Early life experience contributes to the developmental programming of depressive-like behaviour, neuroinflammation and oxidative stress

Réus, Gislaine Z.; Fernandes, Gabrielly C.; Moura, Airam B. de; Silva, Ritele H.; Darabas, Ana Caroline; Souza, Thays G. de; Abelaira, Helena M.; Carneiro, Celso; Wendhausen, Diogo; Michels, Monique; Pescador, Bruna; Dal‐Pizzol, Felipe; Macêdo, Danielle Silveira; Quevedo, João

doi:10.1016/j.jpsychires.2017.08.020

Cited by 65 publications

(56 citation statements)

References 60 publications

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“…Animal findings confirmed that ELS (e.g., maternal separation) has a significant impact on parameters of OXS in mitochondrial function and has shown an association with reactive oxygen species, mitochondrial glutathione, ATP and cytochrome c release in cardiac tissue (251). Furthermore, decreased levels of superoxide dismutase and catalase activity, as well as higher levels of protein carbonylation have been reported in the brain of adult animals exposed to ELS (252). Human research been successfully replicated similar findings.…”

Section: Redox State and Antioxidant Defensessupporting

confidence: 59%

Developmental Trajectories of Early Life Stress and Trauma: A Narrative Review on Neurobiological Aspects Beyond Stress System Dysregulation

et al. 2019

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Early life stressors display a high universal prevalence and constitute a major public health problem. Prolonged psychoneurobiological alterations as sequelae of early life stress (ELS) could represent a developmental risk factor and mediate risk for disease, leading to higher physical and mental morbidity rates in later life. ELS could exert a programming effect on sensitive neuronal brain networks related to the stress response during critical periods of development and thus lead to enduring hyper- or hypo-activation of the stress system and altered glucocorticoid signaling. In addition, alterations in emotional and autonomic reactivity, circadian rhythm disruption, functional and structural changes in the brain, as well as immune and metabolic dysregulation have been lately identified as important risk factors for a chronically impaired homeostatic balance after ELS. Furthermore, human genetic background and epigenetic modifications through stress-related gene expression could interact with these alterations and explain inter-individual variation in vulnerability or resilience to stress. This narrative review presents relevant evidence from mainly human research on the ten most acknowledged neurobiological allostatic pathways exerting enduring adverse effects of ELS even decades later (hypothalamic-pituitary-adrenal axis, autonomic nervous system, immune system and inflammation, oxidative stress, cardiovascular system, gut microbiome, sleep and circadian system, genetics, epigenetics, structural, and functional brain correlates). Although most findings back a causal relation between ELS and psychobiological maladjustment in later life, the precise developmental trajectories and their temporal coincidence has not been elucidated as yet. Future studies should prospectively investigate putative mediators and their temporal sequence, while considering the potentially delayed time-frame for their phenotypical expression. Better screening strategies for ELS are needed for a better individual prevention and treatment.

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Section: Redox State and Antioxidant Defensessupporting

confidence: 59%

Developmental Trajectories of Early Life Stress and Trauma: A Narrative Review on Neurobiological Aspects Beyond Stress System Dysregulation

et al. 2019

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“…Moreover, a meta-analysis study, was confirmed that IL-6 and TNF-α levels are elevated in MDD patients (Muller, 2014). Previous study shown to reduce levels of IL-10 contributed to an increase in the expression of IL-6 in the brains of aged mice, moreover, was demonstrated that early life stress induces an increase in IL-6 levels and a decrease in IL-10 levels in a rat model of early-life stress (Reus et al, 2017). Thus, changes in inflammatory mediators in the periphery could increase inflammation in the CNS.…”

Section: Introductionmentioning

confidence: 64%

Childhood trauma and increased peripheral cytokines in young adults with major depressive: Population-based study

Moreira

Wiener

Jansen

et al. 2018

Journal of Neuroimmunology

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“…In preclinical animal models, exposure to ELS increases the density, size, and propensity to release inflammation within CNS by microglia (Bilbo & Schwarz, ; Calcia et al, ; Delpech et al, ; Réus et al, ; Wang et al, ), which has also been linked to behaviors associated with anxiety and depression in rodents (Johnson & Kaffman, ). Indeed, two of these experimental studies have explicitly linked ELS to behavioral phenotypes associated with depression in adulthood through this neuroinflammatory pathway (Réus et al, ; Wang et al, ) and one showed that the behavioral phenotype associated with depression could be resolved with pharmacological agents that blocked microglia activation (Wang et al, ). ELS may also lead to greater permeability of the BBB (Kuvacheva et al, ), which allows more peripheral inflammatory cytokines and cells to access the CNS.…”

Section: Discussionmentioning

confidence: 99%

Early life stress sensitizes individuals to the psychological correlates of mild fluctuations in inflammation

Kuhlman

Robles

Haydon

et al. 2019

Developmental Psychobiology

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Background Early life stress (ELS) has been linked to health disparities across the human lifespan, particularly increased risk for depression and its recurrence. In this study we explore two plausible and competing pathways through which ELS may lead to depression via inflammation. Methods Participants (ages 18–22; n = 41) completed the Early Trauma Inventory as a measure of ELS. Participants then completed consecutive daily diaries of mood and other sickness behavior for the 7 days prior to and 7 days after receiving the annual influenza vaccine. Circulating concentrations of plasma interleukin‐6 (IL‐6) were measured immediately before and 24 hr after vaccination. Results ELS was not associated with the magnitude of change in IL‐6 from pre‐ to post‐vaccine, however, exposure to ELS moderated the association between change in IL‐6 from pre‐ to post‐vaccine and changes in both cognitive difficulty and depressed mood. Individuals exposed to greater ELS showed greater psychological sensitivity to increases in IL‐6. Conclusions Exposure to ELS may increase sensitivity to peripheral inflammation in the central nervous system. Future studies elaborating on the impact of ELS on the sensitivity of specific neural circuits and cells to inflammation are needed.

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Early life experience contributes to the developmental programming of depressive-like behaviour, neuroinflammation and oxidative stress

Cited by 65 publications

References 60 publications

Developmental Trajectories of Early Life Stress and Trauma: A Narrative Review on Neurobiological Aspects Beyond Stress System Dysregulation

Developmental Trajectories of Early Life Stress and Trauma: A Narrative Review on Neurobiological Aspects Beyond Stress System Dysregulation

Childhood trauma and increased peripheral cytokines in young adults with major depressive: Population-based study

Early life stress sensitizes individuals to the psychological correlates of mild fluctuations in inflammation

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