Telomere length and telomerase in a well-characterized sample of individuals with major depressive disorder compared to controls

Simon, Naomi M.; Walton, Zandra E.; Bui, Éric; Prescott, Jennifer; Hoge, Elizabeth A.; Keshaviah, Aparna; Schwarz, Noah; Dryman, Taylor; Ojserkis, Rebecca A.; Kovachy, Benjamin; Mischoulon, David; Worthington, John J.; Vivo, Immaculata De; Fava, Maurizio; Wong, Kwok-Kin

doi:10.1016/j.psyneuen.2015.04.004

Cited by 45 publications

(41 citation statements)

References 58 publications

(79 reference statements)

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“…Methods have been described elsewhere (Simon et al, 2015). Participants were assessed for psychiatric disorders in person by trained, experienced doctoral-level (MD or PhD) clinicians, using the Structured Clinical Interview for DSM-IV (SCID; First et al, 2002), who also completed interviewer-rated measures.…”

Section: Methodsmentioning

confidence: 99%

“…Use of any psychiatric medication in the 2 weeks (4 weeks for fluoxetine) prior to screen or of anti-inflammatory medications in the 3 days prior to blood draw was exclusionary (prior use of psychiatric medications was allowed). In case of an acute infection, systematically assessed by a trained clinician using the Cumulative Illness Rating Scale (CIRS), or of antibiotic use, participants returned for phlebotomy 1 week after symptom resolution or completion of any antibiotics (Simon et al, 2015). …”

Section: Methodsmentioning

confidence: 99%

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Inflammatory cytokines in major depressive disorder: A case–control study

Cassano

Bui

Rogers

et al. 2016

Aust N Z J Psychiatry

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Introduction: There is mixed evidence in the literature on the role of inflammation in major depressive disorder. Contradictory findings are attributed to lack of rigorous characterization of study subjects, to the presence of concomitant medical illnesses, to the small sample sizes, and to the limited number of cytokines tested.Methods: Subjects aged 18-70 years, diagnosed with major depressive disorder and presenting with chronic course of illness, as well as matched controls (n = 236), were evaluated by trained raters and provided blood for cytokine measurements. Cytokine levels in EDTA plasma were measured with the MILLIPLEX Multi-Analyte Profiling Human Cytokine/ Chemokine Assay employing Luminex technology. The Wilcoxon rank-sum test was used to compare cytokine levels between major depressive disorder subjects and healthy volunteers, before (interleukin [IL]-1β, IL-6, and tumor necrosis factor-α) and after Bonferroni correction for multiple comparisons (IL-1α, IL-2, IL-3, IL-4, IL-5, IL-7, IL-8, IL-10, IL-12(p40), IL-12(p70), IL-13, IL-15, IFN-γ-inducible protein 10, Eotaxin, interferon-γ, monotype chemoattractant protein-1, macrophage inflammatory protein-1α, granulocyte-macrophage colony-stimulating factor and vascular endothelial growth factor).Results: There were no significant differences in cytokine levels between major depressive disorder subjects and controls, both prior to and after correction for multiple analyses (significance set at p ⩽ 0.05 and p ⩽ 0.002, respectively). Conclusion:Our well-characterized examination of cytokine plasma levels did not support the association of major depressive disorder with systemic inflammation. The heterogeneity of major depressive disorder, as well as a potential sampling bias selecting for non-inflammatory depression, might have determined our findings discordant with the literature.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Inflammatory cytokines in major depressive disorder: A case–control study

Cassano

Bui

Rogers

et al. 2016

Aust N Z J Psychiatry

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“…Recent studies have investigated TL in relation to numerous psychiatric disorders [2, unpublished], and several studies have shown shortened TL in MDD [6–13], although exceptions exist [14–16]. Shortened LTL in MDD and other psychiatric disorders could have pathophysiological significance by indicating accelerated aging at the cellular level and by synergizing with depression diagnosis in predicting mortality in certain populations [17].…”

Section: Introductionmentioning

confidence: 99%

Leukocyte Telomere Length Predicts SSRI Response in Major Depressive Disorder: A Preliminary Report

Hough

Bersani

Mellon³

et al. 2016

Complex Psychiatry

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Short leukocyte telomere length (LTL) may be associated with several psychiatric disorders, including major depressive disorder (MDD). Short LTL has previously been associated with poor response to psychiatric medications in bipolar disorder and schizophrenia, but no studies have prospectively assessed the relationship of LTL to selective serotonin reuptake inhibitor (SSRI) response in MDD. We assessed pre-treatment LTL, depression severity [using the Hamilton Depression Rating Scale (HDRS)], and self-reported positive and negative affect in 27 healthy, unmedicated adults with MDD. The subjects then underwent open-label treatment with an SSRI antidepressant for 8 weeks, after which clinical ratings were repeated. The analyses were corrected for age, sex, and body mass index. ‘Non-responders' to treatment (HDRS improvement <50%) had significantly shorter pre-treatment LTL than ‘responders' (p = 0.037). Further, shorter pre-treatment LTL was associated with less improvement in negative affect (p < 0.010) but not with changes in positive affect (p = 0.356). This preliminary study is the first to assess the relationship between LTL and response to SSRIs in MDD and among the first to prospectively assess its relationship to treatment outcome in any psychiatric illness. Our data suggest that short LTL may serve as a vulnerability index of poorer response to SSRI treatment, but this needs examination in larger samples.

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“…Nevertheless, [33] concurrently assessed telomere length and telomerase activity in individuals presenting clinically significant, chronic major depressive disorder and matched controls but failed to provide strong evidence of an association of major depressive disorder with shorter LTL, while telomerase activity was lower in men with major depressive disorder. Despite that result, [34], from a comprehensive meta-analysis, described the significant relationship between depression and shorter telomere length as consistent with the notion positing that psychological distress, such as experienced in depression, results in physiological changes leading to shortened telomere length.…”

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confidence: 99%

Exercise Influences in Depressive Disorders: Symptoms, Biomarkers and Telomeres

Archer¹

2017

Clin Depress

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EditorialThe exact mechanisms concerning how exercise affects the brain, under conditions of health or disorder, are not fully understood and the literature lacks a sufficiency of well-designed studies concerning the effects of exercise training on depressive disorders. Nevertheless, the observed antidepressant actions of exercise are strong enough to warrant its application as a viable alternative to current medications in the treatment of depressive disorders [1]. The beneficial effects of exercise upon cognitive, executive function and working memory, emotional, self-esteem and depressed mood, motivational, anhedonia and psychomotor retardation, and somatic/physical, sleep disturbances and chronic aches and pains, categories of depression are discussed. The ameliorative effects of physical exercise upon several biomarkers associated with depressive states: hypothalamicpituitary-adrenal (HPA) axis homeostasis, anti-neurodegenerative effects, monoamine metabolism regulation and neuro-immune functioning have been outlined [2]. The notion that physical exercise may function as "scaffolding" that buttresses available network circuits, anti-inflammatory defences and neuroreparative processes, e.g. brain-derived neurotrophic factor (BDNF), holds a certain appeal. In older adults, it has been observed that exercise was associated with significantly lower levels of depressive symptom severity [3]. An activity program based on "nordic walking", i.e. using staves, was shown to induce a positive effect on depressive symptoms and sleeping disorders in elderly patients, suggesting that Nordic walking based exercise programs should be developed for the elderly who suffer from depression or a sleeping disorder [4][5].The notion of physical exercise as a "scaffolding" to buttress damage experienced under such conditions as traumatic brain damage and aging provokes the metaphor of transient measures, external to the buildings, that provides for construction, reconstruction and maintenance but not the buildings themselves. Scaffolding provides a normal process that continues across the lifespan involving that application and development of complementary, alternative neural circuits to achieve a particular cognitive goal (252); it is protective of cognition in the aging (or disabled) brain and is reinforced by physical exercise and cognitive engagement (which is harnessed during exercise. Under conditions of traumatic brain injury the notion of scaffolding suggests that exercise buttresses, more or less dependent on extent of injury, the surviving adaptive and neuroreparative processes [6][7]. Studies in transgenic mice and primary human skeletal myocyte studies have shown the critical influence of exercise-responsive transcriptional co-activator PGC-1α (Peroxisome proliferator-activated receptor gamma coactivator 1-alpha, which regulates the genes controlling energy metabolism), in coordinating intramuscular lipid-dropletprogramming leading to mitochondrial remodeling. PGC-1α regulates also mitochondrial biogenesis and function...

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Telomere length and telomerase in a well-characterized sample of individuals with major depressive disorder compared to controls

Cited by 45 publications

References 58 publications

Inflammatory cytokines in major depressive disorder: A case–control study

Inflammatory cytokines in major depressive disorder: A case–control study

Leukocyte Telomere Length Predicts SSRI Response in Major Depressive Disorder: A Preliminary Report

Exercise Influences in Depressive Disorders: Symptoms, Biomarkers and Telomeres

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