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Pathophysiology and Pharmacology in Psychiatry
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Pathophysiology and Pharmacology in Psychiatry

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: 20 October 2025 | Viewed by 3495

Special Issue Editor

Prof. Dr. Galila Agam

E-Mail Website
Guest Editor
Department of Clinical Biochemistry and Pharmacology and Psychiatry Research Unit, Ben-Gurion University of the Negev and Mental Health Center, Beer-Sheva, Israel
Interests: etiology of bipolar disorder; mechanism of mood stabilization; lithium; mitochondrial function; autophagy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

For this Special Issue, we invite authors to delve into the intricate pathophysiological underpinnings and pharmacological mechanisms underlying the attenuation of psychiatric disorders. We wish that this comprehensive collection will highlight the latest advances in understanding how physiological abnormalities contribute to improper frequent (depression, anxiety, schizophrenia and bipolar disorder) and rare (Khyâl Cap, Kufungisisa, clinical Lycanthropy, etc.) mental health conditions. We call upon papers emphasizing a multidisciplinary approach, such as combining molecular biology, genetics, neuroimaging and neurochemistry, which intersect to reveal novel insights into psychiatric pathology.

In parallel, hope for this Special Issue to include papers emphasizing the importance of pharmacological studies dealing with developing effective treatments, namely cutting-edge studies on new pharmacological agents, their mechanisms of action and their therapeutic potential. Research on psychopharmacology, including the efficacy and side effects of existing medications such as GRAS drugs as novel therapeutic strategies is also welcomed.

Bringing together pioneering research from various scientific domains, we expect that this Special Issue will foster a deeper understanding of the complex interplay between physiological processes and psychiatric disorders. It will, thus, serve as a central resource for translational science investigators, clinicians and healthcare professionals dedicated to advancing the field of psychiatry to improve patient outcomes through innovative physiological and pharmacological interventions.

This Special Issue is supervised by Prof. Dr. Galila Agam, who is assisted by our Topical Advisory Panel Member: Dr. Odeya Damri.

Prof. Dr. Galila Agam
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

  • psychiatric disorders
  • mental health
  • pathophysiology
  • neuropsychopharmacology
  • brain

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Published Papers (2 papers)

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21 pages, 6640 KiB  
Article
Combining Network Pharmacology and Transcriptomic Strategies to Explore the Pharmacological Mechanism of Total Ginsenoside Ginseng Root and Its Impact on Antidepressant Effects
by Weijia Chen, Pengli Guo, Lili Su, Xiangjuan Guo, Meiling Shi, Jianan Geng, Ying Zong, Yan Zhao, Rui Du and Zhongmei He
Int. J. Mol. Sci. 2024, 25(23), 12606; https://doi.org/10.3390/ijms252312606 - 24 Nov 2024
Viewed by 1260
Abstract
Depression is one of the most common neurological diseases, which imposes a substantial social and economic burden on modern society. The purpose of this study was to explore the mechanism of total ginsenoside ginseng root (TGGR) in the treatment of depression through a [...] Read more.
Depression is one of the most common neurological diseases, which imposes a substantial social and economic burden on modern society. The purpose of this study was to explore the mechanism of total ginsenoside ginseng root (TGGR) in the treatment of depression through a comprehensive strategy combining network pharmacology, transcriptomics, and in vivo experimental validation. The Traditional Chinese Medicine Systematic Pharmacology (TCMSP) database and literature were used to collect the main components and targets of TGGR. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were applied to explore the underlying mechanisms. In addition, the chronic unpredictable mild stress (CUMS)-induced C57BL/6 mouse model was used to evaluate the antidepressant activity of TGGR. The results showed that TGGR improved depression-like behavior in mice and increased the decrease in serum 5-hydroxytryptamine (5-HT) and brain-derived neurotrophic factor (BDNF) levels caused by CUMS. Combined network pharmacology and transcriptomic analysis showed that the AMP-activated kinase (AMPK) signaling pathway mainly enriched the core target. Immunohistochemistry, Western blotting, and reverse transcription quantitative polymerase chain reaction (RT-qPCR) were used to confirm whether TGGR exerts antidepressant effects by regulating this pathway. The results showed that TGGR has a regulatory impact on related proteins in the AMPK pathway, and the regulatory effect of TGGR on proteins was inhibited after the administration of related pathway inhibitors. In summary, total ginsenosides may regulate the AMPK signaling pathway and activate the sirtuin 1 (SIRT1) peroxisome proliferator-activated receptor-gamma coactivator 1-alpha (PGC-1α) pathway to have therapeutic effects on depression. Full article
(This article belongs to the Special Issue Pathophysiology and Pharmacology in Psychiatry)
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10 pages, 739 KiB  
Review
Lithium, Inflammation and Neuroinflammation with Emphasis on Bipolar Disorder—A Narrative Review
by Odeya Damri and Galila Agam
Int. J. Mol. Sci. 2024, 25(24), 13277; https://doi.org/10.3390/ijms252413277 - 11 Dec 2024
Cited by 2 | Viewed by 1802
Abstract
This narrative review examines lithium’s effects on immune function, inflammation and cell survival, particularly in bipolar disorder (BD) in in vitro studies, animal models and clinical studies. In vitro studies show that high lithium concentrations (5 mM, beyond the therapeutic window) reduce interleukin [...] Read more.
This narrative review examines lithium’s effects on immune function, inflammation and cell survival, particularly in bipolar disorder (BD) in in vitro studies, animal models and clinical studies. In vitro studies show that high lithium concentrations (5 mM, beyond the therapeutic window) reduce interleukin (IL)-1β production in monocytes and enhance T-lymphocyte resistance, suggesting a protective role against cell death. Lithium modulates oxidative stress in lipopolysaccharide (LPS)-activated macrophages by inhibiting nuclear factor (NF)-ƙB activity and reducing nitric oxide production. At therapeutically relevant levels, lithium increased both pro-inflammatory [interferon (INF)-γ, IL-8 and tumor necrosis factor (TNF)-α)] and anti-inflammatory (IL-10) cytokines on whole blood supernatant culture in healthy volunteers, influencing the balance of pro- and anti-inflammatory responses. Animal models reveal lithium’s potential to alleviate inflammatory diseases by reducing pro-inflammatory cytokines and enhancing anti-inflammatory responses. It also induces selective macrophage death in atherosclerotic plaques without harming other cells. In primary rat cerebellum cultures (ex vivo), lithium prevents neuronal loss and inhibits astroglial growth, impacting astrocytes and microglia. Clinical studies show that lithium alters cytokine profiles and reduces neuroinflammatory markers in BD patients. Chronic treatment decreases IL-2, IL-6, IL-10 and IFN-γ secretion from peripheral blood leukocytes. Lithium response correlates with TNF-α levels, with poor responders showing higher TNF-α. Overall, these findings elucidate lithium’s diverse mechanisms in modulating immune responses, reducing inflammation and promoting cell survival, with significant implications for managing BD and other inflammation-related conditions. Yet, to better understand the drug’s impact in BD and other inflammatory/neuroinflammatory conditions, further research is warranted to appreciate lithium’s therapeutic potential and its role in immune regulation. Full article
(This article belongs to the Special Issue Pathophysiology and Pharmacology in Psychiatry)
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