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The role of abnormal mitochondrial dynamics in the pathogenesis of Alzheimer's disease
被引:230
作者:
Wang, Xinglong
[1
]
Su, Bo
[1
]
Zheng, Ling
[2
]
Perry, George
[1
,3
]
Smith, Mark A.
[1
]
Zhu, Xiongwei
[1
]
机构:
[1] Case Western Reserve Univ, Dept Pathol, Cleveland, OH 44106 USA
[2] Wuhan Univ, Coll Life Sci, Wuhan 430072, Peoples R China
[3] Univ Texas San Antonio, Coll Sci, San Antonio, TX USA
关键词:
Alzheimer disease;
DLP1;
mitochondrial distribution;
mitochondrial dynamics;
mitochondrial dysfunction;
synaptic dysfunction;
DOMINANT OPTIC ATROPHY;
AMYLOID-BETA;
CALCIUM HOMEOSTASIS;
FISSION MACHINERY;
FUSION MEDIATORS;
2-HIT HYPOTHESIS;
AXONAL-TRANSPORT;
MAMMALIAN-CELLS;
GTPASE;
OPA1;
D O I:
10.1111/j.1471-4159.2009.05867.x
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:
Mitochondria play critical roles in neuronal function and almost all aspects of mitochondrial function are altered in Alzheimer neurons. Emerging evidence shows that mitochondria are dynamic organelles that undergo continuous fission and fusion, the balance of which not only controls mitochondrial morphology and number, but also regulates mitochondrial function and distribution. In this review, after a brief overview of the basic mechanisms involved in the regulation of mitochondrial fission and fusion and how mitochondrial dynamics affects mitochondrial function, we will discuss in detail our and others' recent work demonstrating abnormal mitochondrial morphology and distribution in Alzheimer's disease (AD) models and how these abnormalities may contribute to mitochondrial and synaptic dysfunction in AD. We propose that abnormal mitochondrial dynamics plays a key role in causing the dysfunction of mitochondria that ultimately damage AD neurons.
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页码:153 / 159
页数:7
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