Disease Prevention

The goal here is to prevent occurrence of disease and symptoms in individuals presumed to be at high risk for the development of Alzheimer's disease or mild cognitive impairment. For this approach to work, we would need both a reliable method or marker for identifying at-risk individuals and therapies that can effectively prevent the disease from developing.

Although we know that the pathological cascade that eventually causes Alzheimer's disease begins decades before symptoms appear, we do not yet possess an early preclinical marker. Performance on neuropsychological tests has thus far been the most sensitive index; subtle changes on specialized imaging studies are being further investigated. Ultimately, the treatment of Alzheimer's disease will occur when an at-risk individual is in his or her twenties, thirties, or forties. Studies are looking at whether the following substances can prevent and, in some cases, modify the

Alzheimer's disease process.

• Antioxidants. Vitamin E and vitamin C have established antioxidant properties, and vitamin E has been shown to ameliorate symptoms of Alzheimer's disease. A current large-scale study cosponsored by the National Institute on Aging and the National Cancer Institute is ongoing to determine if a combination of vitamin E and selenium also conveys a preventive benefit.

• High-dose vitamins. A multicenter clinical trial sponsored by the National Institute on Aging aims to find out if highdose supplements of folate and vitamins B6 and B 12 can slow the progression of Alzheimer's disease. These vitamins appear to moderate blood levels of homocysteine, an amino acid that can damage delicate blood vessels and render a person more vulnerable to cerebrovascular disorders and Alzheimer's disease. I discussed homocysteine as a potential contributory factor in Alzheimer's disease and other forms of dementia in Chapter 5.

• Nonsteroidal anti-inflammatory drugs (NSAIDs). NSAIDs constitute a class of painkillers that includes ibuprofen (Advil, Motrin, and others), naproxen (Aleve, Anaprox, and others), and celecoxib (Celebrex). These medicines have been studied for their potential to prevent and treat Alzheimer's disease. Scientists also think that because these agents reduce inflammation throughout the body, they should be able to reduce the nerve cell inflammation that is associated with the disease. Hopes have also been raised by laboratory and animal studies showing that some of these drugs interfere with the production of beta-amyloid plaques.

Findings have thus far been mixed. Epidemiological studies involving thousands of people have found that frequent use of NSAIDs seems to be associated with decreased likelihood of future development of Alzheimer's disease. Only two of these drugs—rofecoxib (Vioxx) and naproxen—have been tested as potential treatments for Alzheimer's disease, but they did not reduce or slow the progression of the symptoms. Rofecoxib was subsequently removed from the market because of dangerous cardiovascular side effects, including stroke and heart attack. Naproxen and celecoxib had been the focus of a large Alzheimer's disease prevention trial by the National Institutes of Health, which was suspended in 2004 after similar concerns were raised regarding cardiovascular side effects. The status of NSAIDs in the prevention of Alzheimer's disease remains unknown at present.

• Statins. Atorvastatin (Lipitor), simvastatin (Zocor), and pravastatin (Pravachol) belong to a commonly prescribed class of cholesterol-lowering medications called statins. Some preliminary research shows that taking statins can reduce the risk of Alzheimer's disease by as much as 70 percent and may also help prevent mild cognitive impairment. On the other hand, a Columbia University study published in 2004 found that people being treated with statins for hyperlipidemia did not have a lower risk of future development of either Alzheimer's disease or vascular dementia.

A 2002 German study of forty-four people with Alzheimer's disease but normal levels of cholesterol examined the effect of simvastatin on beta-amyloid. After twenty-six weeks, people with mild Alzheimer's disease experienced a significant decrease in beta-amyloid concentration measured in the cerebrospinal fluid. However, there was no change in cerebrospinal fluid levels of beta-amyloid in people with moderate or severe disease. A current large multicenter study sponsored by the National Institute on Aging is investigating simvastatin as a treatment for slowing the progression of Alzheimer's disease.

It stands to reason that statins might help either prevent or treat Alzheimer's disease. We have abundant evidence of a relationship between cholesterol and the formation of beta-amyloid plaques; people with the ApoE e4 allele gene are at increased risk of hypercholesterolemia as well as Alzheimer's disease. We don't yet know enough about the efficacy of statins for the treatment of Alzheimer's disease to recommend that people take these drugs specifically to lower their risk of the disease. But in the meantime, if you have high cholesterol and are taking a statin to control it, you may realize a double benefit: lowering your cholesterol and reducing your risk of memory disorder.

• Estrogen therapy. Although recent large studies have found that hormone replacement therapy actually increases the risk of dementia in healthy postmenopausal women, there is some evidence that estrogen therapy may be helpful in the treatment of women with established Alzheimer's disease. One clinical trial is looking at raloxifene (Evista), an estrogen-like compound that is prescribed for osteoporosis and, unlike menopausal hormone therapy, is not associated with an increased risk of cancer and other illnesses. The purpose of the study is to determine if raloxifene can improve cognitive function and skills required for independent living in women with Alzheimer's disease. A trial sponsored by the National Institutes of Health is evaluating whether estrogen therapy, either alone or in combination with progestin, a synthetic hormone, can improve memory and related functions in postmenopausal women with mild to moderate Alzheimer's disease.

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