Dataset Information

Midlife Marital Dissolution and the Onset of Cognitive Impairment.

ABSTRACT:

Background and objectives

Marital dissolution has become more common in midlife with the doubling of the divorce rate among middle-aged adults. Guided by the stress model that stipulates losing economic, social, and psychological resources lowers well-being, we posited that midlife adults who experienced divorce or widowhood were at greater risk of cognitive impairment than the continuously married. Subsequent repartnering was expected to negate the increased risk.

Research design and methods

We used data from the 1998-2016 Health and Retirement Study to estimate discrete-time event history models using logistic regression to predict cognitive impairment onset for men and women.

Results

Roughly 27% of men who experienced spousal death in midlife went on to experience mild cognitive impairment by age 65. For women, experiencing divorce or widowhood was associated with higher odds of cognitive impairment onset although these differentials were accounted for by economic, social, and psychological resources. Men and women who repartnered after marital dissolution did not appreciably differ from their continuously married counterparts in terms of their likelihoods of cognitive impairment onset.

Discussion and implications

A stressful life event, midlife marital dissolution can be detrimental to cognitive well-being, placing individuals at increased risk of developing dementia in later life. The growing diversity of partnership experiences during the second half of life points to the continued importance of examining how union dissolution and formation shape health and well-being.

SUBMITTER: Brown SL

PROVIDER: S-EPMC8437503 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

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.