Diseases such as Alzheimer’s that lead to decline in mental faculties are associated with a complex multitude of risk factors, including nutrient deficiencies and genetic predisposition. This study on mice showed that supplementation of diet with a variety of compounds, such as vitamin E, folic acid, iron and other nutrients such as DHA (docosahexaenoic acid), ALA (alpha-lipoic acid) etc., help reduce oxidative stress and could delay the decline in cognitive abilities. These agents reduced oxidative stress-causing radicals by 57% when compared to mice that were not given these agents in the diet.
Studies have shown that the elderly, who are at a greater risk of cognitive decline and disease like Alzheimer’s, may be at risk of certain nutrient deficiencies and genetic predispositions. Studies in laboratory animals such as mice have shown that dietary restrictions may lead to similar cognitive decline whereas supplementation of diet with certain nutrients helps in preventing cognitive deterioration. This means that in genetically susceptible individuals, appropriate dietary supplements can help in the prevention of cognitive damage. It is also known that with age and other factors, oxidative damage to the brain cells plays a large role in cognitive decline. This study attempted to see if dietary supplementation with nutrients that showed antioxidant capacity in laboratory mice could also prevent cognitive damage. The exact efficacy of these nutrients on oxidative stress was assessed.
- A total of 9 adult mice aged 9-12 months were divided into three groups with three mice in each group. Some of the mice lacked genes that would allow them to utilize vitamin E effectively and these mice were termed “ApoE minus”.
- One group received folic acid and vitamin E, while the other did not. This second group was given Iron supplementation that produces oxidative stress.
- A third group of mice received both the above diets and were also given in addition a formulation of agents such as “ALA, ALCAR (acetyl-L-carnitine), DHA, GPC (glycerophosphocoline), and PS (phosphatidylserine)”.
- Results showed that there was marked oxidative stress in the brains of the two groups of mice that received the diet deficient in vitamin E and folic acid. ApoE minus mice showed more oxidative stress when given a vitamin E- and folic acid-deficient diet.
- However, when these two groups, with or without vitamin A and folic acid supplementation, received the formulation, oxidative stress causing-radicals fell by 57% causing a marked fall in brain oxidative stress. The ApoE minus mice also showed a decline in oxidative stress when given the formulation.
- The mice that were not on vitamin E and folic acid but were on the formulation, showed a 15% improvement in cognitive functions and performance.
Authors admit that they did not fully explore the reason why these nutrients aid in protecting the nerves of the brain and improving cognitive performance. They speculate that the formulation containing DHA, GPC and PS may help in the formation of new cells. They suggest further studies that explore the mechanisms by which these nutrients can help in the prevention of cognitive decline.
This study reveals that supplementation of diet with vitamin E and folic acid and other agents such as ALA, DHA, and GPC may aid in decreasing oxidative stress of mouse brains even in mice genetically incapable of using antioxidants such as vitamin E. Taken further, this reveals that such dietary supplementation also helps improve cognitive performance in the normal mice. This study is a significant step towards development of newer preventive nutritional therapies in the elderly who are susceptible to cognitive decline and related diseases such as Alzheimer’s. It also enables an understanding of the involvement of oxidative stress and other molecular mechanisms that lead to age-related loss of cognitive abilities.
For More Information:
Dietary Supplementation Reduces Oxidative Damage to Mouse Brain and Improves Cognitive Performance
Nutrition Research, 2009
By James Suchy; Amy Chan
From the University of Massachusetts Lowell, Lowell, Massachusetts
*FYI Living Lab Reports Are Summaries of the Original Research.