介导阿尔茨海默病小鼠模型中的淀粉样β毒性。
Cell. 2010 Aug 6;142(3):387-97. doi: 10.1016/j.cell.2010.06.036. Epub 2010 Jul 22.
9
BACE1 deficiency causes altered neuronal activity and neurodegeneration.BACE1 缺失导致神经元活动改变和神经退行性变。
J Neurosci. 2010 Jun 30;30(26):8819-29. doi: 10.1523/JNEUROSCI.1334-10.2010.
10
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J Alzheimers Dis. 2010;21(2):527-42. doi: 10.3233/JAD-2010-100204.