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.
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。
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本文引用的文献
1
APP Family Regulates Neuronal Excitability and Synaptic Plasticity but Not Neuronal Survival.
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.
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.
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.
Elife. 2015 Nov 9;4:e09743. doi: 10.7554/eLife.09743.
5
Acute function of secreted amyloid precursor protein fragment APPsα in synaptic plasticity.
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.
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.
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.
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.
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.
Proc Natl Acad Sci U S A. 2003 Feb 18;100(4):1729-34. doi: 10.1073/pnas.0437908100. Epub 2003 Jan 31.
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