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阿尔茨海默病和额颞叶痴呆的动物模型:一种观点。

Animal models for Alzheimer's disease and frontotemporal dementia: a perspective.

机构信息

Alzheimer's and Parkinson's Disease Laboratory, Brain and Mind Research Institute, University of Sydney, Camperdown, NSW 2050, Australia.

出版信息

ASN Neuro. 2009 Nov 9;1(4):e00019. doi: 10.1042/AN20090042.

DOI:10.1042/AN20090042
PMID:19839939
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2785514/
Abstract

In dementia research, animal models have become indispensable tools. They not only model aspects of the human condition, but also simulate processes that occur in humans and hence provide insight into how disease is initiated and propagated. The present review discusses two prominent human neurodegenerative disorders, Alzheimer's disease and frontotemporal dementia. It discusses what we would like to model in animals and highlights some of the more recent achievements using species as diverse as mice, fish, flies and worms. Advances in imaging and therapy are explored. We also discuss some anticipated new models and developments. These will reveal how key players in the pathogenesis of Alzheimer's disease and frontotemporal dementia, such as the peptide Aβ (amyloid β) and the protein tau, cause neuronal dysfunction and eventually, neuronal demise. Understanding these processes fully will lead to early diagnosis and therapy.

摘要

在痴呆症研究中,动物模型已成为不可或缺的工具。它们不仅模拟了人类状况的某些方面,还模拟了在人类中发生的过程,从而深入了解疾病的发生和传播方式。本综述讨论了两种突出的人类神经退行性疾病,即阿尔茨海默病和额颞叶痴呆。它讨论了我们希望在动物中模拟的内容,并重点介绍了使用老鼠、鱼类、苍蝇和蠕虫等多种物种取得的一些最新成就。探讨了成像和治疗方面的进展。我们还讨论了一些预期的新模型和发展。这些模型将揭示阿尔茨海默病和额颞叶痴呆发病机制中的关键因素,如肽 Aβ(淀粉样蛋白β)和蛋白 tau,如何导致神经元功能障碍,最终导致神经元死亡。全面了解这些过程将导致早期诊断和治疗。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3834/2785514/b1c436b82d40/an001e019f05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3834/2785514/56db2ca9ca01/an001e019f01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3834/2785514/d0e161d4eed1/an001e019f02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3834/2785514/cab703f6d870/an001e019f03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3834/2785514/c3b940ef353b/an001e019f04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3834/2785514/b1c436b82d40/an001e019f05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3834/2785514/56db2ca9ca01/an001e019f01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3834/2785514/d0e161d4eed1/an001e019f02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3834/2785514/cab703f6d870/an001e019f03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3834/2785514/c3b940ef353b/an001e019f04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3834/2785514/b1c436b82d40/an001e019f05.jpg

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Genome-wide association study identifies variants at CLU and PICALM associated with Alzheimer's disease.
重新审视 sigma-1 受体作为治疗情感和认知障碍的生物靶点。
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Characterization of an APP/tau rat model of Alzheimer's disease by positron emission tomography and immunofluorescent labeling.通过正电子发射断层扫描和免疫荧光标记对阿尔茨海默病的APP/tau大鼠模型进行表征。
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Preclinical Marmoset Model for Targeting Chronic Inflammation as a Strategy to Prevent Alzheimer's Disease.针对慢性炎症作为预防阿尔茨海默病策略的临床前狨猴模型
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