The ratio and interaction between neurotrophin and immune signaling during electroconvulsive therapy in late-life depression

Background: Electroconvulsive therapy (ECT) is the most effective treatment for severe late-life depression (LLD), and several hypotheses on the precise working mechanism have been proposed. Preclinical evidence suggests that ECT induces changes in neurotrophin and inflammatory signaling and that th...

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Autores principales: Dore Loef, Kristof Vansteelandt, Mardien L. Oudega, Philip van Eijndhoven, Angela Carlier, Eric van Exel, Didi Rhebergen, Pascal Sienaert, Mathieu Vandenbulcke, Filip Bouckaert, Annemiek Dols
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Publicado: Elsevier 2021
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spelling oai:doaj.org-article:6417081e3724470eb6ea325840db9d922021-11-20T05:14:18ZThe ratio and interaction between neurotrophin and immune signaling during electroconvulsive therapy in late-life depression2666-354610.1016/j.bbih.2021.100389https://doaj.org/article/6417081e3724470eb6ea325840db9d922021-12-01T00:00:00Zhttp://www.sciencedirect.com/science/article/pii/S2666354621001927https://doaj.org/toc/2666-3546Background: Electroconvulsive therapy (ECT) is the most effective treatment for severe late-life depression (LLD), and several hypotheses on the precise working mechanism have been proposed. Preclinical evidence suggests that ECT induces changes in neurotrophin and inflammatory signaling and that these neurotrophic and inflammatory systems affect each other. We examine the relation, interaction, and ratio between the neurotrophic brain-derived neurotrophic factor (BDNF) and the proinflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor α (TNF-α), and depression severity during ECT. Methods: In this naturalistic longitudinal study, linear mixed models were used to analyze the relation between BDNF, IL-6, TNF-α, and depression severity (determined by the Montgomery-Åsberg Depression Rating Scale; MADRS) in 99 patients with severe LLD before ECT (T0), three weeks after the first ECT (T1), and one week after the last ECT (T2). Results: No significant association was found between BDNF, IL-6 and TNF-α, and MADRS scores at any time point. However, a significant interaction between TNF-α and BDNF in relation to MADRS was established (p ​= ​.020) at all time points. With higher levels of TNF-α, the relation between BDNF and MADRS becomes more negative. Furthermore, a higher ratio of TNF-α/BDNF was associated with a higher score on the MADRS (p ​= ​.007). Conclusion: A possible explanation for the absence of a significant coevolution between the proinflammatory cytokines and BDNF could be that the study design was unable to determine parameters shortly after ECT sessions. However, the TNF-α/BDNF ratio was positively associated with depression severity, and the association of BDNF-level and depression severity depended on the level of TNF-α. This suggests that the interaction and balance between neurotrophin and immune signaling, specifically BDNF and TNF-α, could be relevant in LLD. This could be a focus in future research regarding treatment and the working mechanism of ECT.Dore LoefKristof VansteelandtMardien L. OudegaPhilip van EijndhovenAngela CarlierEric van ExelDidi RhebergenPascal SienaertMathieu VandenbulckeFilip BouckaertAnnemiek DolsElsevierarticleElectroconvulsive therapy (ECT)DepressionBrain-derived neurotrophic factor (BDNF)Interleukin-6 (IL-6)Tumor necrosis factor α (TNF-α)Neurosciences. Biological psychiatry. NeuropsychiatryRC321-571ENBrain, Behavior, & Immunity - Health, Vol 18, Iss , Pp 100389- (2021)
institution DOAJ
collection DOAJ
language EN
topic Electroconvulsive therapy (ECT)
Depression
Brain-derived neurotrophic factor (BDNF)
Interleukin-6 (IL-6)
Tumor necrosis factor α (TNF-α)
Neurosciences. Biological psychiatry. Neuropsychiatry
RC321-571
spellingShingle Electroconvulsive therapy (ECT)
Depression
Brain-derived neurotrophic factor (BDNF)
Interleukin-6 (IL-6)
Tumor necrosis factor α (TNF-α)
Neurosciences. Biological psychiatry. Neuropsychiatry
RC321-571
Dore Loef
Kristof Vansteelandt
Mardien L. Oudega
Philip van Eijndhoven
Angela Carlier
Eric van Exel
Didi Rhebergen
Pascal Sienaert
Mathieu Vandenbulcke
Filip Bouckaert
Annemiek Dols
The ratio and interaction between neurotrophin and immune signaling during electroconvulsive therapy in late-life depression
description Background: Electroconvulsive therapy (ECT) is the most effective treatment for severe late-life depression (LLD), and several hypotheses on the precise working mechanism have been proposed. Preclinical evidence suggests that ECT induces changes in neurotrophin and inflammatory signaling and that these neurotrophic and inflammatory systems affect each other. We examine the relation, interaction, and ratio between the neurotrophic brain-derived neurotrophic factor (BDNF) and the proinflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor α (TNF-α), and depression severity during ECT. Methods: In this naturalistic longitudinal study, linear mixed models were used to analyze the relation between BDNF, IL-6, TNF-α, and depression severity (determined by the Montgomery-Åsberg Depression Rating Scale; MADRS) in 99 patients with severe LLD before ECT (T0), three weeks after the first ECT (T1), and one week after the last ECT (T2). Results: No significant association was found between BDNF, IL-6 and TNF-α, and MADRS scores at any time point. However, a significant interaction between TNF-α and BDNF in relation to MADRS was established (p ​= ​.020) at all time points. With higher levels of TNF-α, the relation between BDNF and MADRS becomes more negative. Furthermore, a higher ratio of TNF-α/BDNF was associated with a higher score on the MADRS (p ​= ​.007). Conclusion: A possible explanation for the absence of a significant coevolution between the proinflammatory cytokines and BDNF could be that the study design was unable to determine parameters shortly after ECT sessions. However, the TNF-α/BDNF ratio was positively associated with depression severity, and the association of BDNF-level and depression severity depended on the level of TNF-α. This suggests that the interaction and balance between neurotrophin and immune signaling, specifically BDNF and TNF-α, could be relevant in LLD. This could be a focus in future research regarding treatment and the working mechanism of ECT.
format article
author Dore Loef
Kristof Vansteelandt
Mardien L. Oudega
Philip van Eijndhoven
Angela Carlier
Eric van Exel
Didi Rhebergen
Pascal Sienaert
Mathieu Vandenbulcke
Filip Bouckaert
Annemiek Dols
author_facet Dore Loef
Kristof Vansteelandt
Mardien L. Oudega
Philip van Eijndhoven
Angela Carlier
Eric van Exel
Didi Rhebergen
Pascal Sienaert
Mathieu Vandenbulcke
Filip Bouckaert
Annemiek Dols
author_sort Dore Loef
title The ratio and interaction between neurotrophin and immune signaling during electroconvulsive therapy in late-life depression
title_short The ratio and interaction between neurotrophin and immune signaling during electroconvulsive therapy in late-life depression
title_full The ratio and interaction between neurotrophin and immune signaling during electroconvulsive therapy in late-life depression
title_fullStr The ratio and interaction between neurotrophin and immune signaling during electroconvulsive therapy in late-life depression
title_full_unstemmed The ratio and interaction between neurotrophin and immune signaling during electroconvulsive therapy in late-life depression
title_sort ratio and interaction between neurotrophin and immune signaling during electroconvulsive therapy in late-life depression
publisher Elsevier
publishDate 2021
url https://doaj.org/article/6417081e3724470eb6ea325840db9d92
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