Neural and motivational mechanisms of age-related change in emotion regulation: Administrative Supplement

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Project Summary: In the progression from middle to older-age, healthy adults typically experience improvements in their emotional functioning, such as increases in positive emotion and greater expertise in managing emotions. However, not everyone shows these age-related improvements, and the mechanisms that give rise to emotional functioning changes across adulthood are still poorly understood. The primary goal of this project is to examine the critical factors that promote positive emotional development in normative aging, and to test whether depression history might moderate this process as a key trait individual difference marker. To this end, we test our proposed Value-Based Cognitive Control Model of Emotion Regulation in ADulthood (VBCC-MERiAD). The VBCC-MERiAD framework suggests a novel insight: that interactions between reward motivation and cognitive control play a central role in understanding both the normative trajectory of emotional functioning in older adults, and conversely, why and how individuals with depression histories may get “off track”. Our primary hypothesis is that emotion regulation (ER) abilities rely upon the integrity of fronto-striatal circuitry (i.e., activity and connectivity between the lateral prefrontal cortex and nucleus accumbens / ventral striatum), to successfully utilize reward motivation as a means of engaging cognitive control (i.e., to update and maintain ER goals). Across three Specific Aims, we will characterize the mechanisms of ER in middle-aged and older adults (N=220, ages 35-75) using a multi-method design involving functional neuroimaging measures, laboratory behavioral assessments, and experience sampling methods, to identify the neural and behavioral indicators of motivation and cognitive control that predict daily emotional functioning, and potential dysregulation in individuals with depression history. We further propose to enrich our understanding of the mechanisms of age-related change in ER, by capitalizing on recent advances in the ability to assess risk of preclinical Alzheimer’s Disease (AD) and AD-related neurodegeneration through the use of blood plasma-based biomarkers. Through new collaborations with Dr. Suzanne Schindler and Dr. Brian Gordon, our partners at both Washington University, Knight Alzheimer’s Disease Research Center, we will utilize state-of-the-art methods, including single-molecule array (Simoa) and mass spectrometry, to comprehensively assess key blood-based biomarkers related to amyloid (APOE, beta-amyloid), tau (ptau181), and neurodegeneration (NfL, GFAP), as well as anatomical MRI biomarkers (e.g., cortical thickness). We propose an Administrative Supplement to provide additional support for us to acquire, process and rigorously analyze AD- related biomarker data. This Supplement will dramatically enhance the scope and impact of our project, by enabling us to extend our understanding of both normative and dysfunctional age-related change in emotional function, by not only identifying mechanisms that promote positive ER in late adulthood, but also determining the degree to which otherwise undetected preclinical AD moderates such effects. In so doing, we will lay the foundation for new interventions to improve quality of life for older adults and individuals with depression history.