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.
| Original language | English |
|---|---|
| Pages (from-to) | 453-456 |
| Number of pages | 4 |
| Journal | Journal of Bioenergetics and Biomembranes |
| Volume | 41 |
| Issue number | 5 |
| DOIs | |
| State | Published - Oct 1 2009 |
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Keywords
- Alzheimer's disease
- Amyloid formation
- COX deficiency
- Oxidative stress
ASJC Scopus subject areas
- Physiology
- Cell Biology
Cite this
The role of cytochrome c oxidase deficiency in ROS and amyloid plaque formation. / Pickrell, Alicia M.; Fukui, Hirokazu; Moraes, Carlos T.
In: Journal of Bioenergetics and Biomembranes, Vol. 41, No. 5, 01.10.2009, p. 453-456.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - The role of cytochrome c oxidase deficiency in ROS and amyloid plaque formation
AU - Pickrell, Alicia M.
AU - Fukui, Hirokazu
AU - Moraes, Carlos T
PY - 2009/10/1
Y1 - 2009/10/1
N2 - 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.
AB - 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.
KW - Alzheimer's disease
KW - Amyloid formation
KW - COX deficiency
KW - Oxidative stress
UR - http://www.scopus.com/inward/record.url?scp=70449433157&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=70449433157&partnerID=8YFLogxK
U2 - 10.1007/s10863-009-9245-3
DO - 10.1007/s10863-009-9245-3
M3 - Article
VL - 41
SP - 453
EP - 456
JO - Journal of Bioenergetics and Biomembranes
JF - Journal of Bioenergetics and Biomembranes
SN - 0145-479X
IS - 5
ER -