期刊
FREE RADICAL BIOLOGY AND MEDICINE
卷 103, 期 -, 页码 14-22出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2016.12.010
关键词
Cell survival pathways; Mechanistic target of rapamycin (mTOR); Mitochondria respiratory chain; Mitochondrial stress; Protein oxidation; Repressor element 1-silencing transcription factor (REST)
资金
- Autonomous Government of Catalonia
- Spanish Ministry of Economy and Competitiveness, Institute of Health Carlos III (FIS) [PI14/00757, PI14/00328]
- Autonomous Government of Catalonia [2014SGR69, 2014SGR168]
- FEDER funds from European Union ('a way to build Europe')
Human brain aging is the physiological process which underlies as cause of cognitive decline in the elderly and the main risk factor for neurodegenerative diseases such as Alzheimer's disease. Humadneurons are functional throughout a healthy adult lifespan, yet the mechanisms that maintain function and protect against neurodegenerative processes during aging are unknown. Here we show that protein oxidative and glycoxidative damage significantly increases during human brain aging, with a breakpoint at 60 years old. This trajectory is coincident with a decrease in the content of the mitochondrial respiratory chain complex I-IV. We suggest that the deterioration in oxidative stress homeostasis during aging induces an adaptive response of stress resistance mechanisms based on the sustained expression of REST, and increased or decreased expression of Akt and mTOR, respectively, over the adult lifespan in order to preserve cell neural survival and function.
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