Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

Journal Browser

Pathogenesis and Treatment Mechanisms of Depression

Special Issue Editors
Special Issue Information
Keywords
Published Papers

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (21 October 2022) | Viewed by 19912

Share This Special Issue

Special Issue Editor

Prof. Dr. Yong-Ku Kim

E-Mail Website
Guest Editor

Department of Psychiatry, College of Medicine, Korea University Ansan Hospital, 123, Jeokgeum-ro, Danwon-gu, Ansan-si, Gyeonggi-do, Seoul 15355, Korea
Interests: psychiatry; depression; mood disorders; stress; schizophrenia; bipolar disorder
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Depression is currently one of the most important causes of mortality and morbidity, and occurs in all genders, ages, and social backgrounds. The pathogenesis and treatment mechanisms of depression are now better understood thanks to multilateral neurobiological studies. The structural and functional brain anomalies of patients with depression have been investigated through brain imaging studies. In addition, genetic mutations have been reported through genetic studies. Molecular biological studies and gene manipulation tests have also contributed to mounting evidence regarding the preclinical grounds associated with depression. Integrated studies on genes, proteins, and animal behavior may help to build a clearer understanding of the pathogenesis and treatment mechanisms of depression, and may enable new drug development and clinical applications. This Special Issue focus on molecular research on depression. Original research articles or reviews are welcome.

Prof. Dr. Yong-Ku Kim
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

molecular biomarker
biological marker
pathophysiology
neurobiology
neural plasticity
immune
endocrine
gene
mTOR
brain–gut
antidepressant
depression
postpartum depression
bipolar depression
psychotic depression
post-schizophrenic depression

Published Papers (5 papers)

Download All Papers

Research

Jump to: Review

22 pages, 3206 KiB

Open AccessArticle

Agomelatine, Ketamine and Vortioxetine Attenuate Energy Cell Metabolism—In Vitro Study

by Matej Ľupták, Zdeněk Fišar and Jana Hroudová

Int. J. Mol. Sci. 2022, 23(22), 13824; https://doi.org/10.3390/ijms232213824 - 10 Nov 2022

Cited by 3 | Viewed by 2888

Abstract

This determination of the mitochondrial effect of pharmacologically different antidepressants (agomelatine, ketamine and vortioxetine) was evaluated and quantified in vitro in pig brain-isolated mitochondria. We measured the activity of mitochondrial complexes, citrate synthase, malate dehydrogenase and monoamine oxidase, and the mitochondrial respiratory rate. Total hydrogen peroxide production and ATP production were assayed. The most potent inhibitor of all mitochondrial complexes and complex I-linked respiration was vortioxetine. Agomelatine and ketamine inhibited only complex IV activity. None of the drugs affected complex II-linked respiration, citrate synthase or malate dehydrogenase activity. Hydrogen peroxide production was mildly increased by agomelatine, which might contribute to increased oxidative damage and adverse effects at high drug concentrations. Vortioxetine significantly reduced hydrogen peroxide concentrations, which might suggest antioxidant mechanism activation. All tested antidepressants were partial MAO-A inhibitors, which might contribute to their antidepressant effect. We observed vortioxetine-induced MAO-B inhibition, which might be linked to decreased hydrogen peroxide formation and contribute to its procognitive and neuroprotective effects. Mitochondrial dysfunction could be linked to the adverse effects of vortioxetine, as vortioxetine is the most potent inhibitor of mitochondrial complexes and complex I-linked respiration. Clarifying the molecular interaction between drugs and mitochondria is important to fully understand their mechanism of action and the connection between their mechanisms and their therapeutic and/or adverse effects. Full article

(This article belongs to the Special Issue Pathogenesis and Treatment Mechanisms of Depression)

► Show Figures

Figure 1

14 pages, 2663 KiB

Open AccessArticle

Association of DNA Methylation of the NLRP3 Gene with Changes in Cortical Thickness in Major Depressive Disorder

by Kyu-Man Han, Kwan Woo Choi, Aram Kim, Wooyoung Kang, Youbin Kang, Woo-Suk Tae, Mi-Ryung Han and Byung-Joo Ham

Int. J. Mol. Sci. 2022, 23(10), 5768; https://doi.org/10.3390/ijms23105768 - 21 May 2022

Cited by 6 | Viewed by 2177

Abstract

The Nod-like receptor pyrin containing 3 (NLRP3) inflammasome has been reported to be a convergent point linking the peripheral immune response induced by psychological stress and neuroinflammatory processes in the brain. We aimed to identify differences in the methylation profiles of the NLRP3 gene between major depressive disorder (MDD) patients and healthy controls (HCs). We also investigated the correlation of the methylation score of loci in NLRP3 with cortical thickness in the MDD group using magnetic resonance imaging (MRI) data. A total of 220 patients with MDD and 82 HCs were included in the study, and genome-wide DNA methylation profiling of the NLRP3 gene was performed. Among the total sample, 88 patients with MDD and 74 HCs underwent T1-weighted structural MRI and were included in the neuroimaging–methylation analysis. We identified five significant differentially methylated positions (DMPs) in NLRP3. In the MDD group, the methylation scores of cg18793688 and cg09418290 showed significant positive or negative correlations with cortical thickness in the occipital, parietal, temporal, and frontal regions, which showed significant differences in cortical thickness between the MDD and HC groups. Our findings suggest that NLRP3 DNA methylation may predispose to depression-related brain structural changes by increasing NLRP3 inflammasome-related neuroinflammatory processes in MDD. Full article

(This article belongs to the Special Issue Pathogenesis and Treatment Mechanisms of Depression)

► Show Figures

Figure 1

Review

Jump to: Research

25 pages, 1030 KiB

Open AccessReview

Selected Biomarkers of Depression: What Are the Effects of Cytokines and Inflammation?

by Stefan Harsanyi, Ida Kupcova, Lubos Danisovic and Martin Klein

Int. J. Mol. Sci. 2023, 24(1), 578; https://doi.org/10.3390/ijms24010578 - 29 Dec 2022

Cited by 41 | Viewed by 6478

Abstract

Depression is one of the leading mental illnesses worldwide and lowers the quality of life of many. According to WHO, about 5% of the worldwide population suffers from depression. Newer studies report a staggering global prevalence of 27.6%, and it is rising. Professionally, depression belonging to affective disorders is a psychiatric illness, and the category of major depressive disorder (MDD) comprises various diagnoses related to persistent and disruptive mood disorders. Due to this fact, it is imperative to find a way to assess depression quantitatively using a specific biomarker or a panel of biomarkers that would be able to reflect the patients’ state and the effects of therapy. Cytokines, hormones, oxidative stress markers, and neuropeptides are studied in association with depression. The latest research into inflammatory cytokines shows that their relationship with the etiology of depression is causative. There are stronger cytokine reactions to pathogens and stressors in depression. If combined with other predisposing factors, responses lead to prolonged inflammatory processes, prolonged dysregulation of various axes, stress, pain, mood changes, anxiety, and depression. This review focuses on the most recent data on cytokines as markers of depression concerning their roles in its pathogenesis, their possible use in diagnosis and management, their different levels in bodily fluids, and their similarities in animal studies. However, cytokines are not isolated from the pathophysiologic mechanisms of depression or other psychiatric disorders. Their effects are only a part of the whole pathway. Full article

(This article belongs to the Special Issue Pathogenesis and Treatment Mechanisms of Depression)

► Show Figures

Figure 1

16 pages, 1638 KiB

Open AccessReview

SUMOylation and Major Depressive Disorder

by Seok-Won Jeoung, Hyun-Sun Park, Zae Young Ryoo, Dong-Hyung Cho, Hyun-Shik Lee and Hong-Yeoul Ryu

Int. J. Mol. Sci. 2022, 23(14), 8023; https://doi.org/10.3390/ijms23148023 - 21 Jul 2022

Cited by 3 | Viewed by 2599

Abstract

Since the discovery of the small ubiquitin-like modifier (SUMO) protein in 1995, SUMOylation has been considered a crucial post-translational modification in diverse cellular functions. In neurons, SUMOylation has various roles ranging from managing synaptic transmitter release to maintaining mitochondrial integrity and determining neuronal health. It has been discovered that neuronal dysfunction is a key factor in the development of major depressive disorder (MDD). PubMed and Google Scholar databases were searched with keywords such as ‘SUMO’, ‘neuronal plasticity’, and ‘depression’ to obtain relevant scientific literature. Here, we provide an overview of recent studies demonstrating the role of SUMOylation in maintaining neuronal function in participants suffering from MDD. Full article

(This article belongs to the Special Issue Pathogenesis and Treatment Mechanisms of Depression)

► Show Figures

Figure 1

39 pages, 827 KiB

Open AccessReview

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

by Laura Orsolini, Simone Pompili, Silvia Tempia Valenta, Virginio Salvi and Umberto Volpe

Int. J. Mol. Sci. 2022, 23(3), 1616; https://doi.org/10.3390/ijms23031616 - 30 Jan 2022

Cited by 39 | Viewed by 4879

Abstract

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. Full article

(This article belongs to the Special Issue Pathogenesis and Treatment Mechanisms of Depression)

► Show Figures