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Personality, Retirement, and Cognitive Impairment: Moderating and Mediating Associations.

ABSTRACT: Objectives: Five-factor model (FFM) personality traits, including higher conscientiousness and lower neuroticism, are associated with lower risk of dementia and cognitive impairment. In this research, we test whether retirement status moderates and/or mediates the relation between personality and cognitive impairment. Method: We used data from the Health and Retirement Study (N = 9899), a longitudinal study of Americans over the age of 50 years, to examine moderating and mediating associations between personality traits and retirement status on risk of dementia and cognitive impairment not dementia (CIND) over an 8-10 year follow-up. Results: Personality and retirement each had strong, independent associations with risk of dementia and CIND. There were not, however, strong or consistent, moderating or mediating associations between personality and retirement predicting impairment risk. Discussion: Overall, these results indicate that personality and retirement are independent risk factors for incident cognitive impairment. Mechanisms other than retirement are likely to explain this association.

SUBMITTER: Strickhouser JE

PROVIDER: S-EPMC7906949 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Although immediate early genes (IEGs) such as Bdnf, Arc and Egr1, have been implicated in plasticity, the larger pathways related to memory and memory disorders are not well understood. Here, we combined statistical Affymetrix microarray and behavioral analyses to identify key genes and pathways associated with aging-related cognitive impairment. Aged rats were separated into cognitively unimpaired (AU) or impaired (AI) groups, based on their Morris water maze performance relative to young-adult (Y) animals. Hippocampal gene expression was assessed in Y, AU and AI on the fifth (last) day of maze training or 21 days posttraining, and in non-trained aged and young animals (eight groups, overall n = 78, one chip/animal). ANOVA, linear contrasts, and overrepresentation analyses identified genes and pathways that differed from Y generally with aging (in both AU and AI) or selectively with cognitive status (only in AI or AU). Plasticity pathways, including insulin/cAMP/IEG signaling, and glycogenolytic and lipogenic pathways, were selectively downregulated (5 days) in AI, whereas Notch2 (regulating oligodendrocyte differentiation) and myelination pathways were upregulated (particularly at 21 days). Downregulation with general aging occurred in signal transduction and axonal growth/transport pathways, whereas upegulation occurred in immune/inflammatory, lipid metabolism/transport (e.g., Lxr-Srebf1), and lysosomal pathways. In AU, receptor/signal transduction genes were selectively upregulated, suggesting possible compensatory mechanisms. Immunohistochemistry confirmed and extended results to the protein level. Thus, this study identified novel cognition-linked processes, suggesting a new model in which energy-intensive, plasticity/lipogenic processes and energy-generating pathways necessary for learning are coordinately downregulated during training, while myelinogenic programs that impair cognition are concurrently activated. Keywords: Immediate Early Genes, Insulin Signaling, Cholesterol, Myelination, Glia, Inflammation, Young and Old comparaison, behavioral-characterization, Aging-related cognitive impairment.

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Personality, Retirement, and Cognitive Impairment: Moderating and Mediating Associations.

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