Mechanisms of impaired mitochondrial energy metabolism in acute and chronic neurodegenerative disorders

Altered mitochondrial energy metabolism contributes to the pathophysiology of acute brain injury caused by ischemia, trauma, and neurotoxins and by chronic neurodegenerative disorders such as Parkinson's and Huntington's diseases. Although much evidence supports that the electron transport...

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Bibliographic Details
Published in:Journal of neuroscience research 2007-11, Vol.85 (15), p.3407-3415
Main Authors: Soane, Lucian, Kahraman, Sibel, Kristian, Tibor, Fiskum, Gary
Format: Article
Language:English
Subjects:
Animals
apoptosis
Apoptosis - physiology
calcium
Energy Metabolism
Humans
Mitochondria - metabolism
Mitochondria - pathology
Mitochondrial Diseases - metabolism
Mitochondrial Diseases - physiopathology
mitochondrial permeability transition
Neurodegenerative Diseases - metabolism
Neurodegenerative Diseases - physiopathology
nitric oxide
PARP-1
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Summary:Altered mitochondrial energy metabolism contributes to the pathophysiology of acute brain injury caused by ischemia, trauma, and neurotoxins and by chronic neurodegenerative disorders such as Parkinson's and Huntington's diseases. Although much evidence supports that the electron transport chain dysfunction in these metabolic abnormalities has both genetic and intracellular environmental causes, alternative mechanisms are being explored. These include direct, reversible inhibition of cytochrome oxidase by nitric oxide, release of mitochondrial cytochrome c, oxidative inhibition of mitochondrial matrix dehydrogenases and adenine nucleotide transport, the availability of NAD for dehydrogenase reactions, respiratory uncoupling by activities such as that of the permeability transition pore, and altered mitochondrial structure and intracellular trafficking. This review focuses on the catabolism of neuronal NAD and the release of neuronal mitochondrial NAD as important contributors to metabolic dysfunction. In addition, the relationship between apoptotic signaling cascades and disruption of mitochondrial energy metabolism is considered in light of the fine balance between apoptotic and necrotic neural cell death. © 2007 Wiley‐Liss, Inc.
ISSN:0360-4012
1097-4547
DOI:10.1002/jnr.21498