Background and Objectives Social connectedness has been linked prospectively to cognitive aging, but there is little agreement about the social mechanisms driving this relationship. This study evaluated nine measures of social connectedness, focusing on two forms of social enrichment – access to an expansive and diverse set of loosely connected individuals (i.e., social bridging) and integration in a supportive network of close ties (i.e., social bonding). Research Design and Methods This study used egocentric network and cognitive data from 311 older adults in the Social Networks in Alzheimer Disease (SNAD) study. Linear regressions were used to estimate the association between social connectedness and global cognitive function, episodic memory, and executive function. Results Measures indicative of social bridging (larger network size, lower density, presence of weak ties, and proportion non-kin) were consistently associated with better cognitive outcomes, while measures of social bonding (close ties, multiplex support, higher frequency of contact, better relationship quality, and being married) largely produced null effects. Discussion and Implications These findings suggest that the protective benefits of social connectedness for cognitive function and memory may operate primarily through a cognitive reserve mechanism that is driven by irregular contact with a larger and more diverse group of peripheral others.

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Sexual satisfaction is understudied among highly religious communities, such as the Church of Jesus Christ of Latter-day Saints (LDS). Through an internet-based self-report survey, this study (N = 266) examined potential predictors of sexual satisfaction among adults living in Utah who had married in the LDS faith, regardless of current faith practice. Both men and women reported their perceived partner satisfaction as the top contributing factor to their own overall sexual satisfaction. These findings have implications for clinicians, educators, and researchers evaluating the sexual lives, including sexual satisfaction, of men and women who have married in the LDS faith.

Background & Aim Primary Sclerosing Cholangitis (PSC) is a cholestatic liver disease characterized by hepatic fibrosis and portal inflammation. Melatonin is synthesized by arylalkylamine N‐acetyltransferase (AANAT) in the pineal gland, as well as extrapineal sites such as cholangiocytes. We previously found that: (i) the MT1 receptor is primarily expressed in cholangiocytes with low and absent expression in hepatic stellate cells and hepatocytes, respectively; (ii) melatonin reduces biliary proliferation via MT1 receptor signaling; and (iii) melatonin treatment for 1 wk decreases biliary proliferation and liver fibrosis in bile duct ligated rats by downregulation of MT1 and clock genes (PER1, CRY1, CLOCK and BMAL1). We aimed to evaluate the beneficial effects of long‐term melatonin treatment and MT1 signaling on biliary phenotypes, liver fibrosis and portal inflammation in Mdr2‐/‐ mice (a model of PSC). Methods Male FVB/NJ and Mdr2‐/‐ mice had access ad libitum to drinking water with/without melatonin for 3 months. We evaluated: (i) ductular reaction (DR) by immunohistochemistry (IHC) for CK19, (ii) liver fibrosis by Sirius Red staining and (iii) portal inflammation by IHC for F4/80. MT1, AANAT, and clock genes immunoreactivity was evaluated by immunofluorescence (IF) co‐stained with CK19 and qPCR in isolated cholangiocytes. Male C3H‐Hej (WT for MT1‐/‐), FVB/NJ (WT for Mdr2‐/‐), MT1‐/‐, Mdr2‐/‐ mice and MT1‐/‐/Mdr2‐/‐ (DKO) mice were euthanized at 12 wk of age. We analyzed: (i) MT1 expression by IF and mRNA expression in total liver by qPCR to validate our model; (ii) liver damage by H&E, DR by IHC for CK19 and liver fibrosis by Sirius Red staining and (iii) portal inflammation by IHC for F4/80 and expression of the inflammatory markers by qPCR in total liver. Results Long‐term melatonin treatment reduces DR, liver fibrosis and portal inflammation in Mdr2‐/‐mice. Prolonged administration of melatonin in Mdr2‐/‐mice improves liver phenotype by decreasing the immunoreactivity of MT1, AANAT and clock genes in Mdr2‐/‐ mice, which suggests the chronobiotic action of melatonin on biliary circadian rhythm. DKO mice have no MT1 expression and display ameliorated liver phenotype compared to Mdr2‐/‐ mice. Conclusion We demonstrated that chronic melatonin treatment improves liver histology and restores the biliary circadian rhythm by interaction with MT1. Suppression of MT1 receptor in Mdr2‐/‐mice ameliorates biliary/liver phenotypes through changes in clock genes and AANAT. Restoration of the circadian rhythm by modulation of melatonin/MT1 signaling may be key for the management of cholangiopathies.