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The Mitochondrion: A Potential Therapeutic Target for Alzheimer's Disease.

作者信息

Lu Mei-Hong, Zhao Xiu-Yun, Yao Pei-Pei, Xu De-En, Ma Quan-Hong

机构信息

Jiangsu Key Laboratory of Neuropsychiatric Diseases and Institute of Neuroscience, Soochow University, Suzhou, 215123, China.

Department of Neurology and Suzhou Clinical Research Center of Neurological Disease, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, China.

出版信息

Neurosci Bull. 2018 Dec;34(6):1127-1130. doi: 10.1007/s12264-018-0310-y. Epub 2018 Nov 12.

DOI:10.1007/s12264-018-0310-y
PMID:30417261
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6246833/
Abstract
摘要

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本文引用的文献

1
Disrupted-in-schizophrenia-1 protects synaptic plasticity in a transgenic mouse model of Alzheimer's disease as a mitophagy receptor.精神分裂症 1 区缺失蛋白作为一种线粒体自噬受体保护阿尔茨海默病转基因小鼠模型的突触可塑性。
Aging Cell. 2019 Feb;18(1):e12860. doi: 10.1111/acel.12860. Epub 2018 Nov 28.
2
Region-specific depletion of synaptic mitochondria in the brains of patients with Alzheimer's disease.阿尔茨海默病患者大脑中特定区域突触线粒体的耗竭。
Acta Neuropathol. 2018 Nov;136(5):747-757. doi: 10.1007/s00401-018-1903-2. Epub 2018 Sep 6.
3
NAD supplementation normalizes key Alzheimer's features and DNA damage responses in a new AD mouse model with introduced DNA repair deficiency.NAD 补充使具有引入的 DNA 修复缺陷的新型 AD 小鼠模型中的关键阿尔茨海默病特征和 DNA 损伤反应正常化。
Proc Natl Acad Sci U S A. 2018 Feb 20;115(8):E1876-E1885. doi: 10.1073/pnas.1718819115. Epub 2018 Feb 5.
4
The Mitochondrial Basis of Aging and Age-Related Disorders.衰老及衰老相关疾病的线粒体基础
Genes (Basel). 2017 Dec 19;8(12):398. doi: 10.3390/genes8120398.
5
A Mouse Model of Alzheimer's Disease with Transplanted Stem-Cell-Derived Human Neurons.移植干细胞衍生的人类神经元的阿尔茨海默病小鼠模型
Neurosci Bull. 2017 Dec;33(6):766-768. doi: 10.1007/s12264-017-0180-8. Epub 2017 Sep 21.
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Trehalose Improves Cognition in the Transgenic Tg2576 Mouse Model of Alzheimer's Disease.海藻糖改善阿尔茨海默病转基因Tg2576小鼠模型的认知功能。
J Alzheimers Dis. 2017;60(2):549-560. doi: 10.3233/JAD-170322.
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Attenuation of β-Amyloid Toxicity In Vitro and In Vivo by Accelerated Aggregation.通过加速聚集在体外和体内减轻β-淀粉样蛋白毒性
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Human wild-type full-length tau accumulation disrupts mitochondrial dynamics and the functions via increasing mitofusins.人类野生型全长tau蛋白的积累通过增加线粒体融合蛋白来破坏线粒体动力学及其功能。
Sci Rep. 2016 Apr 21;6:24756. doi: 10.1038/srep24756.