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Molecular Research on Potential New Antidepressant Drugs
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Molecular Research on Potential New Antidepressant Drugs

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

Deadline for manuscript submissions: 20 May 2026 | Viewed by 5100

Special Issue Editors

Dr. Marta Jóźwiak-Bębenista

E-Mail Website
Guest Editor
Department of Pharmacology and Toxicology, Medical University of Lodz, Zeligowskiego 7/9, 90-752 Lodz, Poland
Interests: antidepressant drug discovery; treatment-resistant depression; neuroinflammation; neuroplasticity; hallucinogens and psychedelics; CNS drug development; molecular targets for depression; neurotransmitter systems; preclinical research; psychiatric disorders
Dr. Anna Stasiak

E-Mail Website
Guest Editor
Department of Hormone Biochemistry, Faculty of Medicine, Medical University of Lodz, Żeligowskiego 7/9 Str., 90-752 Lodz, Poland
Interests: neurodegeneration; CNS diseases; Alzheimer's disease; Parkinson's disease; novel treatments for CNS diseases; neuroprotective agents; dual targeting drugs; multi-targeting drugs; histamine; histamine receptors; biogenic amines
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Despite advances in neuroscience, effective treatment options for depression, particularly treatment-resistant depression, remain limited. The search for new antidepressant drugs requires deeper exploration of the brain's molecular landscape, especially the intricate network of neurotransmitters and signaling pathways involved in mood regulation.

Serotonin, norepinephrine, and dopamine have long been central to the development of antidepressants, but recent studies highlight the importance of other molecular targets, such as glutamate receptors, neurotrophic factors, and inflammatory markers. The discovery of novel compounds and multitarget drugs that can modulate these systems offers hope for more effective therapies with fewer side effects.

We welcome contributions focusing on the identification of new molecular targets, the synthesis of innovative compounds, and the pharmacological evaluation of potential antidepressants. The submission of preclinical research, including in vitro and in vivo studies on novel mechanisms of action, is particularly encouraged, especially in the context of treatment-resistant depression. This Special Issue will feature original research and review articles focused on the development of novel pharmacological agents, their mechanisms of action, and the molecular pathways involved.

Dr. Marta Jóźwiak-Bębenista
Dr. Anna Stasiak
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 250 words) can be sent to the Editorial Office for assessment.

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

  • antidepressant drug discovery
  • treatment-resistant depression
  • neuroinflammation
  • neuroplasticity
  • hallucinogens and psychedelics
  • CNS drug development
  • molecular targets for depression
  • neurotransmitter systems (serotonin, norepinephrine, dopamine)
  • preclinical research (in vitro, in vivo, in silico)
  • psychiatric disorders

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Published Papers (2 papers)

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Research

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19 pages, 2820 KB  
Article
Differential Gene Expression in Differentiated Human Neuroblastoma SH-SY5Y Cells in Response to a Cocktail of Monoamine Oxidase Inhibitors
by Prakshit Niraula, Rachel A. Page, Barry R. Palmer and Penelope Truman
Int. J. Mol. Sci. 2026, 27(4), 1689; https://doi.org/10.3390/ijms27041689 - 9 Feb 2026
Viewed by 520
Abstract
Differentiated human neuroblastoma (SH-SY5Y) cells were exposed to either 0.2 μM nicotine, a tobacco smoke preparation (TPM) diluted to the same nicotine concentration, or a cocktail of seven tobacco smoke monoamine oxidase inhibitors (MAOIs) at the concentrations measured in the TPM. Treatment occurred [...] Read more.
Differentiated human neuroblastoma (SH-SY5Y) cells were exposed to either 0.2 μM nicotine, a tobacco smoke preparation (TPM) diluted to the same nicotine concentration, or a cocktail of seven tobacco smoke monoamine oxidase inhibitors (MAOIs) at the concentrations measured in the TPM. Treatment occurred for 3 days, such that the cellular monoamine oxidase (MAO) concentration was reduced by approximately 50% in both the TPM and MAOI cocktail exposure groups. Changes in MAO gene expression after exposure to the different treatments were determined using qPCR, and the effect of these exposure treatments on global gene expression was also examined using mRNA sequencing. No change in MAOA and MAOB gene expression levels was observed, after any treatment, either using qPCR or mRNA sequencing. The MAOI versus control treatment comparison revealed that four genes were >2-fold down-regulated (ZNF727, RP11-310E22.4, CRYM, SEMA3F), and 19 genes were up-regulated after 3 days’ exposure to the MAOI cocktail. Many of these differentially expressed genes were linked with disease conditions related to smoking and addiction. Exposure to nicotine and TPM each resulted in up- and down-regulation of different sets of genes. The results indicate that changes in MAO gene expression are unlikely to be responsible for the changes in MAO activity. The association between genes whose expression changes with tobacco MAO treatment and smoking-related diseases and addiction suggests the central role that MAO inhibition may play in mediating the effects of smoking on smokers. Full article
(This article belongs to the Special Issue Molecular Research on Potential New Antidepressant Drugs)
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Review

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39 pages, 1453 KB  
Review
Molecular Mechanisms of Emerging Antidepressant Strategies: From Ketamine to Neuromodulation
by Mateusz Kowalczyk, David Aebisher, Jakub Szpara, Sara Czech, Dorota Bartusik-Aebisher and Gabriela Henrykowska
Int. J. Mol. Sci. 2026, 27(1), 344; https://doi.org/10.3390/ijms27010344 - 28 Dec 2025
Cited by 2 | Viewed by 3781
Abstract
Depression is a common, debilitating, and potentially life-threatening mental disorder affecting individuals across all age groups and populations. It represents one of the major challenges of contemporary medicine. It is estimated that more than 300 million people worldwide are affected, and patients with [...] Read more.
Depression is a common, debilitating, and potentially life-threatening mental disorder affecting individuals across all age groups and populations. It represents one of the major challenges of contemporary medicine. It is estimated that more than 300 million people worldwide are affected, and patients with major depressive disorder (MDD) exhibit a significantly increased risk of suicide, underscoring the urgent need for effective and long-lasting therapeutic strategies. Growing evidence indicates that the pathophysiology of depression involves a complex interplay of genetic vulnerability, chronic stress, dysregulation of the hypothalamic–pituitary–adrenal (HPA) axis, neuroinflammation, oxidative stress, mitochondrial dysfunction, and impaired synaptic plasticity, collectively contributing to symptom heterogeneity and treatment resistance. In this review, we synthesize data derived from PubMed, Google Scholar, and ClinicalTrials.gov databases concerning pharmacological and non-pharmacological treatment strategies, with particular emphasis on their cellular and molecular mechanisms of action. We present currently used classes of antidepressant drugs, including selective serotonin reuptake inhibitors (SSRIs), serotonin–norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants (TCAs), and monoamine oxidase inhibitors (MAOIs), discussing their limitations in the context of contemporary pathophysiological models of depression. We then focus on emerging therapies targeting the glutamatergic, GABAergic, and dopaminergic systems, including ketamine, esketamine, (R)-ketamine, the dextromethorphan–bupropion combination (DMX–BUP), neurosteroids (zuranolone, brexanolone), as well as selective serotonin receptor modulators (gepirone ER) and dopaminergic modulators (cariprazine). The review is complemented by a discussion of non-pharmacological neuromodulatory approaches, such as transcranial magnetic stimulation (TMS), transcranial direct current stimulation (tDCS), and photobiomodulation. Rather than providing another summary of clinical response indicators, this article integrates the molecular underpinnings of novel antidepressant agents and neuromodulation techniques with current concepts of depression pathophysiology, highlighting their relevance for the development of precise, mechanistically targeted, and multimodal treatment strategies. Full article
(This article belongs to the Special Issue Molecular Research on Potential New Antidepressant Drugs)
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