Cytokine Alterations in Bipolar Disorder: A Meta-Analysis of 30 Studies

Modabbernia, Amirhossein; Taslimi, Shervin; Brietzke, Elisa; Ashrafi, Mandana

doi:10.1016/j.biopsych.2013.01.007

Cited by 525 publications

(395 citation statements)

References 101 publications

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“…15 In contrast, Mansour et al 16 reported no difference in telomere length between BD patients and a healthy control group. Multiple mechanisms might be implicated in telomere shortening in BD, including oxidative stress 28 leading to secondary DNA damage, 29 inflammation, 30 and glucocorticoid load. 7 Mechanistically, oxidative stress can lead to the formation of 8-oxo-7,8-dihydro-2 0 -deoxyguanosine (8-oxodG) at the GGG triplet in telomere sequences, 31 which is noted to be increased in patients with BD.…”

Section: Discussionmentioning

confidence: 99%

Shortened telomere length in bipolar disorder: a comparison of the early and late stages of disease

Barbé-Tuana

Parisi

Panizzutti

et al. 2016

Rev. Bras. Psiquiatr.

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Objective: Bipolar disorder (BD) has been associated with increased rates of age-related diseases, such as type II diabetes, metabolic syndrome, osteoporosis, and cardiovascular disorders. Several biological findings have been associated with age-related disorders, including increased oxidative stress, inflammation, and telomere shortening. The objective of this study was to compare telomere length among participants with BD at early and late stages and age-and gender-matched healthy controls. Methods: Twenty-six euthymic subjects with BD and 34 healthy controls were recruited. Genomic DNA was extracted from peripheral blood and mean telomere length was measured using real-time quantitative polymerase chain reaction. Results: Telomere length was significantly shorter in both the early and late subgroups of BD subjects when compared to the respective controls (p = 0.002 and p = 0.005, respectively). The sample size prevented additional subgroup analyses, including potential effects of medication, smoking status, and lifestyle. Conclusion: This study is concordant with previous evidence of telomere shortening in BD, in both early and late stages of the disorder, and supports the notion of accelerated aging in BD.

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Section: Discussionmentioning

confidence: 99%

Shortened telomere length in bipolar disorder: a comparison of the early and late stages of disease

Barbé-Tuana

Parisi

Panizzutti

et al. 2016

Rev. Bras. Psiquiatr.

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“…Meta-analyses of clinical studies showed that, compared to controls, bipolar patients have small-to-moderate elevation in levels of proinflammatory cytokines (Modabbernia et al, 2013) and of CRP (Dargél et al, 2015). Systemic inflammation can be observed not only during symptomatic episodes, but also in euthymic phases (Dargél et al, 2015), suggesting that inflammation may be a latent vulnerability factor (or trait markers) rather than a (state) marker of disease severity.…”

Section: Observational Studies In Humansmentioning

confidence: 99%

Psychoneuroimmunology of Early-Life Stress: The Hidden Wounds of Childhood Trauma?

Danese

Lewis

2016

Neuropsychopharmacol

295

191

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The brain and the immune system are not fully formed at birth, but rather continue to mature in response to the postnatal environment. The two-way interaction between the brain and the immune system makes it possible for childhood psychosocial stressors to affect immune system development, which in turn can affect brain development and its long-term functioning. Drawing from experimental animal models and observational human studies, we propose that the psychoneuroimmunology of early-life stress can offer an innovative framework to understand and treat psychopathology linked to childhood trauma. Earlylife stress predicts later inflammation, and there are striking analogies between the neurobiological correlates of early-life stress and of inflammation. Furthermore, there are overlapping trans-diagnostic patterns of association of childhood trauma and inflammation with clinical outcomes. These findings suggest new strategies to remediate the effect of childhood trauma before the onset of clinical symptoms, such as anti-inflammatory interventions and potentiation of adaptive immunity. Similar strategies might be used to ameliorate the unfavorable treatment response described in psychiatric patients with a history of childhood trauma.

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“…6 Two recent meta-analyses listed increased serum levels of interleukin (IL)-4, IL-10, tumour necrosis factor (TNF)-α, sIL-2R, sIL-6R and sTNF-R1 as the most consistent findings in patients with bipolar disorder. 7,8 However, previous studies on inflammatory markers have rarely accounted for potential confounders, such as body mass index (BMI), smoking and ongoing medication use. Moreover, the interpretation of the findings is hampered by the fact that elevated inflammatory markers in the blood cannot be presumed to reflect inflammatory processes in the central nervous system (CNS).…”

Section: Introductionmentioning

confidence: 99%

Monocyte and microglial activation in patients with mood-stabilized bipolar disorder

Jakobsson

Bjerke

Sahebi

et al. 2015

jpn

100

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Cytokine Alterations in Bipolar Disorder: A Meta-Analysis of 30 Studies

Cited by 525 publications

References 101 publications

Shortened telomere length in bipolar disorder: a comparison of the early and late stages of disease

Shortened telomere length in bipolar disorder: a comparison of the early and late stages of disease

Psychoneuroimmunology of Early-Life Stress: The Hidden Wounds of Childhood Trauma?

Monocyte and microglial activation in patients with mood-stabilized bipolar disorder

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