Thesis (Ph. D.)--University of Rochester. Department of Brain and Cognitive Sciences, 2024.Older adults aged 85 years and older are at highest risk for Alzheimer's disease (AD), a progressive neurodegenerative disease characterized by abnormal accumulation of amyloid beta and tau proteins, neurodegeneration, and cognitive impairment. However, not all older adults with AD neuropathology ultimately develop AD, suggesting that there are unaccounted for factors that contribute to the nonlinear relationship between brain aging and cognition. This observation motivated the concept of cognitive reserve (CR) to explain why some individuals are better able to cope with brain pathology than others. However, existing operationalizations fail to capture the fundamental conceptual components of CR, particularly cognitive change (i.e., plasticity). As a result, there is little to no mechanistic evidence for CR. This dissertation presents a novel conceptual framework for CR that uses multidimensional (i.e., trait, state, level, and stability) psychosomatic factors to explain individual variability in the relationship between brain aging and cognition, encompassing both cognitive level and cognitive change. First, we establish a relationship between a psychosomatic factor, trait fatigue, and brain topology, and second, we identify a potential brain mechanism associated with brain aging and fatigue (Chapter 2). Next, we assess the relationship between fatigue and CR and examine how different dimensions of fatigue affect this relationship in older adults with and without mild cognitive impairment (MCI; Chapter 3). Finally, we test the moderating role of a second psychosomatic factor, positive affective experience, on the relationship between neurodegeneration and cognitive change in MCI, and whether preserved resting-state network functional connectivity attenuates the adverse effects of neurodegeneration on older adults' capacity for plasticity (Chapter 4). By using psychosomatic dimensions as different "operational" definitions of timescale, we show that psychosomatic factors differentially moderate the adverse effects of neurodegeneration on cognition, which in turn promote cognitive resilience or exacerbate vulnerability to brain aging. The inclusion of timescale captures an individual's capacity for plasticity, a component that has been theoretically implied in the existing literature but not operationally implemented. To our knowledge, these findings provide the first empirically viable evidence for CR and establish a foundation for future confirmatory research