FINALLY, A WORD ABOUT PREVENTION
Numerous risk factors have been associated with an increased risk for AD (see Table 4).2,3 Some, like age and genetics, are nonmodifiable, while others—particularly cardiovascular risk factors—can be modified.1 There are also factors associated with decreased risks—most notably, physical exercise and participation in cognitively stimulating activities.3 Identification of these factors has led to the hope that addressing them can prevent AD.
But association does not equal causation. In 2010, a report from the National Institutes of Health concluded that, although there are modifiable factors associated with AD, there is insufficient evidence that addressing any of them will actually prevent AD.43 In fact, there is good evidence that some of these factors (eg, statin therapy) are not effective in reducing the incidence of dementia and that others (eg, vitamin E and estrogen therapy) are potentially harmful.44
The absence of empirically supported preventive interventions does not mean, however, that we should disregard these risks and protective factors. Encouraging social engagement, for example, may improve both emotional health and quality of life. Addressing cardiovascular risk factors can reduce the rate of coronary and cerebrovascular disease, potentially including vascular dementia, even if it does not reduce the rate of AD.
Studies are evaluating the use of monoclonal antibodies with anti-amyloid properties for prevention of AD in individuals who have APOE ε4 genotypes or high amyloid loads on neuroimaging.45 It will be several years before results are available, however, and the outcome of these studies is uncertain, as the use of anti-amyloid agents for treating established dementia has not been effective.46,47
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