Commentary: APP as a Mediator of the Synapse Pathology in Alzheimer's Disease.
作者信息
Schreurs An, Latif-Hernandez Amira, Uwineza Alice
机构信息
Brain & Cognition, Faculty of Psychology and Educational Sciences, KU Leuven - University of Leuven, Leuven, Belgium.
Neurology & Neurological Sciences, Stanford University School of Medicine, Stanford, CA, United States.
出版信息
Front Cell Neurosci. 2018 May 31;12:150. doi: 10.3389/fncel.2018.00150. eCollection 2018.
Abstract
摘要
相似文献
1
Commentary: APP as a Mediator of the Synapse Pathology in Alzheimer's Disease.述评：淀粉样前体蛋白作为阿尔茨海默病突触病理学的介质
Front Cell Neurosci. 2018 May 31;12:150. doi: 10.3389/fncel.2018.00150. eCollection 2018.
2
Rifampicin is a candidate preventive medicine against amyloid-β and tau oligomers.利福平是一种针对淀粉样β和tau 寡聚物的候选预防药物。
Brain. 2016 May;139(Pt 5):1568-86. doi: 10.1093/brain/aww042. Epub 2016 Mar 28.
3
Modeling Alzheimer's disease in transgenic mice: effect of age and of presenilin1 on amyloid biochemistry and pathology in APP/London mice.转基因小鼠中阿尔茨海默病的建模：年龄和早老素1对APP/伦敦小鼠淀粉样蛋白生物化学及病理学的影响
Exp Gerontol. 2000 Sep;35(6-7):831-41. doi: 10.1016/s0531-5565(00)00149-2.
4
Human tau increases amyloid β plaque size but not amyloid β-mediated synapse loss in a novel mouse model of Alzheimer's disease.在一种新型阿尔茨海默病小鼠模型中，人tau蛋白会增加β淀粉样蛋白斑块大小，但不会增加β淀粉样蛋白介导的突触损失。
Eur J Neurosci. 2016 Dec;44(12):3056-3066. doi: 10.1111/ejn.13442. Epub 2016 Nov 12.
5
Regulation of Synaptic Amyloid-β Generation through BACE1 Retrograde Transport in a Mouse Model of Alzheimer's Disease.在阿尔茨海默病小鼠模型中通过β-分泌酶1逆向转运调控突触淀粉样β蛋白的生成
J Neurosci. 2017 Mar 8;37(10):2639-2655. doi: 10.1523/JNEUROSCI.2851-16.2017. Epub 2017 Feb 3.
6
Mutation-induced loss of APP function causes GABAergic depletion in recessive familial Alzheimer's disease: analysis of Osaka mutation-knockin mice.突变诱导的 APP 功能丧失导致隐性家族性阿尔茨海默病中 GABA 能神经元缺失：对大阪突变敲入小鼠的分析。
Acta Neuropathol Commun. 2017 Jul 31;5(1):59. doi: 10.1186/s40478-017-0461-5.
7
Amyloid-induced neurofibrillary tangle formation in Alzheimer's disease: insight from transgenic mouse and tissue-culture models.淀粉样蛋白诱导的阿尔茨海默病神经原纤维缠结形成：来自转基因小鼠和组织培养模型的见解。
Int J Dev Neurosci. 2004 Nov;22(7):453-65. doi: 10.1016/j.ijdevneu.2004.07.013.
8
Hypercholesterolemia accelerates intraneuronal accumulation of Aβ oligomers resulting in memory impairment in Alzheimer's disease model mice.高胆固醇血症加速了 Aβ 寡聚物在神经元内的积累，导致阿尔茨海默病模型小鼠的记忆损伤。
Life Sci. 2012 Dec 10;91(23-24):1169-76. doi: 10.1016/j.lfs.2011.12.022. Epub 2012 Jan 17.
9
Amyloid-β dimers in the absence of plaque pathology impair learning and synaptic plasticity.无淀粉样蛋白斑块病理的β 淀粉样蛋白二聚体损害学习和突触可塑性。
Brain. 2016 Feb;139(Pt 2):509-25. doi: 10.1093/brain/awv355. Epub 2015 Dec 10.
10
The Amyloid Precursor Protein Intracellular Domain Is an Effector Molecule of Metaplasticity.淀粉样前体蛋白细胞内域是化学性可塑性的效应分子。
Biol Psychiatry. 2018 Mar 1;83(5):406-415. doi: 10.1016/j.biopsych.2016.12.015. Epub 2016 Dec 22.
引用本文的文献
1
Ameliorating Alzheimer's-like Pathology by Minocycline via Inhibiting Cdk5/p25 Signaling.通过抑制 Cdk5/p25 信号通路来米诺环素改善阿尔茨海默病样病变。
Curr Neuropharmacol. 2022 Aug 3;20(9):1783-1792. doi: 10.2174/1570159X19666211202124925.
2
Passive immunotherapy for N-truncated tau ameliorates the cognitive deficits in two mouse Alzheimer's disease models.针对N端截短型tau蛋白的被动免疫疗法可改善两种小鼠阿尔茨海默病模型的认知缺陷。
Brain Commun. 2020 Apr 6;2(1):fcaa039. doi: 10.1093/braincomms/fcaa039. eCollection 2020.
本文引用的文献
1
Practical considerations for choosing a mouse model of Alzheimer's disease.选择阿尔茨海默病小鼠模型的实用考虑因素。
Mol Neurodegener. 2017 Dec 22;12(1):89. doi: 10.1186/s13024-017-0231-7.
2
Human Brain-Derived Aβ Oligomers Bind to Synapses and Disrupt Synaptic Activity in a Manner That Requires APP.人脑源性β淀粉样蛋白寡聚体以一种需要淀粉样前体蛋白（APP）的方式与突触结合并破坏突触活动。
J Neurosci. 2017 Dec 6;37(49):11947-11966. doi: 10.1523/JNEUROSCI.2009-17.2017. Epub 2017 Nov 3.
3
LTP and memory impairment caused by extracellular Aβ and Tau oligomers is APP-dependent.细胞外淀粉样前体蛋白（Aβ）和 Tau 寡聚体引起的长时程增强（LTP）和记忆损伤是由淀粉样前体蛋白（APP）依赖的。
Elife. 2017 Jul 11;6:e26991. doi: 10.7554/eLife.26991.
4
Not just amyloid: physiological functions of the amyloid precursor protein family.不仅是淀粉样蛋白：淀粉样前体蛋白家族的生理功能。
Nat Rev Neurosci. 2017 May;18(5):281-298. doi: 10.1038/nrn.2017.29. Epub 2017 Mar 31.
5
Embryonic mosaic deletion of APP results in displaced Reelin-expressing cells in the cerebral cortex.APP的胚胎嵌合缺失导致大脑皮层中表达Reelin的细胞移位。
Dev Biol. 2017 Apr 15;424(2):138-146. doi: 10.1016/j.ydbio.2017.03.007. Epub 2017 Mar 8.
6
Network abnormalities and interneuron dysfunction in Alzheimer disease.阿尔茨海默病中的网络异常与中间神经元功能障碍。
Nat Rev Neurosci. 2016 Dec;17(12):777-792. doi: 10.1038/nrn.2016.141. Epub 2016 Nov 10.
7
APP and APLP2 interact with the synaptic release machinery and facilitate transmitter release at hippocampal synapses.APP和APLP2与突触释放机制相互作用，并促进海马突触处的递质释放。
Elife. 2015 Nov 9;4:e09743. doi: 10.7554/eLife.09743.
8
The genetic landscape of Alzheimer disease: clinical implications and perspectives.阿尔茨海默病的遗传图谱：临床意义与展望。
Genet Med. 2016 May;18(5):421-30. doi: 10.1038/gim.2015.117. Epub 2015 Aug 27.
9
Soluble amyloid-β oligomers as synaptotoxins leading to cognitive impairment in Alzheimer's disease.可溶性淀粉样β寡聚体作为导致阿尔茨海默病认知障碍的突触毒素。
Front Cell Neurosci. 2015 May 26;9:191. doi: 10.3389/fncel.2015.00191. eCollection 2015.
10
The amyloid precursor protein controls adult hippocampal neurogenesis through GABAergic interneurons.淀粉样前体蛋白通过γ-氨基丁酸能中间神经元控制成年海马神经发生。
J Neurosci. 2014 Oct 1;34(40):13314-25. doi: 10.1523/JNEUROSCI.2848-14.2014.
Zotero 插件