Tuesday, November 18, 2008

A role of nutrition in the prevention of Alzheimer Disease
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Alzheimer Disease is the most prevalent form of dementia, i.e. diseases showing severe loss of cognitive ability, during aging. Alzheimer Disease is a heterogeneous neurodegenerative disorder, clinically characterized by progressive and irreversible cognitive deficits and behavioral alterations that affect memory and learning ability, activities of daily living and quality of life, already in an early stage of the disease. The prevalence of Alzheimer Disease is only 1% above the age of 60 but increases dramatically to 40% above the age of 85. In addition to the increased life expectancy, also the association between nutrition and life style disorders may add to the predicted global burden of Alzheimer Disease considerably as well.

There is a growing interest in the role of nutrition in aging diseases such as dementia, in particular sporadic or late-onset Alzheimer Disease. The evidence to date supports a contribution of food and food components particularly in the prevention of and risk on Alzheimer's Disease. Older people may already be at nutritional risk because of changes in taste and smell, impaired digestion, absorption or utilization of nutrients due to chronic diseases or drug-nutrient interactions. Although epidemiological studies sometimes report conflicting results, specific associations between nutritional components and the risk for Alzheimer Disease have been found, especially in frail elderly people at risk of deficiencies. These include the potential protective effects of, for instance, specific polyunsaturated fats, B-vitamins and antioxidants. These macro- and micronutrients are dietary components that can influence brain structure and function.

Nutritional intake may provide specific nutrients that can be used as building blocks for membrane and synapse formation and neurotransmitter production but can also directly influence the availability of nutrients, energy and oxygen to the brain. The neuronal loss, amyloid and Tau protein pathology in the Alzheimer brain, as well as possible dysfunction of the cerebrovascular system and energy metabolism may act together to accelerate the downhill cascade in cognitive and behavioral function. The potential of nutrition for neuronal maintenance rather than as an energy substrate is illustrated by the increasing evidence that nutrients not only stimulate neural plasticity but also ameliorate the ongoing neurodegenerative process and show the ability to reduce the pathological burden in the brain. With the limited therapeutic utility of current pharmacological treatments for Alzheimer Disease, the question arises what nutrition may contribute to our toolbox to address the specific needs of the Alzheimer patient. We advocate that a multi-nutrient composition specifically targeting membrane formation has the capacity to modulate all of these processes and may provide a useful way, in conjunction with the pharmaceutical route, to treat the Alzheimer patient effectively.

The contribution of both macro- and micronutrients in this respect is supported by epidemiological data that emphasize the relevance of diet context (i.e. a multi-nutrient approach) rather than single nutrients, and also by recent findings from our lab and others. In addition, recent mechanistic studies specifically support benefits of selective nutritional components in counteracting some of the neurodegenerative and pathological processes. The potential synergy between nutritional components to stimulate neuronal plasticity and function and reduce neuropathology provides a solid basis to investigate the potential benefits of such nutrient combinations in a clinical setting. The modulating capacity of such a specifically designed nutritional approach may show disease modifying capacity rather than symptomatic, especially during the prodromal and early stage of Alzheimer's Disease. European Journal of Pharmacology Volume 585, Issue 1, 6 May 2008, Pages 197-207

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