阿尔茨海默病和帕金森病的线粒体动态为治疗干预提供了重要机会。
The mitochondrial dynamics of Alzheimer's disease and Parkinson's disease offer important opportunities for therapeutic intervention.
机构信息
Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA.
出版信息
Curr Pharm Des. 2011;17(31):3374-80. doi: 10.2174/138161211798072562.
Abstract
Mitochondrial dynamics play a crucial role in the pathobiology underlying Alzheimer's disease (AD) and Parkinson's disease (PD). Although a complete scientific understanding of these devastating conditions has yet to be realized, alterations in mitochondrial fission and fusion, and in the protein complexes that orchestrate mitochondrial fission and fusion, have been well established in AD- and PD-related neurodegeneration. Whether fission/fusion disruption in the brain is a causal agent in neuronal demise or a product of some other upstream disturbance is still a matter of debate; however, in both AD and PD, the potential for successful therapeutic amelioration of degeneration via mitochondrial protection is high. We here discuss the role of mitochondrial dynamics in AD and PD and assess the need for their therapeutic exploitation.
摘要
线粒体动态在阿尔茨海默病（AD）和帕金森病（PD）的病理生物学中起着至关重要的作用。尽管人们尚未完全了解这些破坏性疾病，但在 AD 和 PD 相关的神经退行性变中，线粒体分裂和融合以及协调线粒体分裂和融合的蛋白质复合物的改变已经得到了很好的证实。在大脑中，分裂/融合的破坏是神经元死亡的原因还是其他上游干扰的产物，这仍然是一个有争议的问题；然而，在 AD 和 PD 中，通过线粒体保护来成功治疗退化的潜力很高。我们在这里讨论了线粒体动态在 AD 和 PD 中的作用，并评估了对其进行治疗性利用的必要性。
相似文献
1
The mitochondrial dynamics of Alzheimer's disease and Parkinson's disease offer important opportunities for therapeutic intervention.阿尔茨海默病和帕金森病的线粒体动态为治疗干预提供了重要机会。
Curr Pharm Des. 2011;17(31):3374-80. doi: 10.2174/138161211798072562.
2
Mitochondrial abnormalities in Parkinson's disease and Alzheimer's disease: can mitochondria be targeted therapeutically?帕金森病和阿尔茨海默病中的线粒体异常：线粒体可以作为治疗靶点吗？
Biochem Soc Trans. 2018 Aug 20;46(4):891-909. doi: 10.1042/BST20170501. Epub 2018 Jul 19.
3
Inhibition of ERK-DLP1 signaling and mitochondrial division alleviates mitochondrial dysfunction in Alzheimer's disease cybrid cell.抑制ERK-DLP1信号传导和线粒体分裂可减轻阿尔茨海默病杂交细胞中的线粒体功能障碍。
Biochim Biophys Acta. 2014 Feb;1842(2):220-31. doi: 10.1016/j.bbadis.2013.11.009. Epub 2013 Nov 16.
4
Mitochondria: a therapeutic target in neurodegeneration.线粒体：神经退行性变的一个治疗靶点。
Biochim Biophys Acta. 2010 Jan;1802(1):212-20. doi: 10.1016/j.bbadis.2009.10.007. Epub 2009 Oct 21.
5
Mitochondria: A Therapeutic Target for Parkinson's Disease?线粒体：帕金森病的治疗靶点？
Int J Mol Sci. 2015 Sep 1;16(9):20704-30. doi: 10.3390/ijms160920704.
6
Redox regulation of mitochondrial fission, protein misfolding, synaptic damage, and neuronal cell death: potential implications for Alzheimer's and Parkinson's diseases.氧化还原调节线粒体分裂、蛋白质错误折叠、突触损伤和神经元细胞死亡：对阿尔茨海默病和帕金森病的潜在影响。
Apoptosis. 2010 Nov;15(11):1354-63. doi: 10.1007/s10495-010-0476-x.
7
Role of protein aggregation in mitochondrial dysfunction and neurodegeneration in Alzheimer's and Parkinson's diseases.蛋白质聚集在阿尔茨海默病和帕金森病线粒体功能障碍及神经退行性变中的作用。
Neuromolecular Med. 2003;4(1-2):21-36. doi: 10.1385/NMM:4:1-2:21.
8
The mitochondrial cascade hypothesis for Parkinson's disease.线粒体级联假说与帕金森病。
Curr Pharm Des. 2011;17(31):3390-7. doi: 10.2174/138161211798072508.
9
The Role of Mitochondria in Neurodegenerative Diseases: the Lesson from Alzheimer's Disease and Parkinson's Disease.线粒体在神经退行性疾病中的作用：阿尔茨海默病和帕金森病的启示。
Mol Neurobiol. 2020 Jul;57(7):2959-2980. doi: 10.1007/s12035-020-01926-1. Epub 2020 May 22.
10
Mitochondrial dysfunction and oxidative damage in Alzheimer's and Parkinson's diseases and coenzyme Q10 as a potential treatment.阿尔茨海默病和帕金森病中的线粒体功能障碍与氧化损伤以及辅酶Q10作为一种潜在治疗方法
J Bioenerg Biomembr. 2004 Aug;36(4):381-6. doi: 10.1023/B:JOBB.0000041772.74810.92.
引用本文的文献
1
Mitochondrial Fragmentation as a Key Driver of Neurodegenerative Disease.线粒体碎片化作为神经退行性疾病的关键驱动因素
Curr Alzheimer Res. 2024;21(9):607-614. doi: 10.2174/0115672050366194250107050650.
2
Cerebral oxygen metabolism from MRI susceptibility.MRI 对脑氧代谢的研究
Neuroimage. 2023 Aug 1;276:120189. doi: 10.1016/j.neuroimage.2023.120189. Epub 2023 May 23.
3
Mitochondrially-Targeted Therapeutic Strategies for Alzheimer's Disease.线粒体靶向治疗阿尔茨海默病策略。
Curr Alzheimer Res. 2021;18(10):753-771. doi: 10.2174/1567205018666211208125855.
4
Ferroptosis as a Major Factor and Therapeutic Target for Neuroinflammation in Parkinson's Disease.铁死亡作为帕金森病神经炎症的主要因素和治疗靶点
Biomedicines. 2021 Nov 12;9(11):1679. doi: 10.3390/biomedicines9111679.
5
Gene network analysis to determine the effect of hypoxia-associated genes on brain damages and tumorigenesis using an avian model.使用禽类模型进行基因网络分析，以确定缺氧相关基因对脑损伤和肿瘤发生的影响。
J Genet Eng Biotechnol. 2021 Jul 8;19(1):100. doi: 10.1186/s43141-021-00184-5.
6
Synaptic basis of Alzheimer's disease: Focus on synaptic amyloid beta, P-tau and mitochondria.阿尔茨海默病的突触基础：聚焦于突触淀粉样β、P-tau 和线粒体。
Ageing Res Rev. 2021 Jan;65:101208. doi: 10.1016/j.arr.2020.101208. Epub 2020 Nov 4.
7
Obesity and Diabetes Mediated Chronic Inflammation: A Potential Biomarker in Alzheimer's Disease.肥胖与糖尿病介导的慢性炎症：阿尔茨海默病的一种潜在生物标志物
J Pers Med. 2020 May 22;10(2):42. doi: 10.3390/jpm10020042.
8
Amyloid Beta and Phosphorylated Tau-Induced Defective Autophagy and Mitophagy in Alzheimer's Disease.淀粉样β和磷酸化 tau 诱导的阿尔茨海默病中的自噬和 mitophagy 缺陷。
Cells. 2019 May 22;8(5):488. doi: 10.3390/cells8050488.
9
Time to get Personal: A Framework for Personalized Targeting of Oxidative Stress in Neurotoxicity and Neurodegenerative Disease.是时候关注个体了：神经毒性和神经退行性疾病中氧化应激个性化靶向治疗的框架。
Curr Opin Toxicol. 2018 Feb;7:127-132. doi: 10.1016/j.cotox.2018.02.003. Epub 2018 Feb 15.
10
Mitochondria and Alzheimer's Disease: the Role of Mitochondrial Genetic Variation.线粒体与阿尔茨海默病：线粒体基因变异的作用
Curr Genet Med Rep. 2018;6(1):1-10. doi: 10.1007/s40142-018-0132-2. Epub 2018 Mar 1.
本文引用的文献
1
DLP1-dependent mitochondrial fragmentation mediates 1-methyl-4-phenylpyridinium toxicity in neurons: implications for Parkinson's disease.DLP1 依赖性线粒体片段化介导 1-甲基-4-苯基吡啶离子对神经元的毒性：帕金森病的相关影响。
Aging Cell. 2011 Oct;10(5):807-23. doi: 10.1111/j.1474-9726.2011.00721.x. Epub 2011 Jun 14.
2
Mechanism of neuroprotective mitochondrial remodeling by PKA/AKAP1.PKA/AKAP1 介导的神经保护线粒体重构机制。
PLoS Biol. 2011 Apr;9(4):e1000612. doi: 10.1371/journal.pbio.1000612. Epub 2011 Apr 19.
3
Regulation of mitochondrial dynamics and neurodegenerative diseases.线粒体动力学调控与神经退行性疾病
Acta Med Okayama. 2011 Feb;65(1):1-10. doi: 10.18926/AMO/43824.
4
Molecular mechanisms of PINK1-related neurodegeneration.PINK1 相关神经退行性变的分子机制。
Curr Neurol Neurosci Rep. 2011 Jun;11(3):283-90. doi: 10.1007/s11910-011-0187-x.
5
Mitophagy in neurodegeneration: an opportunity for therapy?神经变性中的自噬：治疗的机会？
Curr Drug Targets. 2011 Jun;12(6):790-9. doi: 10.2174/138945011795528813.
6
Mitochondria: the common upstream driver of amyloid-β and tau pathology in Alzheimer's disease.线粒体：阿尔茨海默病中淀粉样β和tau 病理学的共同上游驱动因素。
Curr Alzheimer Res. 2011 Aug;8(5):563-72. doi: 10.2174/156720511796391872.
7
Mechanisms of mitophagy.线粒体自噬的机制。
Nat Rev Mol Cell Biol. 2011 Jan;12(1):9-14. doi: 10.1038/nrm3028.
8
Aberrant mitochondrial fission in neurons induced by protein kinase C{delta} under oxidative stress conditions in vivo.体内氧化应激条件下蛋白激酶 C{delta}诱导神经元中线粒体的异常分裂。
Mol Biol Cell. 2011 Jan 15;22(2):256-65. doi: 10.1091/mbc.E10-06-0551. Epub 2010 Nov 30.
9
Alzheimer disease.阿尔茨海默病
Dis Mon. 2010 Sep;56(9):484-546. doi: 10.1016/j.disamonth.2010.06.001.
10
Web-based application to project the burden of Alzheimer's disease.基于网络的应用程序，用于预测阿尔茨海默病的负担。
Alzheimers Dement. 2010 Sep;6(5):425-8. doi: 10.1016/j.jalz.2010.01.014. Epub 2010 Aug 5.
Zotero 插件