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β淀粉样蛋白对线粒体作用的研究进展 被引量:2

Advances in understanding the effect of amyloid-β on mitochondrial
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摘要 阿尔茨海默病的一个重要病理特征是胞外β淀粉样蛋白沉积形成的老年斑,β淀粉样蛋白可以引起氧化损伤以及神经细胞凋亡等。随着研究的深入,在细胞内也发现了β淀粉样蛋白的存在。线粒体是细胞内ATP和活性氧自由基产生的主要部位,在氧化损伤和细胞凋亡过程中起到重要的作用。近年的研究表明,β淀粉样蛋白对线粒体有很重要的作用。该文主要针对这一领域的进展,介绍了阿尔茨海默病中β淀粉样蛋白对线粒体多个生理过程的作用以及这些作用在阿尔茨海默病中产生的影响。 Alzheimer's disease (AD) is characterized by the impairment of cognitive functions and changes in behavior and personality. Mitochondrial oxidative damage and synaptic pathology have recently been reported as early events in AD progression. Increasing evidence suggests that amyloid-β might be the causal factor of mitochondrial oxidative damage and synaptic pathology in AD and the effect of amyloid-β on mitochondrial might be an upstream event in the pathogenesis of AD. In this review we made a summary of the effect of amyloid-β on mitochondrial in Alzheimer's disease.
出处 《生命科学》 CSCD 北大核心 2009年第4期504-507,共4页 Chinese Bulletin of Life Sciences
基金 北京市属高等学校人才强教计划资助项目(PHR20090513)
关键词 Β淀粉样蛋白 线粒体 阿尔茨海默病 amyloid-β mitochondrial Alzheimer's disease
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参考文献21

  • 1Huang HC, Jiang ZF. Accumulated amyloid-β peptide and hyperphosphorylated tan protein: relationship and links in Alzheimer's Disease. J Alzheimers Dis, 2009, 16(1): 15-27.
  • 2Melov S, Adlard PA, Hinerfeld D, et al. Mitochondrial oxidative stress causes hyperphosphorylation of tau. PLoS ONE, 2007, 2(6):e536.
  • 3Reddy PH. Amyloid β, mitochondrial structural and functional dynamics in Alzheimer's disease. Exp Neurol, 2009, 218(2):286-92.
  • 4Wang XL, Su B, Zhu X, et al. Insights into amyloid-β-induced mitochondrial dysfunction in Alzheimer disease. Free Radic Biol Med, 2007, 43(12):1569-73.
  • 5Falkevall A, Alikhani N, Johnson KA, et al. Degradation of the amyloid β-protein by the novel mitochondrial peptidasome, PreP. J Biol Chem, 2006, 281(39):29096-104.
  • 6Hansson Petersen CA, Alafuzoff I, Leinonen V, et al. The amyloid β-peptide is imported into mitochondria via the TOM import machinery and localized to mitochondrial cristae. Proc Natl Acad Sci USA, 2008, 105(35):13145-50.
  • 7Sirk D, Zhu Z, Fong J, et al. Chronic exposure to sub-lethal β-amyloid (Aβ) inhibits the import of nuclear-encoded proteins to mitochondria in differentiated PC12 cells. J Neurochem, 2007, 103(5):1989-2003.
  • 8Wang XL, Su B, Zheng L, et al. The role of abnormal, mitochondrial dynamics in the pathogenesis of Alzheimer's disease. J Neurochem, 2009, 109:153-9.
  • 9Knott AB, Bossy-Wetzel E. Impairing the mitochondrial fission and fusion balance: a new mechanism of neurodegeneration. Ann N Y Acad Sci, 2008, 1147:283-92.
  • 10Wang XL, Su B, Siedlak SL, et al. Amyloid-β overproduction causes abnormal mitochondrial dynamics via differential modulation of mitochondrial fission/fusion proteins. Proc Natl Acad Sci USA, 2008, 105(49): 19318-23.

同被引文献30

  • 1Ankarcrona M, Mangialasche F, Winblad B. Rethin- king Alzheimer' s disease therapy: are mitochondria the key? [J]. J Alzheimers Dis, 2010, 20 (suppl 2): 579-590.
  • 2Maruszak A, Zekanowski C. Mitochondrial dysfunction and Alzheimer's disease [ J]. Prog Neuropsychophar- macol Biol Psychiatry, 2010, Jul 16 [Epub ahead of print ].
  • 3Hirai K, Aliev G, Nunomura A, et al. Mitochondrial abnormalities in Alzheimer' s disease [ J]. J Neuros- ci, 2001, 21 (9): 3017-3023.
  • 4Manczak M, Anekonda TS, Henson E, et al. Mito- chondria are a direct site of a beta accumulation in Alzheimer' s disease neurons : implications for free rad- ical generation and oxidative damage in disease progres- sion [J]. Hum Mol Genet, 2006, 15 (9): 1437- 1449.
  • 5Seshadri S, Beiser A, Selhub J, et al. Plasma homo- cysteine as a risk factor for dementia and Alzheimer' sdisease [J]. N Engl J Med, 2002, 346 (7): 476- 483.
  • 6Nakamura T, Watanabe A, Fujino T, et al. Apoli- poprotein E4 (1 -272 ) fragment is associated with mi- tochondrial proteins and affects mitochondrial function in neuronal cells [ J ]. Mol Neurodegener, 2009, 4: 35.
  • 7Pratico D. Evidence of oxidative stress in Alzheimers disease brain and antioxidant therapy: lights and shad- ows [J]. Ann N Y Acad Sci, 2005, 1147:70 -78.
  • 8Reddy PH, Beal MF. Amyloid beta, mitochondrial dysfunction and synaptie damage: implications for cog- nitive decline in aging and Alzheimer' s disease [J]. Trends Mol Med, 2008, 14 (2) : 45 -53.
  • 9Nunomura A, Perry G, Hirai K, et al. Neuronal RNA oxidation in Alzheimer' s disease and Down' s syndrome [J]. Ann N Y Aead Sci, 1999, 893:362 364.
  • 10Nunomura A, Perry G, Pappolla MA, et al. RNA ox- idation is a prominent feature of vulnerable neurons in Alzheimer' s disease [ J]. J Neurosci, 1999, 19 (6) : 1959 - 1964.

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