Mitochondria, Cybrids, Aging, and Alzheimer's Disease

被引:79
作者
Swerdlow, R. H. [1 ]
Koppel, S. [1 ]
Weidling, I. [1 ]
Hayley, C. [1 ]
Ji, Y. [1 ]
Wilkins, H. M. [1 ]
机构
[1] Univ Kansas, Sch Med, Landon Ctr Aging, Alzheimers Dis Ctr, Kansas City, KS 66160 USA
来源
MOLECULAR BIOLOGY OF AGING | 2017年 / 146卷
关键词
CYTOCHROME-C-OXIDASE; AMYLOID PRECURSOR PROTEIN; MATERNAL FAMILY-HISTORY; COMPLEX I INHIBITOR; PRODROMAL METABOLIC PHENOTYPE; ELECTRON-TRANSPORT CHAIN; MTDNA CONTROL-REGION; A-BETA ACCUMULATION; GRAY-MATTER VOLUME; POLY-T LENGTH;
D O I
10.1016/bs.pmbts.2016.12.017
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Mitochondrial and bioenergetic function change with advancing age and may drive aging phenotypes. Mitochondrial and bioenergetic changes are also documented in various age-related neurodegenerative diseases, including Alzheimer's disease (AD). In some instances AD mitochondrial and bioenergetic changes are reminiscent of those observed with advancing age but are greater in magnitude. Mitochondrial and bioenergetic dysfunction could, therefore, link neurodegeneration to brain aging. Interestingly, mitochondrial defects in AD patients are not brain-limited, and mitochondrial function can be linked to classic AD histologic changes including amyloid precursor protein processing to beta amyloid. Also, transferring mitochondria from AD subjects to cell lines depleted of endogenous mitochondrial DNA (mtDNA) creates cytoplasmic hybrid (cybrid) cell lines that recapitulate specific biochemical, molecular, and histologic AD features. Such findings have led to the formulation of a "mitochondrial cascade hypothesis" that places mitochondrial dysfunction at the apex of the AD pathology pyramid. Data pertinent to this premise are reviewed.
引用
收藏
页码:259 / 302
页数:44
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