Mitochondrial inhibition and oxidative stress: Reciprocating players in neurodegeneration

Gail D. Zeevalk, L. P. Bernard, C. Song, M. Gluck, J. Ehrhart

Research output: Contribution to journalReview articlepeer-review

73 Scopus citations


Although the etiology for many neurodegenerative diseases is unknown, the common findings of mitochondrial defects and oxidative damage posit these events as contributing factors. The temporal conundrum of whether mitochondrial defects lead to enhanced reactive oxygen species generation, or conversely, if oxidative stress is the underlying cause of the mitochondrial defects remains enigmatic. This review focuses on evidence to show that either event can lead to the evolution of the other with subsequent neuronal cell loss. Glutathione is a major antioxidant system used by cells and mitochondria for protection and is altered in a number of neurodegenerative and neuropathological conditions. This review also addresses the multiple roles for glutathione during mitochondrial inhibition or oxidative stress. Protein aggregation and inclusions are hallmarks of a number of neurodegenerative diseases. Recent evidence that links protein aggregation to oxidative stress and mitochondrial dysfunction will also be examined. Lastly, current therapies that target mitochondrial dysfunction or oxidative stress are discussed.

Original languageEnglish
Pages (from-to)1117-1139
Number of pages23
JournalAntioxidants and Redox Signaling
Issue number9-10
StatePublished - Sep 2005


Dive into the research topics of 'Mitochondrial inhibition and oxidative stress: Reciprocating players in neurodegeneration'. Together they form a unique fingerprint.

Cite this