Mitochondrial energy metabolism and redox signaling in brain aging and neurodegeneration.
CONCLUSIONS
The mitochondrial energy-transducing capacity is essential for the maintenance of neuronal function, and the impairment of energy metabolism and redox homeostasis is a hallmark of brain aging, which is particularly accentuated in the early stages of neurodegenerative diseases.


BACKGROUND
The communications between mitochondria and the rest of the cell by energy- and redox-sensitive signaling establish a master regulatory device that controls cellular energy levels and the redox environment. Impairment of this regulatory devise is critical for aging and the early stages of neurodegenerative diseases.


RESULTS
This review focuses on a coordinated metabolic network-cytosolic signaling, transcriptional regulation, and mitochondrial function-that controls the cellular energy levels and redox status as well as factors which impair this metabolic network during brain aging and neurodegeneration.


CONCLUSIONS
Characterization of mitochondrial function and mitochondria-cytosol communications will provide pivotal opportunities for identifying targets and developing new strategies aimed at restoring the mitochondrial energy-redox axis that is compromised in brain aging and neurodegeneration.
1 Department of Pharmacology and Pharmaceutical Sciences, School of Pharmacy, University of Southern California , Los Angeles, California.
Fei
F
Yin
Alberto
A
Boveris
Enrique
E
Cadenas
D000375:Aging / Q000378:metabolism*; D000818:Animals; D001921:Brain / Q000378:metabolism*; D002467:Cell Nucleus / Q000235:genetics / Q000378:metabolism; D016922:Cellular Senescence; D003600:Cytosol / Q000378:metabolism; D004734:Energy Metabolism; D005786:Gene Expression Regulation; D006706:Homeostasis; D006801:Humans; D008928:Mitochondria / Q000378:metabolism*; D019636:Neurodegenerative Diseases / Q000235:genetics / Q000378:metabolism*; D010084:Oxidation-Reduction; D015398:Signal Transduction; D014158:Transcription, Genetic