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Alzheimer disease is a disease of old age that affects 68% of the population aged 65 y and 30% of the population aged 85 y (1). As the world's population ages, we can expect that, without intervention, the incidence of this devastating disease will continue to increase. In the coming decades we should focus our efforts on the prevention or delay of onset of Alzheimer disease.
Recent epidemiologic studies indicating no regional differences in the prevalence of Alzheimer disease may discourage some from seeking preventative therapies because these data could be interpreted to mean that environmental factors do not affect the age of onset or prevalence of Alzheimer disease. However, this lack of difference could also be attributable to difficulties in early diagnosis of the disease and to confounding by early death from other causes with potentially overlapping etiologies. Furthermore, several lines of evidence indicate that preventive therapy is possible. Long-term users of nonsteroidal antiinflammatory drugs (NSAIDs), such as individuals with rheumatoid arthritis or osteoarthritis, are less likely to be afflicted with Alzheimer disease, indicating that NSAIDs offer protection against this disease. There are also indications that estrogen therapy is protective against Alzheimer disease. Furthermore, because oxidative stress is increasingly being implicated in Alzheimer disease, there is the possibility of a protective effect of antioxidants. Finally, epidemiologic data indicate that deficiencies in the B vitamins, particularly those involved in homocysteine metabolism, may play a role in the development of Alzheimer disease. Alzheimer disease itself may also affect the patient's nutritional status and weight loss often occurs as the disease progresses.
Taken together, these data indicate that intervention in the prevalence or age of onset of Alzheimer disease is possible. Like the advances that have been made over the past decades in the prevention of another disease of aging, heart disease, advances in the prevention of Alzheimer disease will likely require both behavioral modifications, such as nutritional modifications, and drug therapies. Determining and testing of therapies for Alzheimer disease will likely be more difficult than the fight against cardiovascular disease because of the more complex nature of Alzheimer disease, the problems associated with it early detection, and the fact that it occurs late in life in conjunction with other life-threatening diseases. However, with concerted effort by experts from various fields, including geriatrics, nutrition, and molecular biology, the possibility of reducing the incidence of Alzheimer disease, even as other measures to prolong life continue, may become a reality.
We thank the Danone Institute, France, for its financial support and the Scientific Council of the institute for its interest in the topics of nutrition, cognitive function, and Alzheimer disease and for its decision to sponsor this workshop.