Inflammatory phenotype of depression symptom structure: A network perspective

Moriarity, Daniel P.; Borkulo, Claudia van; Alloy, Lauren B.

doi:10.1016/j.bbi.2020.12.005

Cited by 29 publications

(42 citation statements)

References 52 publications

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“…My dissertation ( Moriarity et al., 2021a , Moriarity et al., 2021b , Moriarity et al., 2021c ) compared this “a priori” approach (assuming all proteins are equally associated with a unidimensional inflammatory construct) to an empirically-identified factor structure of eight proteins (C-reactive protein (CRP), interleukin (IL)-6, IL-8, IL-10, tumor necrosis factor-α (TNF-α), fibrinogen, E-selectin, and intercellular adhesion molecule (ICAM)-1)) using a “bass-ackward” factor analysis ( Goldberg, 2006 ). This analysis supported a hierarchical factor structure with two first-order factors (Factor-A = CRP, IL-6, and fibrinogen; Factor-B = TNF-α, IL-8, IL-10, ICAM-1, and IL-6), and one higher-order general inflammation factor.…”

Section: Methodsmentioning

confidence: 99%

Building a replicable and clinically-impactful immunopsychiatry: Methods, phenotyping, and theory integration

Moriarity

2021

Brain, Behavior, & Immunity - Health

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Immunopsychiatry is a subfield of psychoneuroimmunology that integrates immunological and psychopathological processes with promise for improving the classification, identification, and treatment of psychopathology. Using research on the relationship between inflammation and depression as a running example, this mini-review will discuss three areas of work that should be emphasized in future research to maximize the replicability and clinical impact of the field: 1) methodology with respect to planning data collection and statistical analyses with measurement properties and conceptually important sources of variance in mind, 2) characterizing inflammatory phenotypes of psychopathology, and 3) the integration of inflammatory processes into robust, extant psychosocial theoretical frameworks of psychopathology risk. Consistent, parallel growth in all three areas will ensure immunopsychiatry research is replicable, contributes to understanding of how (and for whom) the immune system is associated with psychiatric symptoms, and increases the flexibility and power of personalized treatment planning.

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Section: Methodsmentioning

confidence: 99%

Building a replicable and clinically-impactful immunopsychiatry: Methods, phenotyping, and theory integration

Moriarity

2021

Brain, Behavior, & Immunity - Health

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“…Somatic symptoms were related to CRP levels (p < 0.001) [48]. A recent network analysis investigated the association between inflammation and a specific depression phenotype [69]. PHQ-9 was administered to a sample of 4157 adults from the NHANES while hs-CRP levels were measured to identify possible inflammatory phenotypes of depression [69].…”

Section: Cross-sectional Studiesmentioning

confidence: 99%

C-Reactive Protein as a Biomarker for Major Depressive Disorder?

Orsolini

Pompili

Valenta

et al. 2022

IJMS

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The etiopathogenesis of depression is not entirely understood. Several studies have investigated the role of inflammation in major depressive disorder. The present work aims to review the literature on the association between C-Reactive Protein (CRP) and depression. A systematic review was performed for the topics of ‘CRP’ and ‘depression’ using the PubMed database from inception to December 2021. Fifty-six studies were identified and included in the review. Evidence suggested the presence of dysregulation in the inflammation system in individuals with depression. In most studies, higher blood CRP levels were associated with greater symptom severity, a specific pattern of depressive symptoms, and a worse response to treatment. Moreover, about one-third of depressed patients showed a low-grade inflammatory state, suggesting the presence of a different major depressive disorder (MDD) subgroup with a distinct etiopathogenesis, clinical course, treatment response, and prognosis, which could benefit from monitoring of CRP levels and might potentially respond to anti-inflammatory treatments. This work provides robust evidence about the potential role of CRP and its blood levels in depressive disorders. These findings can be relevant to developing new therapeutic strategies and better understanding if CRP may be considered a valuable biomarker for depression.

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“…In particular, identifying modifiable risk factors that are causally related to depression and elevated inflammatory physiology could be effective targets for intervention and, thus, of relevance to public policy. Finally, inflammation in depression may be particularly associated with somatic symptoms (e.g., fatigue) and/or cognitive dysfunction (e.g., difficulties in concentration/decision-making) and consequently a deeper understanding of inflammation in depression may contribute to a better understanding of depression's heterogeneous clinical presentation ( Chu et al., 2019 ; Fried et al., 2019 ; Moriarity et al., 2020 ). In particular, such an approach may inform our understanding of cognitive dysfunction in depression, which is of particular importance given the clinical heterogeneity of depression and that cognitive dysfunction is differentially associated with worse functional impairment in depression ( Jaeger et al., 2006 ; Whiteford et al., 2013 ; Woo et al., 2016 ).…”

Section: What Are the Benefits Of Incorporating These Approaches?mentioning

confidence: 99%

Inflammation and depression: Research designs to better understand the mechanistic relationships between depression, inflammation, cognitive dysfunction, and their shared risk factors

Giollabhui

2021

Brain, Behavior, & Immunity - Health

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There is convergent evidence that the immune system is dysregulated in some depressed individuals. A psychoneuroimmunology-based understanding of depression is advancing rapidly; however, a question of fundamental importance is poorly understood: does inflammation play a causal role in the etiology of depression or are elevated inflammatory biomarkers a downstream effect of depressive behaviors? Although longitudinal studies suggest that the relationship between depression and inflammation is characterized by complex bidirectional associations, existing prospective, longitudinal research designs are poorly equipped to investigate the dynamic interplay of depression and inflammation that unfolds over a relatively short time period. In addition, the precise role played by multiple, shared, and overlapping risk factors (e.g., diet, adiposity, stress, sleep dysregulation) in the etiology of depression and a pro-inflammatory phenotype (or both) is poorly understood. In this manuscript, I highlight the benefits of research designs that (i) manipulate constructs of interest (depression/inflammation) using intervention or treatment designs and (ii) use intensive sampling approaches with an ultimate goal of better understanding the temporal sequence and causal relationships of depression, inflammation, cognitive dysfunction, and their shared risk factors. For instance, are improved depressive symptoms a downstream effect of changes in inflammatory activity caused by increases in exercise or, alternatively, are changes in inflammatory activity and depression sequelae of improvements in sleep quality caused by increases in exercise? Potential benefits of these research designs are discussed in terms of their contribution to a better understanding of the etiology of depression and a pro-inflammatory phenotype, their relevance to structural health inequalities, and better characterizing the heterogeneous clinical presentation of depression, particularly relating to the etiology of cognitive dysfunction in depression.

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Inflammatory phenotype of depression symptom structure: A network perspective

Cited by 29 publications

References 52 publications

Building a replicable and clinically-impactful immunopsychiatry: Methods, phenotyping, and theory integration

Building a replicable and clinically-impactful immunopsychiatry: Methods, phenotyping, and theory integration

C-Reactive Protein as a Biomarker for Major Depressive Disorder?

Inflammation and depression: Research designs to better understand the mechanistic relationships between depression, inflammation, cognitive dysfunction, and their shared risk factors

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