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Lipids and lipoxidation in human brain aging. Mitochondrial ATP-synthase as a key lipoxidation target

Journal

REDOX BIOLOGY
Volume 23, Issue -, Pages -

Publisher

ELSEVIER
DOI: 10.1016/j.redox.2018.101082

Keywords

Advanced lipoxidation end products; Aging; Antioxidants; Cytoskeleton; Energy metabolism; Lipidomics; Neurotransmission; Oxidative stress; Proteostasis; Reactive carbonyl species; Redox proteomics

Funding

  1. Spanish Ministry of Economy and Competitiveness (Institute of Health Carlos III, Spain, FIS grants ) [PI14/00757, PI14/00328PI14/00328]
  2. Autonomous Government of Catalonia (Catalonia, Spain) [2017SGR696]
  3. FEDER funds from the European Union ('A way to build Europe')

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The human brain is a target of the aging process like other cell systems of the human body. Specific regions of the human brain exhibit differential vulnerabilities to the aging process. Yet the underlying mechanisms that sustain the preservation or deterioration of neurons and cerebral functions are unknown. In this review, we focus attention on the role of lipids and the importance of the cross-regionally different vulnerabilities in human brain aging. In particular, we first consider a brief approach to the lipidomics of human brain, the relationship between lipids and lipoxidative damage, the role of lipids in human brain aging, and the specific targets of lipoxidative damage in human brain and during aging. It is proposed that the restricted set of modified proteins and the functional categories involved may be considered putative collaborative factors contributing to neuronal aging, and that mitochondrial ATP synthase is a key lipoxidative target in human brain aging.

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