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Depression gets old fast: do stress and depression accelerate cell aging?

Depression and Anxiety (Impact Factor: 4.29). 04/2010; 27(4):327 - 338. DOI: 10.1002/da.20686

ABSTRACT Depression has been likened to a state of “accelerated aging,” and depressed individuals have a higher incidence of various diseases of aging, such as cardiovascular and cerebrovascular diseases, metabolic syndrome, and dementia. Chronic exposure to certain interlinked biochemical pathways that mediate stress-related depression may contribute to “accelerated aging,” cell damage, and certain comorbid medical illnesses. Biochemical mediators explored in this theoretical review include the hypothalamic–pituitary–adrenal axis (e.g., hyper- or hypoactivation of glucocorticoid receptors), neurosteroids, such as dehydroepiandrosterone and allopregnanolone, brain-derived neurotrophic factor, excitotoxicity, oxidative and inflammatory stress, and disturbances of the telomere/telomerase maintenance system. A better appreciation of the role of these mediators in depressive illness could lead to refined models of depression, to a re-conceptualization of depression as a whole body disease rather than just a “mental illness,” and to the rational development of new classes of medications to treat depression and its related medical comorbidities. Depression and Anxiety, 2010. © 2010 Wiley-Liss, Inc.

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    • "This may be due in part to possible neuropathological contributors of each disorder including white matter damage, not assessed in the study. For example, a recent review suggests that depression might represent accelerated cellular aging, reflected in abnormalities in cortisol, neurotrophic factors, oxidative damage, and telomere length (Wolkowitz et al., 2010). Diabetes may play a role in brain aging as well. "
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    ABSTRACT: Objective The purpose of this study was to examine the relationship between verbal learning and memory performance and hippocampal volume in subjects with co-morbid type 2 diabetes and major depression compared with healthy control subjects and subjects with type 2 diabetes alone. Methods Twenty four subjects with type 2 diabetes and 20 subjects with type 2 diabetes and major depression were recruited from endocrinology clinics and were compared with 32 healthy control subjects recruited from the community. Subjects were scanned on a 1.5 T GE scanner, and hippocampal volumes were measured using Freesurfer. The California Verbal Learning Test assessed learning and memory. Significant predictors of verbal learning performance (e.g., age, gender, education, blood pressure, stroke risk, hemoglobin A1c, and hippocampal volume) were determined using a stepwise linear regression. ResultsSubjects with diabetes and depression had significantly worse performance on verbal list learning compared with healthy control subjects. Hippocampal volume was a strong predictor of performance in healthy control subjects, and age and hippocampal volume were strong predictors in subjects with type 2 diabetes alone. Age alone was a significant predictor of verbal learning performance in subjects with diabetes and depression. Conclusions The relationship between hippocampal volume and performance on the California Verbal Learning Test is decoupled in subjects with type 2 diabetes and major depression and this decoupling may contribute to poor verbal learning and memory performance in this study population. Copyright (c) 2014 John Wiley & Sons, Ltd.
    International Journal of Geriatric Psychiatry 04/2015; 30(4). DOI:10.1002/gps.4149 · 3.09 Impact Factor
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    • "Furthermore, in the peripheral blood mononuclear cells from patients with systemic diseases, it has been shown that telomeres were short and that telomeric erosion could result from chronic stress exposure (Georgin-Lavialle et al., 2010). However, the correlation between telomere erosion and depression are not consensual (Hartmann et al., 2010; Hoen et al., 2011; Wolkowitz et al., 2010) probably because of differences in the status of depressive symptoms in the populations studied (endogeneous/secondary depression). "
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    ABSTRACT: Mastocytosisis a rare diseaseassociated with chronic symptoms related to mast cell mediator release.Patients with mastocytosis display high level of negative emotionality such as depression and stress sensibility. Brain mast cells are mainly localized in the diencephalon, which is linked to emotion regulatory systems. Negative emotionality has been shown to be associated with telomere shortening. Taken together these observations led us to hypothesize that mast cells activity could be involved in both negative emotionality and telomere shortening in mastocytosis. To demonstrate a possible relationship between negative emotionality in mastocytosis and leukocytes telomere length. Leukocyte telomere length and telomerase activity were measured amongmastocytosispatients and were correlated with perceived stress and depressionassessed by the Beck Depression Inventory revised and the Perceived Stress Scale. Mild-severe depression scores were frequent (78.9%) as well as high perceived stress (42.11%). Telomere length was correlated to perceived stress (r=0.77; p= 0.0001) but not to depression in our population. Patients displaying Wild-type KIT significantly presented higher perceived stress levels. Patients with the D816VC KIT mutation who had high perceived stress scores displayed significantly shorter telomere but not if they had high depression scores. These findings suggest that high perceived stress in mastocytosis could accelerate the rate of leukocytes telomere shortening. Since mastocytosis is, by definition, a mast cell mediated disease; these cells could be involved in this phenomenon. Mechanistic causal relationships between these parameters need to be investigated.
    Brain Behavior and Immunity 07/2013; 35. DOI:10.1016/j.bbi.2013.07.009 · 6.13 Impact Factor
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    • "E. Puterman et al. / Brain, Behavior, and Immunity 33 (2013) 65–73 69 increases inflammation and reactive oxygen species, accelerating loss of telomeres by increasing cell turnover and DNA damage (Wolkowitz et al., 2010). From a neurologic perspective, adaptive emotion regulation and social connections also reduce activity in brain regions associated with depression that induce autonomic, neuroendocrine, and inflammatory responses (Eisenberger et al., 2007; Lieberman et al., 2007; Slavich et al., 2010). "
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    ABSTRACT: Major depressive disorder has been associated with reduced leukocyte telomere length (LTL). It is not known, however, whether psychosocial and behavioral protective factors moderate this association. In the current study, we examine whether multisystem resiliency - defined by healthy emotion regulation, strong social connections, and health behaviors (sleep and exercise) - predicts LTL and mitigates previously demonstrated associations between depression diagnosis and LTL. LTL was measured, using a quantitative PCR assay, in 954 patients with stable cardiovascular disease in the Heart and Soul Study. In a fully adjusted model, high multisystem resiliency predicted longer LTL (b = 80.00, se = 27.17, p = .003), whereas each individual factor did not. Multisystem resiliency significantly moderated the MDD-LTL association (p = .02). Specifically, MDD was significantly related to LTL at 1 SD below the mean of multisystem resiliency (b = -142.86, SE = 56.46, p = .01), but not at 1 SD above the mean of the profile (b = 49.07, se = 74.51, p =.51). This study suggests that MDD associations with biological outcomes should be examined within a psychosocial-behavioral context, because this context shapes the nature of the direct relationship. Further research should explore the cognitive, neural, and other physiological pathways through which multisystem resiliency may confer biological benefit.
    Brain Behavior and Immunity 05/2013; 33. DOI:10.1016/j.bbi.2013.05.008 · 6.13 Impact Factor
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