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      Oxytocin administration prevents cellular aging caused by social isolation

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          Abstract

          Chronic stressors, such as chronic isolation in social mammals, can elevate glucocorticoids, which can affect cellular mechanisms of aging, including increased levels of oxidative stress and shortened telomere lengths. Recent work in the selectively social prairie vole ( Microtus ochrogaster) suggests that oxytocin and social support may mitigate some of the negative consequences of social isolation, possibly by reducing glucocorticoid levels. We investigated the influences of isolation, social support, and daily oxytocin injections in female prairie voles. Glucocorticoid levels, oxidative damage, telomere length, and anhedonia, a behavioral index of depression, were measured throughout the study. We found that six weeks of chronic isolation led to increased glucocorticoid levels, oxidative damage, telomere degradation and anhedonia. However, daily oxytocin injections in isolated voles prevented these negative consequences. These findings demonstrate that chronic social isolation in female prairie voles is a potent stressor that results in depression-like behavior and accelerated cellular aging. Importantly, oxytocin can completely prevent the negative consequences of social isolation.

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          Most cited references54

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          Telomeres and aging.

          Telomeres play a central role in cell fate and aging by adjusting the cellular response to stress and growth stimulation on the basis of previous cell divisions and DNA damage. At least a few hundred nucleotides of telomere repeats must "cap" each chromosome end to avoid activation of DNA repair pathways. Repair of critically short or "uncapped" telomeres by telomerase or recombination is limited in most somatic cells and apoptosis or cellular senescence is triggered when too many "uncapped" telomeres accumulate. The chance of the latter increases as the average telomere length decreases. The average telomere length is set and maintained in cells of the germline which typically express high levels of telomerase. In somatic cells, telomere length is very heterogeneous but typically declines with age, posing a barrier to tumor growth but also contributing to loss of cells with age. Loss of (stem) cells via telomere attrition provides strong selection for abnormal and malignant cells, a process facilitated by the genome instability and aneuploidy triggered by dysfunctional telomeres. The crucial role of telomeres in cell turnover and aging is highlighted by patients with 50% of normal telomerase levels resulting from a mutation in one of the telomerase genes. Short telomeres in such patients are implicated in a variety of disorders including dyskeratosis congenita, aplastic anemia, pulmonary fibrosis, and cancer. Here the role of telomeres and telomerase in human aging and aging-associated diseases is reviewed.
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            Telomere length in early life predicts lifespan.

            The attrition of telomeres, the ends of eukaryote chromosomes, is thought to play an important role in cell deterioration with advancing age. The observed variation in telomere length among individuals of the same age is therefore thought to be related to variation in potential longevity. Studies of this relationship are hampered by the time scale over which individuals need to be followed, particularly in long-lived species where lifespan variation is greatest. So far, data are based either on simple comparisons of telomere length among different age classes or on individuals whose telomere length is measured at most twice and whose subsequent survival is monitored for only a short proportion of the typical lifespan. Both approaches are subject to bias. Key studies, in which telomere length is tracked from early in life, and actual lifespan recorded, have been lacking. We measured telomere length in zebra finches (n = 99) from the nestling stage and at various points thereafter, and recorded their natural lifespan (which varied from less than 1 to almost 9 y). We found telomere length at 25 d to be a very strong predictor of realized lifespan (P < 0.001); those individuals living longest had relatively long telomeres at all points at which they were measured. Reproduction increased adult telomere loss, but this effect appeared transient and did not influence survival. Our results provide the strongest evidence available of the relationship between telomere length and lifespan and emphasize the importance of understanding factors that determine early life telomere length.
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              Understanding the Links Between Social Support and Physical Health: A Life-Span Perspective With Emphasis on the Separability of Perceived and Received Support.

              Social support has been reliably related to physical health outcomes. However, the conceptual basis of such links needs greater development. In this article, I argue for a life-span perspective on social support and health that takes into account distinct antecedent processes and mechanisms that are related to measures of support over time. Such a view highlights the need to distinguish measures of perceived and received support and its links to more specific diseases (e.g., chronic, acute) and stages of disease development (e.g., incidence). I discuss both the novel implications of these theoretical arguments for research on social support and physical health, as well as the potential intervention approaches that are apparent from this perspective.
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                Author and article information

                Journal
                7612148
                6787
                Psychoneuroendocrinology
                Psychoneuroendocrinology
                Psychoneuroendocrinology
                0306-4530
                1873-3360
                31 August 2020
                08 January 2019
                May 2019
                07 September 2020
                : 103
                : 52-60
                Affiliations
                [a ]Department of Psychology, Bucknell University, Lewisburg, PA, USA
                [b ]Department of Biology, Bucknell University, Lewisburg, PA, USA
                [c ]Institute of Biodiversity Animal Health and Comparative Medicine, University of Glasgow, Scotland, United Kingdom
                Author notes
                [1]

                Shared first authorship.

                [* ]Corresponding author at: 215 O’Leary Center, 1 Dent Drive, Bucknell University, Lewisburg, PA, 17837, United States. j.stevenson@ 123456bucknell.edu (J.R. Stevenson).
                Article
                NIHMS1624385
                10.1016/j.psyneuen.2019.01.006
                7476076
                30640038
                ea5c6fa5-d5ec-4bb6-a64b-00fe5bbfc379

                This is an open access article under the CC BY-NC-ND license ( http://creativecommons.org/licenses/BY-NC-ND/4.0/).

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                Categories
                Article

                Endocrinology & Diabetes
                oxytocin,telomeres,oxidative stress,stress,social support,aging
                Endocrinology & Diabetes
                oxytocin, telomeres, oxidative stress, stress, social support, aging

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