Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.
Mice with (a) high spontaneous neurological activity, or subjected to (b) moderate exercise or (c) dietary supplemented with high doses of vitamin E from 28 weeks of age to senescence (76 wk of age), showed an increased survival and a retardation in the development of the neurological deficits associated to aging. During aging there was an increase in dysfunctional brain mitochondria, characterized by an increased content of oxidation products and by a diminished functional activity. The mitochondrial oxidative damage observed in adult (52 wk) and senescent mice (76 wk) was partially ameliorated in the groups of animals subject to the mentioned experimental conditions, and this decrease in mitochondrial oxidative damage was related to the improvement in neurological performance. In brain mitochondria, the activities of enzymes that are critical for mitochondrial function (mtNOS, NADH-dehydrogenase, and cytochrome oxidase) decreased progressively during aging and constituted aging markers. Usual clinical recommendations for aged humans, such as increased neurological activity, moderate exercise, and vitamin E supplementation, proved to be effective in increasing mice survival and neurological performances, along with a better mitochondrial function and a lower content of oxidation products.