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阿尔茨海默病的线粒体功能紊乱机制 被引量：7

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摘要 线粒体对于神经元的生存发挥关键作用,氧化应激引起细胞凋亡是AD早期的主要特征。线粒体形态结构发生改变和线粒体DNA突变都可以造成线粒体功能紊乱,表现为电子传递链的损伤如细胞色素氧化酶活性降低,线粒体动力学异常如线粒体自噬增加、分裂融合失衡、生物合成障碍、转运功能下降等,淀粉样蛋白生成进一步增加,最终导致不可逆的神经元损伤,散发性AD发生。针对线粒体损伤的治疗措施,为AD的治疗带来新的选择。
作者 李玉梅 付剑亮
机构地区 上海交通大学附属第六人民医院神经内科
出处 《国际神经病学神经外科学杂志》 2013年第1期70-74,共5页 Journal of International Neurology and Neurosurgery
关键词 阿尔茨海默病 线粒体 Β-淀粉样蛋白 氧化应激
分类号 R749.16 [医药卫生—神经病学与精神病学]
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参考文献28

  • 1Sperling RA, Aisen PS, Beckett LA, et al. Toward defining the preclinical stages of Alzheimer' s disease: recommenda- tions from the National Institute on Aging-Alzheimer' s Asso- ciation workgroups on diagnostic guidelines for Alzheimer' s disease. Alzhelmers Dement, 2011 , 7 ( 3 ) : 280-292.
  • 2Swerdlow RH, Khan SM. A " mitochondrial cascade hypothe- sis" for sporadic Alzheimer' s disease. Med Hypotheses, 2004, 63(1) : 8-20.
  • 3Bosetti F, Brizzi F, Barogi S, et al. Cytochrome e oxidase and mitochondrial F1 F0-ATPase ( ATP synthase ) activities in platelets and brain from patients with Alzheimer ' s disease. Neurobiol Aging, 2004, 25(1) : 105-110.
  • 4Alleyne T, Mohan N, Joseph J, et al. Unraveling the role of metal ions and low catalytic activity of eytochrome C oxidase in Alzheimer' s disease. J Mol Neurosci, 2011, 43 (3) : 284-289.
  • 5黄丹华,周珊珊,张黎明.氧化应激与阿尔茨海默病[J].国际神经病学神经外科学杂志,2012,39(3):268-270. 被引量：2
  • 6Zhang F, Wang S, Gan L, et al. Protective effects and mechanisms of sirtuins in the nervous system. Prog Neurobiol, 2011, 95(3) : 373-395.
  • 7Finkel T. Signal transduction by reactive oxygen species. J Cell Biol, 2011, 194(1) : 7-15.
  • 8Adler V, Yin Z, Tew KD, et al. Role of" redox potential and reactive oxygen species in stress signaling. Oncogene, 1999, 18(45): 6104-6111.
  • 9Guo X, Wu X, Ren L, et al. Epigenetic mechanisms of am- yloid-β production in anisomycin-treated SH-SY5Y cells. Neuroscience, 2011 , 194 : 272-281.
  • 10刘蓉,叶兰,徐运.阿尔茨海默病中β淀粉样多肽与线粒体异常及靶向治疗[J].国际神经病学神经外科学杂志,2010,37(3):270-274. 被引量：5

二级参考文献49

  • 1Wang X, Su B, Perry G, et al. Insights into amyloid-β-induced mitochondrial dysfunction in Alzheimer disease. Free Radic Biol Med, 2007, 43( 12): 1569-1573.
  • 2Hansson-Petersen CA, Alikhani N, Behbahani H, et al. The amyloidβ-peptide is imported into mitochondria via the TOM import machinery and localized to mitochondrial cristae. Proc Natl Acad Sci U S A, 2008, 105 (35): 13145- 13150.
  • 3Butterfield DA, Reed T, Newman SF, et al. Roles of amytoid β-peptide-associated oxidative stress and brain protein modifications in the pathogenesis of Alzheimer' s disease and mild cognitive impairment. Free Radic Biol Med, 2007, 43 (5) : 658-677.
  • 4Manczak M, Anekonda TS, Henson E, et al. Mitochondria are a direct site of A beta accumulation in Alzheimer' s disease neurons: implications for free radical generation and oxidative damage in disease progression. Hum Mol Genet, 2006, 15(9): 1437-1449.
  • 5Devi L, Prabhu BM, Galati DF, et al. Accumulation of amyloid precursor protein in the mitochondrial import channels of human Alzheimer' s disease brain is associated with mitochondrial dysfunction. J Neurosci, 2006, 26 (35): 9057- 9068.
  • 6Sirk D, Zhu Z, Wadia JS, et al. Chronic exposure to sublethal beta-amyloid inhibits the import of nuclear encoded proteins to mitochondria in differentiated PC 12 cells. J Neurochem, 2007, 103(5): 1989-2003.
  • 7Reddy PH. Amyloid beta, mitochondrial structural and functional dynamics in Alzheimer' s disease. Exp Neurol, 2009, 218(2) : 286-292.
  • 8Hong WK, Han EH, Kim DG, et al. Amyloid-beta-peptide reduces the expression level of mitochondrial cytochrome oxidase subunits. Neurochem Res, 2007, 32 (9): 1483- 1488.
  • 9Wang X, Su B, Fujioka H, et al. Dynamin-Like Protein 1 Reduction Underlies Mitochondrial Morphology and Distribution Abnormalities in Fibroblasts from Sporadic Alzheimer' s Disease Patients. Am J Pathol, 2008, 173(2) : 470-482.
  • 10Twig G, Elorza A, Molina A J, et al. Fission and selective fusion govern mitochondrial segregation and elimination by autophagy. EMBO J, 2008, 27(2) : 433-446.

共引文献5

同被引文献137

  • 1高欣,唐希灿.神经退行性疾病的早期信号:线粒体功能障碍[J].生命科学,2006,18(2):138-144. 被引量：15
  • 2周仲瑛.中医内科学[M].北京:中国中医药出版社,2007:297
  • 3Burns A, Iliffe S. Alzheimer's disease[J]. BMJ, 2009, 338: b158.
  • 4Zieske LR. A perspective on the use of iTRAQ reagent tech nology for protein complex and profiling studies[J]. Exp Bot, 2006, 57: 1501-1508.
  • 5Ralhan R, Desouza LV, Matta A, et al. Discovery and verifi- cation of head-and-neck cancer biomarkers by differential pro tein expression analysis using iTRAQ labeling, multidimen sional liquid chromatography, and tandem mass spectrometry [J]. MolCellProteomics, 2008,7: 1162-1173.
  • 6Pierce A, Unwin RD, Evans CA, et al. Eight-channel iTRAQ enables comparison of the activity of six leukemogen- ic tyrosine kinases[J]. Mol Cell Proteomics, 2008, 7: 853- 863.
  • 7Huang DW, Sherman BT, Lempicki RA. Systematic and integrative analysis of large gene lists using DAVID bioinfor- maties resourees[J]. Nat Protoc, 2009,4:44-57.
  • 8Sweatt JD. Mitogen activated protein kinases in synaptic plas ticityand memory[J]. Curr Opin Neurobiol, 2004 ,14 : 311-317.
  • 9Feld M, Dimant B, Delorenzi A, et al. Phosphorylation of extra nuclear ERK/MAPK is required for long-term memory consolidation in the crab Chasmagnathus[J]. Behav Brain Res,2005,158:251 -261.
  • 10Subramaniam S, Zirrgiebel U, von BUHO, et al. ERK acti- vation promotes neuronal degeneration predominantly through plasma membrane damage and independently of caspase 3[J]. Cell Biol, 2004, 165: 357-369.

引证文献7

二级引证文献45

国际神经病学神经外科学杂志
2013年 第1期

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