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Pathophysiology of Neuropsychiatric Disease
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Pathophysiology of Neuropsychiatric Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 July 2020) | Viewed by 13323

Special Issue Editors

Dr. Won-Myong Bahk

E-Mail Website
Guest Editor
Department of Psychiatry, Yeouido ST. Mary’s Hospital, The Catholic University of Korea, Seoul, Korea
Interests: mood disorder; bipolar disorder; depression; psychopharmacology; clinical trial
Prof. Dr. Young Sup Woo

E-Mail Website
Co-Guest Editor
Department of Psychiatry, Yeouido ST. Mary’s Hospital, The Catholic University of Korea, Seoul, Korea

Special Issue Information

Dear Colleagues,

Neuropsychiatric disorders comprise a wide range of disorders. None of them are single homogenous disorders, but rather are complex, heterogeneous disorders resulting from the interaction of various factors, including genetic, neurological, physical, and environmental. As a result, past research inevitably focused on investigating their pathophysiology by understanding symptomatic presentations such as clinical signs and symptoms of different disorders. However, with the rise of predictive, preventive, and personalized medicine, increasing studies emphasize the importance of biomarkers in the diagnosis and treatment of neuropsychiatric disorders. Recent advancements in molecular, biological, genetic, and neuroimaging techniques and analyses have also led to a much better understanding of their pathophysiology.

In accordance with these innovative translational researches and technologies, the brain–gut–microbiome theory is receiving increasing attention regarding important causative factors of various neuropsychiatric disorders. Correlation among depression, physical weakness evidenced by lowered muscle mass, and cognitive change highlight the importance of correlation among emotion, brain, and body. The medications for diabetes are now being tested for depression, so we must understand the role of insulin in mood disorders. The impact of neuro-inflammation and glucocorticoid receptors, which has been the important focus for decades, have recently been investigated using novel approaches such as epigenetics and mass data from nation-wide cohort studies. The classical interests including serotonin dysfunction correlated with evoked potential, circadian rhythm associated with mood disorder, and the neurophysiology of suicide have also been updated, needing comprehensive discussion.

In this Special Issue of IJMS, the focus will be on the pathophysiology of neuropsychiatric disease by considering the novel biomarkers of mood and geriatric disorders.

Dr. Won-Myong Bahk
Prof. Dr. Young Sup Woo
Guest Editors

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

  • mood disorders
  • neurophysiology
  • cognition
  • brain reserve
  • circadian rhythm
  • inflammation

Published Papers (3 papers)

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Research

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12 pages, 2210 KiB  
Article
Effects of Early Life Stress on Epigenetic Changes of the Glucocorticoid Receptor 17 Promoter during Adulthood
by Mi Kyoung Seo, Seon-gu Kim, Dae-Hyun Seog, Won-Myong Bahk, Seong-Ho Kim, Sung Woo Park and Jung Goo Lee
Int. J. Mol. Sci. 2020, 21(17), 6331; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21176331 - 31 Aug 2020
Cited by 15 | Viewed by 2944
Abstract
Growing evidence suggests that early life stress (ELS) has long-lasting effects on glucocorticoid receptor (GR) expression and behavior via epigenetic changes of the GR exon 17 promoter. However, it remains unclear whether ELS regulates histone modifications of the GR exon 17 [...] Read more.
Growing evidence suggests that early life stress (ELS) has long-lasting effects on glucocorticoid receptor (GR) expression and behavior via epigenetic changes of the GR exon 17 promoter. However, it remains unclear whether ELS regulates histone modifications of the GR exon 17 promoter across the life span. We investigated the effects of maternal separation (MS) on histone acetylation and methylation of GR exon 17 promoter in the hippocampus, according to the age of adults. Depression-like behavior and epigenetic regulation of GR expression were examined at young and middle adulthood in mice subjected to MS from postnatal day 1 to 21. In the forced swimming test, young adult MS mice showed no effect on immobility time, but middle-aged MS mice significantly increased immobility time. Young adult and middle-aged MS mice showed decreased GR expression. Their two ages showed decreased histone acetylation with increased histone deacetylases (HDAC5) levels, decreased permissive methylation, and increased repressive methylation at the GR exon 17 promoter. The extent of changes in gene expression and histone modification in middle adulthood was greater than in young adulthood. These results indicate that MS in early life causes long-term negative effects on behavior via histone modification of the GR gene across the life span. Full article
(This article belongs to the Special Issue Pathophysiology of Neuropsychiatric Disease)
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Review

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17 pages, 269 KiB  
Review
The Brain–Gut–Microbiome Axis in Psychiatry
by Seung-Ho Jang, Young Sup Woo, Sang-Yeol Lee and Won-Myong Bahk
Int. J. Mol. Sci. 2020, 21(19), 7122; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21197122 - 27 Sep 2020
Cited by 25 | Viewed by 5373
Abstract
Beginning with the concept of the brain–gut axis, the importance of the interaction between the brain and the gastrointestinal tract has been extended to the microbiome with increasing clinical applications. With the recent development of various techniques for microbiome analysis, the number of [...] Read more.
Beginning with the concept of the brain–gut axis, the importance of the interaction between the brain and the gastrointestinal tract has been extended to the microbiome with increasing clinical applications. With the recent development of various techniques for microbiome analysis, the number of relevant preclinical and clinical studies on animals and human subjects has rapidly increased. Various psychotic symptoms affect the intestinal microbiome through the hypothalamus–pituitary–adrenal gland axis. Conversely, the intestinal microbiome regulates the gastrointestinal tract environment and affects psychological factors by means of the microorganisms or their metabolites, either acting directly on the brain or through the synthesis of various neurotransmitters. This review discusses the clinical applicability of the brain–gut–microbiome axis and directions for improving psychological symptoms based on the studies published to date. Full article
(This article belongs to the Special Issue Pathophysiology of Neuropsychiatric Disease)
32 pages, 487 KiB  
Review
Clinical Evidence of Antidepressant Effects of Insulin and Anti-Hyperglycemic Agents and Implications for the Pathophysiology of Depression—A Literature Review
by Young Sup Woo, Hyun Kook Lim, Sheng-Min Wang and Won-Myong Bahk
Int. J. Mol. Sci. 2020, 21(18), 6969; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21186969 - 22 Sep 2020
Cited by 17 | Viewed by 4556
Abstract
Close connections between depression and type 2 diabetes (T2DM) have been suggested by many epidemiological and experimental studies. Disturbances in insulin sensitivity due to the disruption of various molecular pathways cause insulin resistance, which underpins many metabolic disorders, including diabetes, as well as [...] Read more.
Close connections between depression and type 2 diabetes (T2DM) have been suggested by many epidemiological and experimental studies. Disturbances in insulin sensitivity due to the disruption of various molecular pathways cause insulin resistance, which underpins many metabolic disorders, including diabetes, as well as depression. Several anti-hyperglycemic agents have demonstrated antidepressant properties in clinical trials, probably due to their action on brain targets based on the shared pathophysiology of depression and T2DM. In this article, we review reports of clinical trials examining the antidepressant effect of these medications, including insulin, metformin, glucagon like peptide-1 receptor agonists (GLP-1RA), and peroxisome proliferator-activated receptor (PPAR)-γ agonists, and briefly consider possible molecular mechanisms underlying the associations between amelioration of insulin resistance and improvement of depressive symptoms. In doing so, we intend to suggest an integrative perspective for understanding the pathophysiology of depression. Full article
(This article belongs to the Special Issue Pathophysiology of Neuropsychiatric Disease)
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