ABSTRACT
Age-related dementia and cognitive decline are substantial public health problems that are projected to increase in the first half of this century as the proportion of older persons in the U.S. population increases (Hebert, Scherr, Bienias, Bennett, & Evans, 2003). Loss of cognitive ability in old age is thought to arise from the interaction of experiential and genetic risk factors with multiple age-related pathologic changes in the brain. On post-mortem examination, late life dementia has been associated with the pathology of Alzheimer's disease (i.e., amyloid deposition, neurofibrillary changes), stroke (i.e., cerebral infarction), and Parkinson's disease (i.e., Lewy bodies). These pathologic changes are also seen in the brains of older people who die without dementia, however, albeit to a lesser degree, suggesting that people differ in their capacity to tolerate the deleterious effects of age-related neuropathology. This ability to maintain function despite the accumulation of pathology in the brain is referred to as neural reserve capacity. Factors are thought to influence risk of late life dementia either by affecting the accumulation of neuropathology or by affecting the brain's ability to function in the presence of such pathology.
