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本文引用的文献

1
Cinnamic acid activates PPARα to stimulate Lysosomal biogenesis and lower Amyloid plaque pathology in an Alzheimer's disease mouse model.肉桂酸通过激活 PPARα 刺激溶酶体生物发生,降低阿尔茨海默病小鼠模型中的淀粉样斑块病理。
Neurobiol Dis. 2019 Apr;124:379-395. doi: 10.1016/j.nbd.2018.12.007. Epub 2018 Dec 19.
2
Aspirin binds to PPARα to stimulate hippocampal plasticity and protect memory.阿司匹林与 PPARα 结合,刺激海马体可塑性,保护记忆。
Proc Natl Acad Sci U S A. 2018 Jul 31;115(31):E7408-E7417. doi: 10.1073/pnas.1802021115. Epub 2018 Jul 16.
3
Aspirin Induces Lysosomal Biogenesis and Attenuates Amyloid Plaque Pathology in a Mouse Model of Alzheimer's Disease via PPARα.阿司匹林通过 PPARα 诱导溶酶体生物发生并减轻阿尔茨海默病小鼠模型中的淀粉样斑块病理
J Neurosci. 2018 Jul 25;38(30):6682-6699. doi: 10.1523/JNEUROSCI.0054-18.2018. Epub 2018 Jul 2.
4
Low-Dose Aspirin Use and Cognitive Function in Older Age: A Systematic Review and Meta-analysis.老年人群中低剂量阿司匹林的使用与认知功能:一项系统评价和荟萃分析。
J Am Geriatr Soc. 2017 Aug;65(8):1763-1768. doi: 10.1111/jgs.14883. Epub 2017 Apr 20.
5
BDNF and Hippocampal Synaptic Plasticity.脑源性神经营养因子与海马突触可塑性
Vitam Horm. 2017;104:153-195. doi: 10.1016/bs.vh.2016.10.004. Epub 2016 Nov 29.
6
Mean Daily Dosage of Aspirin and the Risk of Incident Alzheimer's Dementia in Patients with Type 2 Diabetes Mellitus: A Nationwide Retrospective Cohort Study in Taiwan.台湾一项全国性回顾性队列研究:2 型糖尿病患者每日平均阿司匹林剂量与新发阿尔茨海默病痴呆风险。
J Diabetes Res. 2016;2016:9027484. doi: 10.1155/2016/9027484. Epub 2016 Oct 27.
7
Identification and characterization of PPARα ligands in the hippocampus.海马体中过氧化物酶体增殖物激活受体α(PPARα)配体的鉴定与表征
Nat Chem Biol. 2016 Dec;12(12):1075-1083. doi: 10.1038/nchembio.2204. Epub 2016 Oct 17.
8
Brain-derived neurotrophic factor protects against tau-related neurodegeneration of Alzheimer's disease.脑源性神经营养因子可预防阿尔茨海默病中与tau相关的神经退行性变。
Transl Psychiatry. 2016 Oct 4;6(10):e907. doi: 10.1038/tp.2016.186.
9
Development of Poly Unsaturated Fatty Acid Derivatives of Aspirin for Inhibition of Platelet Function.用于抑制血小板功能的阿司匹林多不饱和脂肪酸衍生物的研发。
J Pharmacol Exp Ther. 2016 Oct;359(1):134-41. doi: 10.1124/jpet.116.234781. Epub 2016 Aug 3.
10
Neuronal activity controls Bdnf expression via Polycomb de-repression and CREB/CBP/JMJD3 activation in mature neurons.神经元活动通过多梳蛋白去抑制以及成熟神经元中CREB/CBP/JMJD3的激活来控制脑源性神经营养因子(Bdnf)的表达。
Nat Commun. 2016 Mar 24;7:11081. doi: 10.1038/ncomms11081.

过氧化物酶体增殖物激活受体α(PPARα)是阿司匹林发挥神经保护作用的新型受体。

PPARα serves as a new receptor of aspirin for neuroprotection.

机构信息

Department of Neurological Sciences, Rush University Medical Center, Chicago, IL, USA.

Division of Research and Development, Jesse Brown Veterans Affairs Medical Center, Chicago, IL, USA.

出版信息

J Neurosci Res. 2020 Apr;98(4):626-631. doi: 10.1002/jnr.24561. Epub 2019 Dec 3.

DOI:10.1002/jnr.24561
PMID:31797405
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7015783/
Abstract

Acetyl salicylic acid, commonly known as aspirin, has been being widely used as an anti-inflammatory drug for almost 100 years. However, there was no receptor known for this popular drug. Recently, we have established that peroxisome proliferator-activated receptor alpha (PPARα) acts as a novel receptor of aspirin. Activation of PPARα by aspirin stimulated a series of downstream signaling pathways that could potentially ameliorate different Alzheimer's disease (AD)-related pathologies. In this mini-review, we have discussed how aspirin-PPARα interaction plays a pivotal role in the amelioration of AD pathology via the stimulation of neurotrophic factors, upregulation of plasticity-associated genes, and removal of plaque burden in hippocampal neurons.

摘要

乙酰水杨酸,俗称阿司匹林,作为一种抗炎药物,已经广泛应用近 100 年。然而,这种广受欢迎的药物却没有已知的受体。最近,我们已经确定过氧化物酶体增殖物激活受体α(PPARα)是阿司匹林的一种新型受体。阿司匹林激活 PPARα 会刺激一系列下游信号通路,这些通路可能有助于改善不同的阿尔茨海默病(AD)相关病理。在这篇简评中,我们讨论了阿司匹林-PPARα 相互作用如何通过刺激神经营养因子、上调与可塑性相关的基因以及清除海马神经元中的斑块负担,在改善 AD 病理方面发挥关键作用。