Neuroinflammatory Biomarkers in Cerebrospinal Fluid From 106 Patients With Recent-Onset Depression Compared With 106 Individually Matched Healthy Control Subjects

Sørensen, Nina Vindegaard; Orlovska-Waast, Sonja; Jeppesen, Rose; Klein-Petersen, Amalie Wandel; Christensen, Rune Haubo Bojesen; Benros, Michael E.

doi:10.1016/j.biopsych.2022.04.002

Cited by 24 publications

(13 citation statements)

References 50 publications

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“…As in our study, previous reports could not establish differences in IL-4 and IL-10 between FED and healthy controls (Lan, Zhou et al 2021, Yang, Liu et al 2021. However, in cerebrospinal fluid (CSF), there was no difference in 25 cytokines/chemokines between individuals with recent-onset depression and healthy controls (Sørensen, Borbye-Lorenzen et al 2023). Other studies were unable to detect alterations in CSF levels of TNF-α, TNF-β, sIL-1RA, and sIL-2R in FED (Yang, Liu et al 2021).…”

Section: Cytokines/chemokines/growth Factors In Fe-mdmdcontrasting

confidence: 84%

“…These findings provide additional evidence that T cell activation, as demonstrated by flow cytometry, is a key factor in severe MDD (Maes, Bosmans et al 1990, Maes, Bosmans et al 1991, Maes, Lambrechts et al 1992, Maes, Stevens et al 1993. Recent meta-analyses indicate that persons with MDD express more activated T cells and have a higher CD4/CD8 ratio (Foley, Parkinson et al 2023, Sørensen, Borbye-Lorenzen et al 2023.…”

Section: Immune Profiles In Fe-mdmdmentioning

confidence: 65%

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T helper-1 activation via interleukin-16 is a key phenomenon in the acute phase of severe, first-episode major depressive disorder and suicidal behaviors

Almulla

Algon

Tunvirachaisakul

et al. 2023

Preprint

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Background: Immune-inflammatory pathways in major depressive disorder are confined to the major dysmood disorder (MDMD) phenotype (Maes et al., 2022). No studies have addressed the immune profile of first episode MDMD (FE-MDMD). Methods: This study examines 48 cytokines/chemokines/growth factors, and classical M1, alternative M2, T helper (Th)-1, Th-2, and Th-17 phenotypes, immune-inflammatory response system (IRS), compensatory immunoregulatory system (CIRS), and neuro-immunotoxicity profiles in the acute phase of FE-MDMD (n=71) versus healthy controls (40). Results: FE-MDMD patients show significantly activated M1, M2, Th-1, IRS, CIRS, and neurotoxicity, but not Th-2 or Th-17, profiles compared to controls. FE-MDMD is accompanied by Th-1 polarization, while there are no changes in M1/M2 or IRS/CIRS ratios. The top single indicator of FE-MDMD was by far interleukin (IL)-16, followed at a distance by TRAIL, IL-2R, tumor necrosis factor (TNF)-β. The severity of depression and anxiety was strongly associated with IRS (positively) and Th-2 (inversely) profiles, whereas suicidal behavior was associated with M1 activation. Around 56-60% of the variance in depression, anxiety, and suicidal behavior scores was explained by IL-16, platelet-derived growth factor (PDGF) (both positively), and IL-1 receptor antagonist (inversely). Increased neurotoxicity is mainly driven by IL-16, TNF-α, TRAIL, IL-6 and chemokine (CCL2, CCL11, CXCL1, CXCL10) signaling. Antidepressant-treated patients show an increased IRS/CIRS ratio as compared with drug-naive FE-MDMD patients. Conclusions: FE-MDMD is accompanied by positive regulation of the IRS mainly driven by Th-1 polarization and T cell activation (via binding of IL-16 to CD4), and TNF, chemokine, and growth factor signaling.

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Section: Cytokines/chemokines/growth Factors In Fe-mdmdcontrasting

confidence: 84%

Section: Immune Profiles In Fe-mdmdmentioning

confidence: 65%

T helper-1 activation via interleukin-16 is a key phenomenon in the acute phase of severe, first-episode major depressive disorder and suicidal behaviors

Almulla

Algon

Tunvirachaisakul

et al. 2023

Preprint

View full text Add to dashboard Cite

show abstract

“…The study was conducted at the facility of Biological and Precision Psychiatry, Copenhagen Research Centre for Mental Health, Mental Health Centre Copenhagen, Copenhagen, Denmark. A study protocol was published prior to this article ( 19 ), and demographic data have previously been published ( 20 ). The study was approved by the Regional Committee on Health Research Ethics and the Danish Data Protection Agency.…”

Section: Methodsmentioning

confidence: 99%

Antineuronal Autoantibodies in the Cerebrospinal Fluid and Serum From 106 Patients With Recent-Onset Depression Compared With 106 Individually Matched Healthy Control Subjects

Sørensen

Nilsson²,

Orlovska-Waast³

et al. 2023

Biological Psychiatry Global Open Science

Self Cite

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“…Proof of abuse of the term "neuroinflammation" is nowhere more apparent than in the sheer number of conditions that are now referred to as "neuroinflammatory," including obesity (Lorena et al, 2021;Miller & Spencer, 2014), pain (De Logu et al, 2021;Li et al, 2022a), epilepsy (Parsons et al, 2022;Pracucci et al, 2021), periodontitis (Li et al, 2022b;Teixeira et al, 2017), sleep loss (Kou et al, 2022;Wisor et al, 2011), autism (Matta et al, 2019;Vargas et al, 2005), depression (Furtado & Katzman, 2015;Sorensen et al, 2022), schizophrenia (Monji & Mizoguchi, 2022;Vallee, 2022), Alzheimer's disease (Leng & Edison, 2021;McGeer et al, 2000), Parkinson's disease (Pfeiffer, 2009;Yang et al, 2020), amyotrophic lateral sclerosis (Arnoux & Dupuis, 2021;Lewis et al, 2012), and the brain's response to air pollution (Block & Calderon-Garciduenas, 2009;Brockmeyer & D'Angiulli, 2016), to name a few. Arguably, this quite indiscriminate spread is facilitated by the fact that few research scientists are trained in neuropathology, a medical specialty that exists in only a handful of countries, making systematic and direct comparative studies between nervous system diseases very difficult.…”

Section: Sizing the Problemmentioning

confidence: 99%

Neuroinflammation: The Abused Concept

Galea,

Graeber

2023

ASN Neuro

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Scientific progress requires the relentless correction of errors and refinement of hypotheses. Clarity of terminology is essential for clarity of thought and proper experimental interrogation of nature. Therefore, the application of the same scientific term to different and even conflicting phenomena and concepts is not useful and must be corrected. Such abuse of terminology has happened and is still increasing in the case of “neuroinflammation,” a term that until the 1990s meant classical inflammation affecting the central nervous system (CNS) and thereon was progressively used to mostly denote microglia activation. The resulting confusion is very wasteful and detrimental not only for scientists but also for patients, given the numerous failed clinical trials in acute and chronic CNS diseases over the last decade with “anti-inflammatory” drugs. Despite this failure, reassessments of the “neuroinflammation” concept are rare, especially considering the number of articles still using the term. This undesirable situation motivates this article. We review the origins and evolution of the term “neuroinflammation,” discuss the unique tissue defense and repair strategies in the CNS, define CNS immunity, and emphasize the notion of gliopathies to help readdress, if not bury, the term “neuroinflammation” as it stands in the way of scientific progress.

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Neuroinflammatory Biomarkers in Cerebrospinal Fluid From 106 Patients With Recent-Onset Depression Compared With 106 Individually Matched Healthy Control Subjects

Cited by 24 publications

References 50 publications

T helper-1 activation via interleukin-16 is a key phenomenon in the acute phase of severe, first-episode major depressive disorder and suicidal behaviors

T helper-1 activation via interleukin-16 is a key phenomenon in the acute phase of severe, first-episode major depressive disorder and suicidal behaviors

Antineuronal Autoantibodies in the Cerebrospinal Fluid and Serum From 106 Patients With Recent-Onset Depression Compared With 106 Individually Matched Healthy Control Subjects

Neuroinflammation: The Abused Concept

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