The role of cytochrome <Emphasis Type="Italic">c</Emphasis> oxidase deficiency in ROS and amyloid plaque formation |
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Authors: | Alicia M Pickrell Hirokazu Fukui Carlos T Moraes |
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Institution: | (1) Department of Cell and Molecular Biology, The Feinberg School of Medicine, Northwestern University, Chicago Avenue, Chicago, IL, USA |
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Abstract: | The multiple dysfunctional changes associated with a brain affected with Alzheimer’s disease (AD) makes the understanding
of primary pathogenic mechanisms challenging. Mitochondrial dysfunction has been associated with almost every neurodegenerative
disease and neurodegenerative-related event. Alzheimer’s disease is no exception with data suggesting mitochondrial malfunctions
ranging from improper organelle dynamics, defective oxidative phosphorylation (OXPHOS), oxidative stress, and harmful beta
amyloid (Aβ) associations with the mitochondria. A major change often associated with AD is impairment of the electron transport
chain at complex IV: cytochrome c oxidase (COX). This mini-review concentrates on recent work by our group that sheds light on the role COX deficiency plays
in the pathophysiology of AD using a transgenic mouse model. Results suggest that neuronal COX deficiency does not increase
oxidative stress and nor increases amyloidal formations in vivo. Conclusions from this work also suggest that Aβ formation is a cause of COX deficiency as opposed to the consequence. |
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