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APP 家族在大脑中做什么?

What Does the APP Family Do in the Brain?

机构信息

Department of Pathology and Cell Biology, Columbia University, 630W 168(th) Street, New York, NY 10032, USA; Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University, 630W 168(th) Street, New York, NY 10032, USA; Department of Medicine, Columbia University, 630W 168(th) Street, New York, NY 10032, USA.

出版信息

Neuron. 2020 Nov 25;108(4):583-585. doi: 10.1016/j.neuron.2020.11.003.

DOI:10.1016/j.neuron.2020.11.003
PMID:33242425
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8379349/
Abstract

Amyloid-β precursor protein (APP) is overshadowed by its degradation product, the Alzheimer protein Aβ. Lee et al. now find a role for the APP family in neuronal excitability, synaptic plasticity, and memory in adulthood, despite the lack of requirement for neuronal survival.

摘要

淀粉样前体蛋白(APP)因其降解产物阿尔茨海默病相关蛋白 Aβ而黯然失色。然而,Lee 等人现在发现 APP 家族在成年期神经元兴奋性、突触可塑性和记忆中具有重要作用,尽管其对于神经元存活没有需求。

相似文献

1
What Does the APP Family Do in the Brain?APP 家族在大脑中做什么?
Neuron. 2020 Nov 25;108(4):583-585. doi: 10.1016/j.neuron.2020.11.003.
2
Roles of amyloid precursor protein and its fragments in regulating neural activity, plasticity and memory.淀粉样前体蛋白及其片段在调节神经活动、可塑性和记忆方面的作用。
Prog Neurobiol. 2003 May;70(1):1-32. doi: 10.1016/s0301-0082(03)00089-3.
3
[Alzheimer disease: cellular and molecular aspects].[阿尔茨海默病:细胞与分子层面]
Bull Mem Acad R Med Belg. 2005;160(10-12):445-9; discussion 450-1.
4
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.
5
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.
6
Amyloid-beta precursor protein mediates neuronal toxicity of amyloid beta through Go protein activation.淀粉样前体蛋白通过激活Go蛋白介导β淀粉样蛋白的神经元毒性。
Neurobiol Aging. 2009 Sep;30(9):1379-92. doi: 10.1016/j.neurobiolaging.2007.11.017. Epub 2008 Jan 10.
7
Neuronal deficiency of presenilin 1 inhibits amyloid plaque formation and corrects hippocampal long-term potentiation but not a cognitive defect of amyloid precursor protein [V717I] transgenic mice.早老素1的神经元缺陷可抑制淀粉样斑块形成并纠正海马长时程增强,但不能纠正淀粉样前体蛋白[V717I]转基因小鼠的认知缺陷。
J Neurosci. 2002 May 1;22(9):3445-53. doi: 10.1523/JNEUROSCI.22-09-03445.2002.
8
Subcellular trafficking of the amyloid precursor protein gene family and its pathogenic role in Alzheimer's disease.淀粉样前体蛋白基因家族的亚细胞运输及其在阿尔茨海默病中的致病作用。
Neurodegener Dis. 2006;3(4-5):218-26. doi: 10.1159/000095259.
9
The upside of APP at synapses.APP 在突触处的好处。
CNS Neurosci Ther. 2012 Jan;18(1):47-56. doi: 10.1111/j.1755-5949.2010.00221.x. Epub 2010 Dec 27.
10
Treadmill exercise enhances synaptic plasticity, but does not alter β-amyloid deposition in hippocampi of aged APP/PS1 transgenic mice.跑步机运动可增强突触可塑性,但不会改变老年APP/PS1转基因小鼠海马体中的β-淀粉样蛋白沉积。
Neuroscience. 2015 Jul 9;298:357-66. doi: 10.1016/j.neuroscience.2015.04.038. Epub 2015 Apr 23.

引用本文的文献

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Combinatorial mechanisms specify cellular location and neurotransmitter identity during regeneration of planarian neurons.组合机制在涡虫神经元再生过程中确定细胞位置和神经递质特性。
bioRxiv. 2025 May 25:2025.05.23.655781. doi: 10.1101/2025.05.23.655781.
2
Re-Arranging the Puzzle between the Amyloid-Beta and Tau Pathology: An APP-Centric Approach.重新排列淀粉样β和 Tau 病理之间的谜题:以 APP 为中心的方法。
Int J Mol Sci. 2023 Dec 23;25(1):259. doi: 10.3390/ijms25010259.
3
Integrative analysis reveals a conserved role for the amyloid precursor protein in proteostasis during aging.综合分析揭示淀粉样前体蛋白在衰老过程中在蛋白质稳定中具有保守作用。
Nat Commun. 2023 Nov 3;14(1):7034. doi: 10.1038/s41467-023-42822-1.
4
Targeting neuroinflammation in Alzheimer's disease: from mechanisms to clinical applications.针对阿尔茨海默病中的神经炎症:从机制到临床应用
Neural Regen Res. 2023 Apr;18(4):708-715. doi: 10.4103/1673-5374.353484.

本文引用的文献

1
APP Family Regulates Neuronal Excitability and Synaptic Plasticity but Not Neuronal Survival.APP 家族调节神经元兴奋性和突触可塑性,但不影响神经元存活。
Neuron. 2020 Nov 25;108(4):676-690.e8. doi: 10.1016/j.neuron.2020.08.011. Epub 2020 Sep 4.
2
Facilitation of glutamate, but not GABA, release in Familial Alzheimer's APP mutant Knock-in rats with increased β-cleavage of APP.在淀粉样前体蛋白(APP)β-切割增加的家族性阿尔茨海默病APP突变敲入大鼠中,谷氨酸释放增加,但γ-氨基丁酸(GABA)释放无变化。
Aging Cell. 2019 Dec;18(6):e13033. doi: 10.1111/acel.13033. Epub 2019 Sep 9.
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
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.
5
Acute function of secreted amyloid precursor protein fragment APPsα in synaptic plasticity.分泌型淀粉样前体蛋白片段 APPsα 在突触可塑性中的急性功能。
Acta Neuropathol. 2015 Jan;129(1):21-37. doi: 10.1007/s00401-014-1368-x. Epub 2014 Nov 29.
6
Physiological functions of APP family proteins.APP 家族蛋白的生理功能。
Cold Spring Harb Perspect Med. 2012 Feb;2(2):a006288. doi: 10.1101/cshperspect.a006288.
7
Endogenous amyloid-β is necessary for hippocampal synaptic plasticity and memory.内源性淀粉样蛋白-β对于海马体突触可塑性和记忆是必需的。
Ann Neurol. 2011 May;69(5):819-30. doi: 10.1002/ana.22313. Epub 2011 Apr 6.
8
Aberrant excitatory neuronal activity and compensatory remodeling of inhibitory hippocampal circuits in mouse models of Alzheimer's disease.阿尔茨海默病小鼠模型中异常的兴奋性神经元活动及海马抑制性回路的代偿性重塑
Neuron. 2007 Sep 6;55(5):697-711. doi: 10.1016/j.neuron.2007.07.025.
9
Loss of presenilin function causes impairments of memory and synaptic plasticity followed by age-dependent neurodegeneration.早老素功能丧失会导致记忆和突触可塑性受损,随后出现年龄依赖性神经退行性变。
Neuron. 2004 Apr 8;42(1):23-36. doi: 10.1016/s0896-6273(04)00182-5.
10
JNK-interacting protein-1 promotes transcription of A beta protein precursor but not A beta precursor-like proteins, mechanistically different than Fe65.JNK相互作用蛋白1促进β淀粉样蛋白前体的转录,但不促进类β淀粉样前体蛋白的转录,其作用机制与Fe65不同。
Proc Natl Acad Sci U S A. 2003 Feb 18;100(4):1729-34. doi: 10.1073/pnas.0437908100. Epub 2003 Jan 31.