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The role of abnormal mitochondrial dynamics in the pathogenesis of Alzheimer’s disease
Author(s) -
Wang Xinglong,
Su Bo,
Zheng Ling,
Perry George,
Smith Mark A.,
Zhu Xiongwei
Publication year - 2009
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2009.05867.x
Subject(s) - mitochondrial fusion , mitochondrion , mitochondrial fission , biology , alzheimer's disease , neuroscience , dnaja3 , organelle , microbiology and biotechnology , function (biology) , neurodegeneration , disease , mitochondrial dna , pathology , medicine , genetics , gene
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.