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Review
, 109 Suppl 1 (Suppl 1), 153-9

The Role of Abnormal Mitochondrial Dynamics in the Pathogenesis of Alzheimer's Disease

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Review

The Role of Abnormal Mitochondrial Dynamics in the Pathogenesis of Alzheimer's Disease

Xinglong Wang et al. J Neurochem.

Abstract

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.

Figures

Figure 1
Figure 1. Schematic Illustration of the Involvement of Abnormal Mitochondrial Dynamics in the Pathogenesis of Alzheimer Disease
Pathogenic factors such as oxidative stress and Aβ impair the delicate balance of mitochondria fission and fusion dynamics in the vulnerable neurons, which not only results in mitochondrial morphological change and structural damage that in turn further enhance ROS production and thus a vicious cycle ensues, but also leads to mitochondrial re-distribution from an evenly distribution pattern to accumulation in the cell body and depletion in the remote area such as axon or dendrite. Together, the abnormal mitochondrial dynamics causes mitochondrial dysfunction and neuronal dysfunction including synaptic dysfunction, and eventually neurodegeneration.

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