Sixty years old is the breakpoint of human frontal cortex aging

Cabré Cucó, Rosanna; Naudí i Farré, Alba; Dominguez Gonzalez, Mayelin; Ayala Jové, Ma. Victoria (Maria Victoria); Jové Font, Mariona; Mota Martorell, Natàlia; Piñol Ripoll, Gerard; Gil Villar, M. Pilar; Rué i Monné, Montserrat; Portero Otín, Manuel; Ferrer, Isidre; Pamplona Gras, Reinald

doi:https://doi.org/10.1016/j.freeradbiomed.2016.12.010

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2017

Author

Cabré Cucó, Rosanna

Naudí i Farré, Alba

Dominguez Gonzalez, Mayelin

Ayala Jové, Ma. Victoria (Maria Victoria)

Jové Font, Mariona

Mota Martorell, Natàlia

Piñol Ripoll, Gerard

Gil Villar, M. Pilar

Rué i Monné, Montserrat

Portero Otín, Manuel

Ferrer, Isidre

Pamplona Gras, Reinald

Suggested citation

Cabré Cucó, Rosanna; Naudí i Farré, Alba; Dominguez Gonzalez, Mayelin; Ayala Jové, Ma. Victoria (Maria Victoria); Jové Font, Mariona; Mota Martorell, Natàlia; ... Pamplona Gras, Reinald. (2017) . Sixty years old is the breakpoint of human frontal cortex aging. Free Radical Biology and Medicine, 2017, vol. 103, p. 14–22. https://doi.org/10.1016/j.freeradbiomed.2016.12.010.

Abstract

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. Human neurons 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.

URI

http://hdl.handle.net/10459.1/60010

DOI

https://doi.org/10.1016/j.freeradbiomed.2016.12.010

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Free Radical Biology and Medicine, 2017, vol. 103, p. 14–22

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Except where otherwise noted, this item's license is described as cc-by-nc-nd (c) Elsevier, 2016