Brain Aging and Mitochondria-Targeted Plastoquinone Antioxidants of SkQ-Type

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N. K. Isaev^1,2,3*, E. V. Stelmashook^2,3, N. N. Stelmashook⁴, I. N. Sharonova², and V. G. Skrebitsky²

¹Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, 119992 Moscow, Russia; fax: (495) 939-3181; E-mail: isaev@genebee.msu.ru

²Research Center of Neurology, Russian Academy of Medical Sciences, Volokolamskoe Shosse 80, 125367 Moscow, Russia

³Institute of Mitoengineering, Lomonosov Moscow State University, 119992 Moscow, Russia

⁴Bauman Moscow State Technical University, 2-ya Baumanskaya ul. 5, 105005 Moscow, Russia

^* To whom correspondence should be addressed.

Received July 11, 2012; Revision received November 2, 2012

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Normal brain aging leads to decrease in cognitive functions, shrink in brain volume, loss of nerve fibers and degenerating myelin, reduction in length and branching of dendrites, partial loss of synapses, and reduction in expression of genes that play central roles in synaptic plasticity, vesicular transport, and mitochondrial functioning. Impaired mitochondrial functions and mitochondrial reactive oxygen species can contribute to the damage of these genes in aging cerebral cortex. This review discusses the possibility of using mitochondria-targeted antioxidants to slow the processes of brain aging.

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KEY WORDS: brain aging, neurons, mitochondria-targeted antioxidants

DOI: 10.1134/S0006297913030127

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