Location: Human Nutrition Research Center on Aging
Title: Fruit Polyphenols and their effects on Neuronal Signaling and Behavior in Senescence. Authors
Submitted to: Annals of the New York Academy of Sciences
Publication Type: Book / Chapter
Publication Acceptance Date: February 22, 2007
Publication Date: May 1, 2007
Citation: Joseph, J.A., Shukitt Hale, B., Lau, F.C. 2007. Fruit Polyphenols and their effects on Neuronal Signaling and Behavior in Senescence. Annals of the New York Academy of Sciences. 1100:470-485. Technical Abstract: The onset of age-related neurodegenerative diseases superimposed on a declining nervous system could exacerbate the motor and cognitive behavioral deficits that normally occur in senescence. It is likely that, in cases of severe deficits in memory or motor function, hospitalization and/or custodial care would be a likely outcome. This means that unless some way is found to reduce these age-related decrements in neuronal function, health care costs will continue to rise exponentially. Thus, it is extremely important to explore methods to retard or reverse the age-related neuronal deficits as well as their subsequent, behavioral manifestations. Applying molecular biological approaches to slow aging in the human condition may be years away. So it is important to determine what methods can be utilized today to increase healthy aging, forestall the onset of these diseases, and create conditions favorable to obtaining a “longevity dividend” in both financial and human terms. In this regard, epidemiological studies indicate that consumption of diets rich in antioxidants and anti-inflammatory compounds, such as those found in fruits and vegetables, may lower the risk of developing age-related neurodegenerative diseases such as Alzheimer or Parkinson Diseases (AD and PD). Research suggests that the polyphenolic compounds found in fruits such as blueberries may exert their beneficial effects by altering stress signaling and neuronal communication, suggesting that interventions may exert protection against age-related deficits in cognitive and motor function. The purpose of this review is to discuss the benefits of these interventions in rodent models and to describe the putative molecular mechanisms involved in their benefits.