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Aging is characterized by a wide a range of changes in cognitive performance and the accumulation of multiple pathologic insults, including misfolded proteins of Alzheimer disease (AD) and related dementias (ADRD) and vascular changes. At the most extreme end of the cognitive decline of aging is the syndrome of dementia (or major neurocognitive disorder according to the DSM-5 criteria1). However, it is well known from clinicopathologic studies, and more recently in vivo measurements of AD-related biomarkers, that a similar neuropathologic burden can be found in cognitively unimpaired or mildly impaired individuals.2 An individual's ability to remain cognitively normal—resilience—in the presence of neuropathologic insults has been attributed to inherent attributes of the brain (brain reserve) and efficiencies that develop through enrichment and acquired skills (cognitive reserve).3,4 In reality, these 2 constructs are likely to overlap, and there are significant gaps in our understanding of the fundamental mechanisms of resilience.
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