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Oxidative Stress, Cognitive Dysfunction, and Brain Aging

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Studies on Veterinary Medicine

Abstract

Oxidative damage is a consistent feature of brain aging in all species studied. Decline in cognitive functions, which accompanies aging, may have a biological basis, and many of the disorders associated with aging may be preventable through dietary modifications that incorporate specific nutrient. Based on previous research and results of both laboratory and clinical studies in the canine model of human aging and disease, antioxidants may be one class of nutrient that may be beneficial. Brains of aged dogs accumulate oxidative damage to proteins and lipids, and mitochondrial dysfunction that may lead to impaired neuronal function. The production of free radicals and lack of increase in compensatory antioxidant enzymes may lead to increased damage to macromolecules within neurons. Reducing oxidative damage and mitochondrial dysfunction through a diet rich in antioxidants and mitochondrial cofactors significantly improves, or slows the decline of, learning and memory in aged dogs. Furthermore, there are clear links between the reduction of brain oxidative damage and mitochondrial impairments and improved or maintained cognitive function. However, determining which compounds, which combinations and dosage range, when to initiate intervention, and long-term effects constitute critical gaps in knowledge.

This work was supported by Grant No. AG12694 from the National Institutes of Aging, U.S. Department of the Army, Contract No. DAMD17-98-1-8622. The content of the information does not necessarily reflect the position or the policy of the government, and no official endorsement should be inferred. Hill’s Pet Nutrition, Topeka, KS, provided additional funding.

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Head, E., Zicker, S.C. (2011). Oxidative Stress, Cognitive Dysfunction, and Brain Aging. In: Mandelker, L., Vajdovich, P. (eds) Studies on Veterinary Medicine. Oxidative Stress in Applied Basic Research and Clinical Practice. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-61779-071-3_7

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