Submitted to: Inflammation in the Pathogenesis of Chronic Diseases
Publication Type: Book / Chapter
Publication Acceptance Date: October 1, 2006
Publication Date: April 1, 2007
Citation: Lau, F.C., Shukitt Hale, B., Joseph, J.A. 2007. Nutritional Intervention in Brain Aging: Reducing the Effects of Inflammation and Oxidative Stress. Inflammation in the Pathogenesis of Chronic Diseases:The COX-2 controversy. Subcellular Biochemistry. Volume 42. New York, NY:Springer Publication. p.299-318. Technical Abstract: It is estimated that by the year 2050 the elderly (aged 65 or older) population will double the population of children (aged 0 – 14) for the first time in history. The expansion of the elderly population has already taken a toll on health care systems. In order to alleviate the health care costs and increase the quality of living in the aging population, it is crucial to explore methods that may retard or reverse the deleterious effects of aging. Inflammation and oxidative stress play important roles in brain aging. Inflammatory markers, as well as cellular and molecular oxidative damage, increase during normal brain aging. This increase is accompanied by the concomitant decline in cognitive and motor performance in the elderly population, even in the absence of neurodegenerative diseases. Epidemiological studies have shown that consumption of diets rich in antioxidant and anti-inflammatory agents, such as those found in fruits and vegetables, may lower the risk of developing age-related neurodegenerative diseases such as Parkinson’s disease and Alzheimer’s disease. Research from our laboratory suggests that dietary supplementation with fruit or vegetable extracts can decrease the age-enhanced vulnerability to oxidative stress and inflammation. Additional research suggests that the polyphenolic compounds found in fruits such as blueberries may exert their beneficial effects through signal transduction and neuronal communication. Thus, nutritional intervention may exert a therapeutic protection against age-related deficits and neurodegenerative diseases.