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Molecular Mechanisms of Drug Discovery, Treatment, and Repurposing in Neuropsychiatric...
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Molecular Mechanisms of Drug Discovery, Treatment, and Repurposing in Neuropsychiatric Disorders

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 April 2025 | Viewed by 1701

Special Issue Editors

Dr. Maria Bogdan

E-Mail Website
Guest Editor
Department of Pharmacology, University of Medicine and Pharmacy Craiova, 200349 Craiova, Romania
Interests: inflammation; anti-inflammatory drugs; depression; antidepressant drugs; biomarkers; drug delivery systems; in vivo animal models
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Liliana Mititelu-Tartau

E-Mail Website
Guest Editor
Department of Pharmacology, Faculty of Medicine, “Grigore T. Popa” University of Medicine and Pharmacy, 700115 Iasi, Romania
Interests: chitosan; biocompatible polymers; biomaterials; biomedical applications; tissue engineering; drug delivery systems; regenerative medicine; wound healing; antimicrobial properties; cancer therapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue is supervised by Prof. Dr. Liliana Mititelu-Tartau and Dr. Maria Bogdan, assisted by our Topical Advisory Panel Member, Dr. Tosin Olasehinde (School of Life Sciences, University of KwaZulu-Natal, Durban, South Africa).

We are delighted to announce a Special Issue which aims to spotlight the promising approach of utilizing existing medications to address various neuropsychiatric conditions, thereby fostering innovative therapeutic strategies and advancements in patient care.

In recent years, drug repurposing has emerged as a compelling strategy in neuropsychiatric research, offering the potential to expedite the development of new treatments by leveraging established pharmacological agents with well-known safety profiles. This approach not only provides opportunities for cost-effective drug development but also holds the promise of addressing unmet medical needs and enhancing patient outcomes.

We cordially invite researchers, and experts in the field to contribute original research articles, reviews, case studies, and perspectives that delve into the multifaceted aspects of drug repurposing in neuropsychiatric disorders. Since IJMS is a journal of molecular science, purely clinical studies will not be suitable. However, clinical or pure model submissions with biomolecular experiments are welcomed.

We eagerly anticipate your valuable contributions to this Special Issue.

Dr. Maria Bogdan
Prof. Dr. Liliana Mititelu-Tartau
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

  • animal models
  • neurodegeneration
  • neuropsychiatric disorders
  • neuroprotection
  • nanoparticles

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Published Papers (2 papers)

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12 pages, 2776 KiB  
Article
Prenatal Constant Light Exposure Induces Behavioral Deficits in Male and Female Rat Offspring: Effects of Prenatal Melatonin Treatment
by Tsveta Stoyanova, Hristina Nocheva, Zlatina Nenchovska, Desislava Krushovlieva, Petya Ivanova and Jana Tchekalarova
Int. J. Mol. Sci. 2025, 26(3), 1036; https://doi.org/10.3390/ijms26031036 - 25 Jan 2025
Viewed by 389
Abstract
Prenatal constant light exposure (CLE) impaired the anxiety response and circadian rhythms of testicular enzymes in adult male rat offspring, while melatonin corrected these deficiencies. However, the mechanism by which CLE induces these long-term behavioral consequences and the impact of melatonin system have [...] Read more.
Prenatal constant light exposure (CLE) impaired the anxiety response and circadian rhythms of testicular enzymes in adult male rat offspring, while melatonin corrected these deficiencies. However, the mechanism by which CLE induces these long-term behavioral consequences and the impact of melatonin system have not been examined. The aim of the present study was to investigate the effects of prenatal CLE and melatonin treatment on anxiety- and depression-like behaviors, and the melatonin system in male and female adult rat offspring. Six groups of male and female rat offspring (P60) exposed to either light/dark (LD) or CL regimes, and treated with vehicle or melatonin (10 mg/kg, s.c.) were evaluated for anxiety by open field (OF), elevated plus maze (EPM), and light/dark (LD) tests, and depressive-like response by splash test and sucrose preference test. Plasma adrenocorticotropic hormone (ACTH), corticosterone (CORT) and melatonin expression, and hippocampal MT1A and MT1b receptor expression were assessed by ELISA. Prenatal CLE induced behavioral deficits and elevated plasma CORT levels, while melatonin levels, their circadian rhythmicity, and hippocampal MT receptor expression were not altered in male and female offspring in the CLE regime. However, prenatal melatonin treatment corrected behavioral deficits in a sex-specific manner by up-regulating hippocampal MT receptors, even without altering systemic melatonin levels or normalizing CORT in either sex. The results of this study suggest critical insights into how prenatal environmental factors and therapeutic interventions shape physiological and behavioral outcomes. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Drug Discovery, Treatment, and Repurposing in Neuropsychiatric Disorders)
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18 pages, 20350 KiB  
Article
Paeoniflorin Inhibits the Activation of Microglia and Alleviates Depressive Behavior by Regulating SIRT1-NF-kB-NLRP3/Pyroptosis Pathway
by Xue Wang, Lili Su, Silu Liu, Zhongmei He, Jianming Li, Ying Zong, Weijia Chen and Rui Du
Int. J. Mol. Sci. 2024, 25(23), 12543; https://doi.org/10.3390/ijms252312543 - 22 Nov 2024
Viewed by 755
Abstract
Inflammation assumes a vital role in the pathogenesis of depression and in antidepressant treatment. Paeoniflorin (PF), a monoterpene glycoside analog possessing anti-inflammatory attributes, exhibits therapeutic efficacy on depression-like behavior in mice. The objective of this study was to evaluate the antidepressant effects of [...] Read more.
Inflammation assumes a vital role in the pathogenesis of depression and in antidepressant treatment. Paeoniflorin (PF), a monoterpene glycoside analog possessing anti-inflammatory attributes, exhibits therapeutic efficacy on depression-like behavior in mice. The objective of this study was to evaluate the antidepressant effects of PF on depression elicited by the chronic unpredictable mild stress (CUMS) model and the precise neural sequence associated with the inflammatory process. In this study, we established an in vivo mouse model induced by CUMS and an in vitro BV2 cell model induced by LPS+ATP. The mechanism of PF for depression was assessed by the SIRT1 selective inhibitor EX-527. The findings demonstrated that PF significantly alleviated the damage of BV2 cells treated with LPS and ATP, inhibited the generation of ROS, up-regulated the expression of SIRT1 mRNA, and down-regulated the expression of nuclear NF-κB, p65, NLRP3, Caspase-1 and GSDMD-N in vitro. In vivo, PF mitigated the depressive-like behavior induced by CUMS, reduced the number of neurons, and decreased the secretion of pro-inflammatory factors IL-1β, IL-6, and TNF-α in the hippocampus. Immunohistochemical results indicated that PF attenuated CUMS-induced hyperactivation of microglia. Moreover, the expression level of SIRT1 in the hippocampus was augmented, while the protein levels of NF-κB, p65, NLRP3, Caspase-1, IL-1β and GSDMD-N were diminished after PF treatment. Additionally, the selective inhibition of SIRT1 attenuated the therapeutic effect of PF on depression. These results imply that PF possesses antidepressant properties that rely on SIRT1 signaling to regulate NLRP3 inflammasome inactivation. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Drug Discovery, Treatment, and Repurposing in Neuropsychiatric Disorders)
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