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阿尔茨海默病:来自基因小鼠模型的见解及人类诱导多能干细胞衍生神经元的当前进展

Alzheimer's Disease: Insights from Genetic Mouse Models and Current Advances in Human IPSC-Derived Neurons.

作者信息

Harasta Anne E, Ittner Lars M

机构信息

Dementia Research Unit, Department of Anatomy, School of Medical Sciences, Faculty of Medicine, The University of New South Wales, Sydney, NSW, 2052, Australia.

Transgenic Animal Unit, Mark Wainwright Analytical Centre, The University of New South Wales, Sydney, NSW, 2052, Australia.

出版信息

Adv Neurobiol. 2017;15:3-29. doi: 10.1007/978-3-319-57193-5_1.

DOI:10.1007/978-3-319-57193-5_1
PMID:28674976
Abstract

Alzheimer's disease was first described in 1906 and since then tremendous efforts have been made to fully understand the disease pathology and to find a cure for this neurodegenerative disease. The diagnosis of Alzheimer's is still difficult, especially in early stages of the disease. Current treatment of Alzheimer's only ameliorates the symptoms but fails to provide a therapy. Over the last decades, animal models have been proven valuable in elucidating insights of the pathology. In vitro models using patient-derived cells are currently emerging and hold great promise in understanding the disease pathophysiology. Here, we introduce the neurobiology and genetic features of Alzheimer's and describe what we have learned from studies employing mouse models and patient-derived induced pluripotent stem cells.

摘要

阿尔茨海默病于1906年首次被描述,自那时起,人们付出了巨大努力来全面了解该疾病的病理,并寻找治疗这种神经退行性疾病的方法。阿尔茨海默病的诊断仍然困难,尤其是在疾病的早期阶段。目前对阿尔茨海默病的治疗仅能缓解症状,但无法提供治愈方法。在过去几十年中,动物模型已被证明在阐明病理见解方面具有重要价值。目前,使用患者来源细胞的体外模型正在兴起,并在理解疾病病理生理学方面具有巨大潜力。在这里,我们介绍阿尔茨海默病的神经生物学和遗传特征,并描述我们从使用小鼠模型和患者来源的诱导多能干细胞的研究中学到的知识。

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Low and High Molecular Weight FGF-2 Have Differential Effects on Astrocyte Proliferation, but Are Both Protective Against Aβ-Induced Cytotoxicity.低分子量和高分子量成纤维细胞生长因子-2对星形胶质细胞增殖有不同影响,但二者均对β-淀粉样蛋白诱导的细胞毒性具有保护作用。
Front Mol Neurosci. 2020 Jan 24;12:328. doi: 10.3389/fnmol.2019.00328. eCollection 2019.
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The Use of Pluripotent Stem Cell-Derived Organoids to Study Extracellular Matrix Development during Neural Degeneration.
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