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Mitochondria and cell bioenergetics: increasingly recognized components and a possible etiologic cause of Alzheimer's disease.线粒体和细胞生物能量学：越来越被认可的阿尔茨海默病的组成部分和可能的病因。
Antioxid Redox Signal. 2012 Jun 15;16(12):1434-55. doi: 10.1089/ars.2011.4149. Epub 2011 Sep 15.
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Mitochondria, Cybrids, Aging, and Alzheimer's Disease.线粒体、胞质杂种、衰老与阿尔茨海默病
Prog Mol Biol Transl Sci. 2017;146:259-302. doi: 10.1016/bs.pmbts.2016.12.017. Epub 2017 Feb 1.
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The Alzheimer's disease mitochondrial cascade hypothesis.阿尔茨海默病线粒体级联假说。
J Alzheimers Dis. 2010;20 Suppl 2(Suppl 2):S265-79. doi: 10.3233/JAD-2010-100339.
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Mitochondria and Mitochondrial Cascades in Alzheimer's Disease.阿尔茨海默病中的线粒体和线粒体级联反应。
J Alzheimers Dis. 2018;62(3):1403-1416. doi: 10.3233/JAD-170585.
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Mitochondria, mitochondrial DNA and Alzheimer's disease. What comes first?线粒体、线粒体DNA与阿尔茨海默病。何者为先？
Curr Alzheimer Res. 2008 Oct;5(5):457-68. doi: 10.2174/156720508785908946.
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Clinical features and pathogenesis of Alzheimer's disease: involvement of mitochondria and mitochondrial DNA.阿尔茨海默病的临床特征和发病机制：线粒体和线粒体 DNA 的参与。
Adv Exp Med Biol. 2010;685:34-44. doi: 10.1007/978-1-4419-6448-9_4.
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The Alzheimer's disease mitochondrial cascade hypothesis: an update.阿尔茨海默病线粒体级联假说：最新进展
Exp Neurol. 2009 Aug;218(2):308-15. doi: 10.1016/j.expneurol.2009.01.011. Epub 2009 Jan 29.
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Mitochondrial dysfunction in Alzheimer's disease: Role in pathogenesis and novel therapeutic opportunities.阿尔茨海默病中的线粒体功能障碍：在发病机制中的作用及新的治疗机会
Br J Pharmacol. 2019 Sep;176(18):3489-3507. doi: 10.1111/bph.14585. Epub 2019 Mar 6.
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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.
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Abnormal mitochondrial morphology in sporadic Parkinson's and Alzheimer's disease cybrid cell lines.散发性帕金森病和阿尔茨海默病胞质杂种细胞系中的线粒体形态异常。
Exp Neurol. 2000 Mar;162(1):37-50. doi: 10.1006/exnr.2000.7333.
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Ubiquitin-Proteasome System Dysregulation in Alzheimer's Disease Impacts Protein Abundance.阿尔茨海默病中泛素-蛋白酶体系统失调影响蛋白质丰度。
bioRxiv. 2025 May 29:2025.05.29.656728. doi: 10.1101/2025.05.29.656728.
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Mitochondrial-based therapies for neurodegenerative diseases: a review of the current literature.基于线粒体的神经退行性疾病治疗方法：当前文献综述
Naunyn Schmiedebergs Arch Pharmacol. 2025 Mar 31. doi: 10.1007/s00210-025-04014-0.
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VDAC1: A Key Player in the Mitochondrial Landscape of Neurodegeneration.电压依赖性阴离子通道1：神经退行性变线粒体格局中的关键角色。
Biomolecules. 2024 Dec 30;15(1):33. doi: 10.3390/biom15010033.
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Viruses and neurodegeneration: a growing concern.病毒与神经退行性变：日益受到关注。
J Transl Med. 2025 Jan 12;23(1):46. doi: 10.1186/s12967-024-06025-6.
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Inhibiting mtDNA transcript translation alters Alzheimer's disease-associated biology.抑制线粒体DNA转录本翻译会改变阿尔茨海默病相关生物学特性。
Alzheimers Dement. 2024 Dec;20(12):8429-8443. doi: 10.1002/alz.14275. Epub 2024 Oct 23.
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Synaptic mitochondria glycation contributes to mitochondrial stress and cognitive dysfunction.突触线粒体糖基化会导致线粒体应激和认知功能障碍。
Brain. 2025 Jan 7;148(1):262-275. doi: 10.1093/brain/awae229.
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Neurotoxic β-amyloid oligomers cause mitochondrial dysfunction-the trigger for PANoptosis in neurons.神经毒性β-淀粉样寡聚体导致线粒体功能障碍——神经元中PANoptosis的触发因素。
Front Aging Neurosci. 2024 May 14;16:1400544. doi: 10.3389/fnagi.2024.1400544. eCollection 2024.
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TOMM40 '523 Genotype Distinguishes Patterns of Cognitive Improvement for Executive Function in APOEɛ3 Homozygotes.TOMM40 '523 基因型区分 APOEɛ3 纯合子执行功能认知改善模式。
J Alzheimers Dis. 2023;95(4):1697-1707. doi: 10.3233/JAD-230066.
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Peripheral Mitochondrial Dysfunction: A Potential Contributor to the Development of Metabolic Disorders and Alzheimer's Disease.外周线粒体功能障碍：代谢紊乱和阿尔茨海默病发展的潜在因素。
Biology (Basel). 2023 Jul 19;12(7):1019. doi: 10.3390/biology12071019.
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Neuroprotective effects of coenzyme Q10 on neurological diseases: a review article.辅酶Q10对神经疾病的神经保护作用：一篇综述文章。
Front Neurosci. 2023 Jun 23;17:1188839. doi: 10.3389/fnins.2023.1188839. eCollection 2023.
本文引用的文献
1
Reduced mitochondria cytochrome oxidase activity in adult children of mothers with Alzheimer's disease.阿尔茨海默病母亲的成年子女中线粒体细胞色素氧化酶活性降低。
J Alzheimers Dis. 2011;27(3):483-90. doi: 10.3233/JAD-2011-110866.
2
The impact of mitochondrial and nuclear DNA variants on late-onset Alzheimer's disease risk.线粒体和核 DNA 变异对迟发性阿尔茨海默病风险的影响。
J Alzheimers Dis. 2011;27(1):197-210. doi: 10.3233/JAD-2011-110710.
3
Amyloid-β-induced mitochondrial dysfunction impairs the autophagic lysosomal pathway in a tubulin dependent pathway.淀粉样蛋白-β诱导的线粒体功能障碍通过微管依赖性途径损害自噬溶酶体途径。
J Alzheimers Dis. 2011;26(3):565-81. doi: 10.3233/JAD-2011-110423.
4
Deficient brain insulin signalling pathway in Alzheimer's disease and diabetes.阿尔茨海默病和糖尿病中大脑胰岛素信号通路缺陷。
J Pathol. 2011 Sep;225(1):54-62. doi: 10.1002/path.2912. Epub 2011 May 19.
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Mild cognitive impairment, dementia, and their subtypes in oldest old women.高龄老年女性的轻度认知障碍、痴呆及其亚型
Arch Neurol. 2011 May;68(5):631-6. doi: 10.1001/archneurol.2011.82.
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The diagnosis of dementia due to Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease.阿尔茨海默病所致痴呆的诊断：美国国家老龄化研究所-阿尔茨海默病协会工作组关于阿尔茨海默病诊断指南的建议。
Alzheimers Dement. 2011 May;7(3):263-9. doi: 10.1016/j.jalz.2011.03.005. Epub 2011 Apr 21.
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The diagnosis of mild cognitive impairment due to Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease.阿尔茨海默病所致轻度认知障碍的诊断：美国国家老龄化研究所-阿尔茨海默病协会诊断指南工作组的建议。
Alzheimers Dement. 2011 May;7(3):270-9. doi: 10.1016/j.jalz.2011.03.008. Epub 2011 Apr 21.
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Toward defining the preclinical stages of Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease.为了定义阿尔茨海默病的临床前阶段：来自美国国家老龄化研究所-阿尔茨海默病协会工作组关于阿尔茨海默病诊断指南的建议。
Alzheimers Dement. 2011 May;7(3):280-92. doi: 10.1016/j.jalz.2011.03.003. Epub 2011 Apr 21.
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Impaired mitochondrial dynamics and abnormal interaction of amyloid beta with mitochondrial protein Drp1 in neurons from patients with Alzheimer's disease: implications for neuronal damage.阿尔茨海默病患者神经元中线粒体动力学受损和淀粉样β蛋白与线粒体蛋白 Drp1 异常相互作用：对神经元损伤的影响。
Hum Mol Genet. 2011 Jul 1;20(13):2495-509. doi: 10.1093/hmg/ddr139. Epub 2011 Mar 31.
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Cognitive impairment and increased Aβ levels induced by paraquat exposure are attenuated by enhanced removal of mitochondrial H(2)O(2).百草枯暴露引起的认知障碍和 Aβ水平升高可通过增强清除线粒体 H₂O₂来减弱。
Neurobiol Aging. 2012 Feb;33(2):432.e15-26. doi: 10.1016/j.neurobiolaging.2011.01.008. Epub 2011 Mar 22.
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