Depression Phenotype, Inflammation, and the Brain

Abstract

Article (Accepted Version) http://sro.sussex.ac.uk Krishnadas, Rajeev and Harrison, Neil (2016) Depression phenotype, inflammation and the brain: implications for future research. Psychosomatic Medicine, 78 (4). pp. [384][385][386][387][388] This version is available from Sussex Research Online: http://sro.sussex.ac.uk/60238/ This document is made available in accordance with publisher policies and may differ from the published version or from the version of record. If you wish to cite this item you are advised to consult the publisher's version. Please see the URL above for details on accessing the published version. Copyright and reuse:Sussex Research Online is a digital repository of the research output of the University.Copyright and all moral rights to the version of the paper presented here belong to the individual author(s) and/or other copyright owners. To the extent reasonable and practicable, the material made available in SRO has been checked for eligibility before being made available.Copies of full text items generally can be reproduced, displayed or performed and given to third parties in any format or medium for personal research or study, educational, or not-for-profit purposes without prior permission or charge, provided that the authors, title and full bibliographic details are credited, a hyperlink and/or URL is given for the original metadata page and the content is not changed in any way.

Bidirectional Associations Between Inflammatory Biomarkers and Depressive Symptoms in Adolescents: Potential Causal Relationships

“…Thus, testing symptom subtypes, or specific symptoms, might provide more replicable findings. Recent commentaries have argued for the importance of investigating inflammatory phenotypes of depression (Felger, Haroon, & Miller, 2018; Krishnadas & Harrison, 2016). This interest inspired a recent review examining experimental evidence for the association between inflammation and depression, which concluded that increased inflammatory activity likely is associated with exaggerated reactivity to negative information, altered reward reactivity, and somatic symptoms but less likely to be associated with deficits in cognitive control (Dooley et al, 2018).…”

How handling extreme C-reactive protein (CRP) values and regularization influences CRP and depression criteria associations in network analyses

“…Further, elevated inflammation only is seen in a subset of individuals with depression (Raison & Miller, 2011). One potential explanation for this is that CRP is not associated equally with all depression symptoms, which has inspired calls for investigations into the inflammatory phenotyping of depression (Felger et al, 2018;Krishnadas & Harrison, 2016) and expanding the scalar variety of psychopathological constructs analyzed in immunopsychiatry research (Moriarity & Alloy, in press).…”

Synergistic Action of Sodium Selenite with some Antidepressants and Diazepam in Mice

“…Current hypotheses regarding the etiology of the depressive disorder tend to integrate monoaminergic, neuroendocrine, and immunological concepts with those based on oxidative stress, neuronal plasticity, and neurogenesis disturbances (the role of brain derived neurotrophic factor, BDNF). Many research papers highlight the involvement of several pathways i.e., serum lipids, hypothalamic–pituitary–adrenal axis (HPA axis), inflammatory system, gut microbiota, kynurenine pathway [5,6,7,8,9,10,11,12,13]. This complexity of various factor interactions may be the cause of increased risk of atherosclerosis and cardiovascular changes such as ischemic heart disease [14] and stroke [15] as well as endocrine dysregulation [16].…”