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Middle-aged and older adults with diabetes are at increased risk for loneliness and functional limitations. Cross-sectional and longitudinal associations between loneliness and functional limitations have been demonstrated among the general population, but have not been established among those with diabetes. The purpose of this study was to directly compare the following models describing the direction of the association between loneliness and functional limitations among people with diabetes: (1) loneliness leads to functional limitations, (2) functional limitations lead to loneliness, and (3) a bidirectional association between loneliness and functional limitations.Data came from the Health and Retirement Study. Participants were middle-aged and older individuals with diabetes in the United States (n = 2934). Loneliness and functional limitations were measured at baseline, 4-year follow-up, and 8-year follow-up. Path models for each of the three models, as well as a stability model, were created. Model fit was compared using Akaike's Information Criteria (AIC).Participants were 54.6% female, 74.98% White, had a mean age of 69.66 years, had an average of 1.48 comorbid chronic conditions, and had diabetes for an average of 10.40 years. The bidirectional model best fit the data as evidenced by the lowest AIC value (AIC = 171,162.81). ∆AIC between the bidirectional model and the next best fitting model was 16.19, indicating strong support for selecting the bidirectional model. Higher levels of loneliness were associated with subsequent higher levels of functional limitations at some time points (βs = 0.07, 0.02) and higher levels of functional limitations were associated with subsequent higher levels of loneliness (βs = 0.13, 0.06) at all time points.Results suggest that the association between loneliness and functional limitations among individuals with diabetes is bidirectional. This study demonstrates the value of directly comparing directional models.

Recent models of emotion regulation suggest that the cognitive costs of reappraisal depend on stimulus intensity and habitual reappraisal. In the current experiment, we tested these hypotheses by manipulating the intensity of unpleasant and pleasant images, which participants reappraised, viewed, or suppressed their emotions to. To assess cognitive costs, we measured participants’ performance on a concurrent simple reaction time task. Participants also reported on their everyday use of reappraisal and suppression. Higher intensity stimuli were associated with greater cognitive costs of reappraisal, for unpleasant, but not pleasant pictures. Also, greater habitual reappraisal predicted lower cognitive costs of reappraisal and greater reductions in subjective feelings. Results support the role of stimulus intensity and habitual use of reappraisal in predicting the cognitive costs of reappraisal.

Several microRNAs (miRNAs) that are either specifically enriched or highly expressed in neurons and glia have been described, but the identification of miRNAs modulating neural stem cell (NSC) biology remains elusive. In this study, we exploited high throughput miRNA expression profiling to identify candidate miRNAs enriched in NSC/early progenitors derived from the murine subventricular zone (SVZ). Then, we used lentiviral miRNA sensor vectors (LV.miRT) to monitor the activity of shortlisted miRNAs with cellular and temporal resolution during NSC differentiation, taking advantage of in vitro and in vivo models that recapitulate physiological neurogenesis and gliogenesis and using known neuronal- and glial-specific miRNAs as reference. The LV.miRT platform allowed us monitoring endogenous miRNA activity in low represented cell populations within a bulk culture or within the complexity of CNS tissue, with high sensitivity and specificity. In this way we validated and extended previous results on the neuronal-specific miR-124 and the astroglial-specific miR-23a. Importantly, we describe for the first time a cell type- and differentiation stage-specific modulation of miR-93 and miR-125b in SVZ-derived NSC cultures and in the SVZ neurogenic niche in vivo, suggesting key roles of these miRNAs in regulating NSC function.