Integrating Health into Cognitive Aging: Toward a Preventive Cognitive Neuroscience of Aging

Summary In this article, we have argued that age is not a causal variable and cannot be viewed usefully as a basis for under-standing cognitive changes. In its place, we suggest an en-hanced consideration of health and disease. This emphasis on health is supported by growing evidence from the cogni-tive neuroscience of aging with its focus on understanding neural substrates of cognitive processes. Furthermore, pro-spective epidemiological studies indicate that there is sub-stantial variability in health among older persons and that numerous aspects of health are associated with cognitive outcomes. Combined with neurological evidence, the “vas-cular hypothesis” suggests that vascular conditions are re-sponsible for a substantial portion of cognitive decline, impairment, and dementia. If true, this suggests that there is much to learn from cardiovascular prevention that can be applied to the identification and treatment of risk factors for cognitive changes with age.To implement a preventive science of cognitive aging, we need to reconsider the way we conduct our research. To iden-tify predictive factors that alter cognitive outcomes, we must first clearly define the outcomes; the recent reconsiderations proposed by the DSM-5 workgroup on neurocognitive disor-ders and by National Institute on Aging and the Alzheimer’s association suggest that the criteria for dementia are in need of revision. Of more concern is the question of the etiology of dementia and whether Alzheimer’s is a vascular or a neu-rodegenerative disease. The introduction of mild cognitive impairment is an attempt to move the diagnosis of dementia earlier into life in order to begin treatment sooner. However, rather than creating a new diagnosis that can be given earlier, it may be more useful to consider Hachinski’s (2007) notion of the “brain at risk” and recognize that such risk begins long before symptoms may become evident. In this respect, there is much we can learn from the success of preventive cardiol-ogy in how to identify at-risk patients and how to treat them to reduce their risk of disease later in life. By clearly defining our outcomes, developing risk indices that predict these out-comes and by initiating treatment earlier in those identified at risk, we have an opportunity to develop a preventive sci-ence of cognitive aging and to reduce the growing burden of cognitive declines in aging. Obviously, we have failed to date in our attempts to cure AD.A second requirement for implementing this preventive science is to enhance our measurement of health. Although self-report measures may be better than ignoring health completely, it is likely that their failure to adequately mea-sure health leads to a substantial misunderstanding of the relative roles of age and health in cognitive change. As Finch (2009) claimed, our science should be mature enough to recognize that ignorance of the health of our samples is unacceptable. Although there may be other causes of cogni-tive changes than health, it seems clear that age per se does not play a causal role. Once we accept this as fact, then we can truly begin to understand the causes of cognitive changes and begin to prevent and treat them.