Posttraumatic stress disorder (PTSD), a chronic disorder resulting from severe trauma, has been linked to immunologic dysregulation. Gene expression profiling has emerged as a promising tool for understanding the pathophysiology of PTSD. However, to date, all but one gene expression study was based on whole blood or unsorted peripheral blood mononuclear cell (PBMC), a complex tissue consisting of several populations of cells. The objective of this study was to utilize RNA sequencing to simultaneously profile the gene expression of four immune cell subpopulations (CD4T, CD8T, B cells, and monocytes) in 39 World Trade Center responders (20 with and 19 without PTSD) to determine which immune subsets play a role in the transcriptomic changes found in whole blood. Transcriptome-wide analyses identified cell-specific and shared differentially expressed genes across the four cell types.FKBP5 and PI4KAP1genes were consistently upregulated across all cell types. Notably,RESTandSEPT4, genes linked to neurodegeneration, were among the top differentially expressed genes in monocytes. Pathway analyses identified differentially expressed gene sets involved in mast cell activation and regulation in CD4T, interferon-beta production in CD8T, and neutrophil-related gene sets in monocytes. These findings suggest that gene expression indicative of immune dysregulation is common across several immune cell populations in PTSD. Furthermore, given notable differences between cell subpopulations in gene expression associated with PTSD, the results also indicate that it may be valuable to analyze different cell populations separately. Monocytes may constitute a key cell type to target in research on gene expression profile of PTSD.

On average, older people remember less and walk more slowly than do younger persons. Some researchers argue that this is due in part to a common biologic process underlying age-related declines in both physical and cognitive functioning. Only recently have longitudinal data become available for analyzing this claim. We conducted a systematic review of English-language research published between 2000 and 2011 to evaluate the relations between rates of change in physical and cognitive functioning in older cohorts. Physical functioning was assessed using objective measures: walking speed, grip strength, chair rise time, flamingo stand time, and summary measures of physical functioning. Cognition was measured using mental state examinations, fluid cognition, and diagnosis of impairment. Results depended on measurement type: Change in grip strength was more strongly correlated with mental state, while change in walking speed was more strongly correlated with change in fluid cognition. Examining physical and cognitive functioning can help clinicians and researchers to better identify individuals and groups that are aging differently and at different rates. In future research, investigators should consider the importance of identifying different patterns and rates of decline, examine relations between more diverse types of measures, and analyze the order in which age-related declines occur.

Fundamental cause theory (FCT) was originally proposed to explain how socioeconomic inequalities in health emerged and persisted over time. The concept was that higher socioeconomic status helped some people to avoid risks and adopt protective strategies using flexible resources: knowledge, money, power, prestige, and beneficial social connections. As a sociological theory, FCT addressed this issue by calling on social stratification, stigma, and racism as they affected medical treatments and health outcomes. The last comprehensive review was completed a decade ago. Since then, FCT has been tested, and new applications have extended central features. The current review consolidates key foci in the literature in order to guide future research in the field. Notable themes emerged around types of resources and their usage, approaches used to test the theory, and novel extensions. We conclude that after 25 years of use, there remain crucial questions to be addressed.

The objective of this study was to examine the association between education and incidence of accelerated cognitive decline. Secondary analyses of data from the Health and Retirement Study (HRS), a nationally representative prospective cohort study of U.S. residents were conducted (N = 28,417). Cox proportional hazards survival models were layered on longitudinal mixed-effects modeling to jointly examine healthy cognitive aging and incidence of accelerated cognitive decline consistent with patterns seen in preclinical Alzheimer’s disease and related dementias (ADRD). Replication analyses were completed on a database including 62,485 additional respondents from HRS sister studies. Life expectancy ratios (LER) and 95% confidence intervals (CIs) were reported. This study replicated research showing that education was positively associated with cognition at baseline. Model fit improved using the survival method compared to random-slopes models alone. Analyses of HRS data revealed that higher education was associated with delayed onset of accelerated cognitive decline (LER = 1.031 95% CI = [1.013–1.015], p < 1E-06). Replication analyses using data from 14 countries identified similar results. These results are consistent with cognitive reserve theory, suggesting that education reduces risk of ADRD-pattern cognitive decline. Follow-up work should seek to differentiate specific dementia types involved and consider potential mechanisms.