C-reactive protein: A differential biomarker for major depressive disorder and bipolar II disorder

Chang, Hui Hua; Wang, Tzu Yun; Lee, I. Hui; Lee, Sheng Yu; Chen, Kao Chin; Huang, San Yuan; Yang, Yen Kuang; Lu, Ru Band; Chen, Po See

doi:10.3109/15622975.2016.1155746

Cited by 51 publications

(44 citation statements)

References 48 publications

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“…BD patients show lower levels of plasma TNF-a and IL-13 (111), and serum IL-1b (112) compared to MDD patients. On the other hand, BD patients presented higher Creactive protein, sTNFR1, soluble IL-6 receptor (sIL-6R), and MCP-1 levels compared to MDD patients (33,113). Another group has tried to investigate the difference in the peripheral inflammatory markers' levels between BD illness phase.…”

Section: Immune Markers As Clinical Outcome and Diagnostic Predictorsmentioning

confidence: 99%

Neuroinflammation in Bipolar Depression

et al. 2020

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Bipolar disorder (BD) is a leading cause of worldwide disability among mood disorders. Pathological mechanisms are still vastly unclear, and current treatments with conventional medications are often unsatisfactory in maintaining symptoms control and an adequate quality of life. Consequently, current research is focusing on shedding new light on disease pathogenesis, to improve therapeutic effectiveness. Recent evidence has suggested a prominent role of inflammation in mood disorders. Elevated levels of peripheral proinflammatory mediators have been reported in BD, as well as in other mood disorders, and people with systemic autoimmune diseases have an increased risk of developing BD. These immunological alterations are stable, and current medications are unable to alter peripheral concentrations even when clinical improvement is evident. These findings have also been replicated in the central nervous system (CNS) milieu, whereas genetic studies have shown that these immune alterations are not due to the disorder itself, being detectable before the illness onset. Moreover, these inflammatory modifications seem to be affected by and linked to other biomarkers of the disorder, such as alterations of white matter (WM) microstructure, metabolism, kynurenine pathway, and circadian rhythmicity. Finally, these immune variations seem to be useful as predictors of therapeutic responsiveness to medications, and in discriminating between clinically different outcomes. The objective of this review is to summarize available evidence on the connection between inflammation and BD, focusing on peripheral inflammatory markers and recent findings on their connection with other typical features of BD, to outline a general overview of the disorder. Moreover, it is meant to analyze the issues with data gathering and interpretation, given the partially contradictory and inconsistent nature of results.

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Section: Immune Markers As Clinical Outcome and Diagnostic Predictorsmentioning

confidence: 99%

Neuroinflammation in Bipolar Depression

et al. 2020

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“…Recent meta-analyses have found decreased levels of kynurenine in MDD versus healthy controls but not in bipolar disorder [67]. Using high-sensitivity testing of fasting plasma CRP levels at baseline and after treatment, Chang and colleagues reported that a baseline CRP level of 621.6 ng/mL could discriminate between bipolar disorder II and MDD [68]. However, Powell et al found that reduced transcription of IL8 could be used to distinguish both MDD and bipolar disorder from control subjects [69].…”

Section: Relationship Between Pro-inflammatory Cytokines and The Braimentioning

confidence: 99%

Role of inflammation in depression relapse

Liu

Zhang

et al. 2019

J Neuroinflammation

119

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Major depressive disorder (MDD) is a leading cause of disability worldwide. After the first episode, patients with remitted MDD have a 60% chance of experiencing a second episode. Consideration of therapy continuation should be viewed in terms of the balance between the adverse effects of medication and the need to prevent a possible relapse. Relapse during the early stages of MDD could be prevented more efficiently by conducting individual risk assessments and providing justification for continuing therapy. Our previous work established the neuroimaging markers of relapse by comparing patients with recurrent major depressive disorder (rMDD) in depressive and remitted states. However, it is not known which of these markers are trait markers that present before initial relapse and, consequently, predict disease course. Here, we first describe how inflammation can be translated to subtype-specific clinical features and suggest how this could be used to facilitate clinical diagnosis and treatment. Next, we address the central and peripheral functional state of the immune system in patients with MDD. In addition, we emphasize the important link between the number of depressive episodes and rMDD and use neuroimaging to propose a model for the latter. Last, we address how inflammation can affect brain circuits, providing a possible mechanism for rMDD. Our review suggests a link between inflammatory processes and brain region/circuits in rMDD.

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“…It is of clinical importance regarding the high prevalence of metabolic disturbance in BD patients (Chang et al, 2009b;Hung Chi et al, 2013;Vancampfort et al, 2013). CRP plays a pivotal role in aspects of inflammation that appears to be related to BD across several important domains (Chang et al, 2016;Goldstein et al, 2009;Leboyer et al, 2012a). Moreover, inflammation has been proposed to be the underlying mechanism that links BD and metabolic disturbances (Kim et al, 2007;Leboyer et al, 2012a;Lee et al, 2013a), as a previous study revealed apparent metabolic disturbances in BD patients with high CRP levels (Tsai et al, 2014).…”

Section: Discussionmentioning

confidence: 99%