Fruit polyphenols and their effects on neuronal signaling and behavior in senescence

被引:81
作者
Joseph, James A. [1 ]
Shukitt-Hale, Barbara [1 ]
Lau, Francis C. [1 ]
机构
[1] Tufts Univ, USDA, HNRCA, Boston, MA 02111 USA
来源
BIOGERONTOLOGY: MECHANISMS AND INTERVENTIONS | 2007年 / 1100卷
关键词
oxidants; antioxidants; Alzheimer's; Parkinson's; life span;
D O I
10.1196/annals.1395.052
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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, healthcare 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 used 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's or Parkinson's 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 article is to discuss the benefits of these interventions in rodent models and to describe the putative molecular mechanisms involved in their benefits.
引用
收藏
页码:470 / 485
页数:16
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