Research Provides Further Support for Lifelong Influences on Brain and Cognitive Health

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Although most studies on AD address changes in late midlife and old age, there is some evidence to suggest that susceptibility to age-related cognitive changes or AD may be related to variables from much earlier in life. One set of evidence comes from studies on epidemiology of AD. For example, a paper from the Nun Study correlated the complexity of nuns' writing styles in late teenage years with their risk of developing AD in later life (Snowdon et al., 1996), and several studies suggest that more education is a protective factor for AD. The idea of "brain reserve" suggests that the more healthy neurons and connections between them can be established when the brain is developing in the fetus and maintained in later stages of development, the more time it will take for the ravages of AD to be manifested clinically. Studies in rats show that exercise can increase the number of neurons in a specific region of the hippocampus, suggesting that behavior modifications can modify the structure of adult brain. Could this be one approach to alleviating age-related decline? Would an enriched environment in early life be protective in our later years?

Another potentially important factor in promoting optimum brain health in later years is diet, even in the fetus. Recent research from investigators at Boston University School of Medicine has shown that alterations in choline availability to pregnant rats at the time the fetal brain is developing result in lifelong behavioral changes (Blusztajn, 1998). Offspring from choline-supplemented mothers were more adept as adults at tasks that measured attention and memory compared to the control and choline-deficient experimental groups. This improvement in cognitive behavior was evident even when the rats became very old. Thus, prenatal choline availability and supplementation alleviated the age-related decline in memory function, suggesting that long-lasting brain structural and functional changes are induced by choline. Could these play a part in defending against the clinical expression of AD? The results of these studies played a key role in the April 1998 decision by the Food and Nutrition Board of the National Academy of Sciences to classify choline as an essential nutrient and to recommend specific adequate intake levels.

Other studies in rats and humans conducted by investigators at the New York University School of Medicine also suggest that diet can play a part in brain defenses against cognitive deficits with age and AD. For example, long-term feeding of rats with a diet supplemented with antioxidant-rich substances such as spinach, strawberries, or vitamin E retarded age-related declines in spatial memory (Joseph et al., 1998). Beginning at 6 months of age, the rats were fed standard lab diets supplemented with extracts of spinach or strawberries, vitamin E, or no supplement and were then compared at 15 months of age for spatial memory performance in the Morris Water Maze task. Those animals receiving diets supplemented with substances rich in antioxidants showed none of the age-related cognitive declines typically seen in this spatial memory task. Spinach supplementation was particularly beneficial to the animals. Each dietary supplement was effective in retarding the age-associated deficits in several measures of brain metabolism. Additionally, the same research team has shown that short-term dietary supplementation with substances rich in antioxidants may partly reverse both cognitive and motor deficits seen with normal aging. Old rats (19 months) were given a diet supplemented with extracts of spinach, strawberries, or blueberries, or no supplement and compared on performance on motor and spatial learning tasks. Results showed that deficits of both motor coordination and spatial memory were reversed in the animals supplemented with blueberry extracts (Joseph et al., 1999). Furthermore, all animals that received any of the three dietary supplements showed improvements in cellular functions involved in transmission of chemical signals in brain.

In humans there are epidemiologic studies showing a correlation between antioxidant supplementation and reduction of risk for AD. Vitamin E has been shown to retard several milestones of AD progression (Sano et al., 1997) and it and other antioxidants are currently being tested in several clinical trials for preventing age-related memory deficits and development of AD. Epidemiologic studies also implicate folate, which is also being tested in an add-on component to the NIA-funded Women's Antioxidant Cardiovascular Study clinical trial for age-related memory impairment . Only the results of this sort of clinical trial and further basic research will show whether there are beneficial effects of dietary supplements on aging and AD.

Source: National Institutes of Health; National Institute on Aging
1999 PROGRESS REPORT ON ALZHEIMER'S DISEASE

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