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Molecular Neuropsychiatry: Target Discovery for Mental Disorders
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Molecular Neuropsychiatry: Target Discovery for Mental Disorders

A Special Issue of Current Issues in Molecular Biology (ISSN 1467-3045) belonging to the section "Molecular Medicine".

Deadline for manuscript submissions: 31 December 2026 | Viewed by 4634

Editors

Dr. Fenfen Ge

E-Mail Website
Guest Editor
1. Department of Medicine and Health Technology Faculty of Health Sciences, Aalborg University, DK-9260 Gistrup, Denmark
2. National Centre for Register-based Research, Department of Public Health, Aarhus University, DK-8000 Aarhus C, Denmark
Interests: artificial intelligence; epidemiology; genetics; statistics
Dr. Yue Wang

E-Mail Website
Guest Editor Assistant
Department of Clinical Medicine, Aarhus University, DK-8000 Aarhus C, Denmark
Interests: genetic predisposition; environmental exposure; neuropsychiatric disorders

Special Issue Information

Dear Colleagues,

We are excited to announce a call for submissions for a Special Issue titled “Molecular Neuropsychiatry: Target Discovery for Mental Disorders.” Neuropsychiatric disorders—including major psychiatric illnesses, neurodevelopmental conditions, and neurodegenerative diseases—represent a substantial and growing global health burden. Elucidating the molecular and cellular mechanisms underlying these complex disorders is essential for the development of innovative diagnostic approaches and effective, targeted therapeutic strategies.

Recent advances have highlighted the critical roles of brain–immune interactions, intricate molecular and signaling networks, synaptic plasticity, and large-scale transcriptomic studies that have identified dysregulated genes and pathways associated with neuropsychiatric conditions. Despite this progress, significant challenges remain in translating molecular discoveries into clinically actionable targets and precision treatments. This Special Issue aims to provide a comprehensive platform for cutting-edge research and critical reviews that advance our understanding of molecular mechanisms in neuropsychiatric disorders.

In this Special Issue, topics of interest include, but are not limited to, the following:

  • Genetic and epigenetic regulation in neuropsychiatric disorders;
  • Non-coding RNAs and their role in brain function and disease progression;
  • Neuroinflammatory and neuroendocrine mechanisms;
  • Synaptic plasticity and dysregulated neural signaling pathways;
  • Biomarker discovery for diagnosis, prognosis, and therapeutic response;
  • Neuroimaging and molecular correlates of psychiatric disorders;
  • Pharmacogenomics and molecular targets for precision therapeutics;
  • Environmental and lifestyle influences on molecular pathways in mental health;
  • Molecular mechanisms underlying comorbidity across neuropsychiatric disorders. 

Dr. Fenfen Ge
Guest Editor

Dr. Yue Wang
 Guest Editor Assistant

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-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Current Issues in Molecular Biology is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2400 CHF (Swiss Francs). 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 targets
  • neuropsychiatric disorders
  • genetic and epigenetic regulation
  • transcriptomics
  • pharmacogenomics
  • brain–immune interactions
  • neural circuits and synaptic plasticity
  • biomarker discovery
  • omics approaches
  • precision psychiatry

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (4 papers)

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Research

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19 pages, 2938 KB  
Article
Plasma-Derived miRNAs as Fluid Biomarkers to Differentiate Alzheimer’s and Frontotemporal Dementia
by Rosalinda Di Gerlando, Francesca Dragoni, Evelyne Minucchi, Maria Garofalo, Giulia Perini, Alfredo Costa, Antonio Pisani, Carlo Morasso, Matteo Cotta Ramusino and Stella Gagliardi
Curr. Issues Mol. Biol. 2026, 48(6), 633; https://doi.org/10.3390/cimb48060633 - 17 Jun 2026
Cited by 1 | Viewed by 639
Abstract
Alzheimer’s disease (AD) and Frontotemporal Dementia (FTD) are complex neurodegenerative disorders, often sharing overlapping symptoms. Non-coding RNAs may be involved in pathological processes in these conditions, hence the study of miRNAs isolated from plasma-derived extracellular vesicles (EVs) could provide exploratory insights into the [...] Read more.
Alzheimer’s disease (AD) and Frontotemporal Dementia (FTD) are complex neurodegenerative disorders, often sharing overlapping symptoms. Non-coding RNAs may be involved in pathological processes in these conditions, hence the study of miRNAs isolated from plasma-derived extracellular vesicles (EVs) could provide exploratory insights into the molecular background. The main aim of this work was to identify shared deregulated miRNAs presenting different expression patterns in the two pathologies. A selection of the identified deregulated miRNAs was further studied with the purpose of identifying their mRNA targets and generating hypotheses on their potential pathological involvement. A total of 340 and 291 differentially expressed miRNAs were found in FTD and AD, respectively. Among the commonly deregulated miRNAs with opposite expression patterns between the two conditions, miR-638 emerged as a candidate of interest, showing consistent patterns across our experimental analyses. Nevertheless, these findings are preliminary and intended to be interpreted cautiously, requiring validation in larger cohorts. In addition, the expression of two of its predicted targets in peripheral blood mononuclear cells (PBMCs) appeared to align with miR-638 expression in the same cell type and may reflect potential differences in underlying brain pathological states. Full article
(This article belongs to the Special Issue Molecular Neuropsychiatry: Target Discovery for Mental Disorders)
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21 pages, 5748 KB  
Article
Estrogen Replacement Therapy in Ovariectomized Rats: Complementary Roles of ER and GPR30 in Alleviating Depressive-like Behavior
by Siyi He, Zhongyu Ren, Lan Wu, Yinping Xie, Limin Sun, Ling Xiao and Gaohua Wang
Curr. Issues Mol. Biol. 2026, 48(5), 519; https://doi.org/10.3390/cimb48050519 - 16 May 2026
Viewed by 588
Abstract
Women are twice as likely to suffer from major depressive disorder (MDD). The underlying mechanism between estrogen and depression is still unknown. We used ovariectomized rats to simulate menopausal status and established a depression model of chronic and acute stress. The therapeutic effects [...] Read more.
Women are twice as likely to suffer from major depressive disorder (MDD). The underlying mechanism between estrogen and depression is still unknown. We used ovariectomized rats to simulate menopausal status and established a depression model of chronic and acute stress. The therapeutic effects of estrogen were systematically studied through behavioral testing, Western blotting, ELISA, LC-MS, and cell experiments. In chronic stress, OVX rats showed depressive-like behaviors, and elevated hippocampal ER, BDNF, IL-1β/IL-18, and body weight. ERT reduced depression-like behavior by 64% to 76% in the behavioral test. ERT also reversed the molecules without affecting GPR30. In acute stress, ERT reduced depression-like behavior by 20% to 58% in the behavioral test. OVX decreased ER, BDNF, P2X7, IL-1β/IL-18, spine density, and microglia and increased the expression of GPR30. ERT reversed all the above. ERT normalized metabolic abnormalities caused by CUMS. Our study demonstrates that estrogen deficiency contributes to the onset and progression of depression in a rat model of menopause-like estrogen deficiency. Estrogen replacement therapy appears to alleviate depressive-like behaviors by reducing brain inflammation and supporting the brain’s adaptive capacities through ER. Furthermore, the dual function positions GPR30 as a promising potential target for future treatments of menopausal depression, and GPR30 regulates neuroinflammation and neuroplasticity through the NLRP3/P2X7/IL-1β pathway. Full article
(This article belongs to the Special Issue Molecular Neuropsychiatry: Target Discovery for Mental Disorders)
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Review

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24 pages, 1500 KB  
Review
Epigenetic and Transcriptomic Pathways Underlying Animal Models of Cognitive and Psychiatric Disorders: A Scoping Review
by Jaishriram Rathored, Ajay Pal and Deepika Sai Painkra
Curr. Issues Mol. Biol. 2026, 48(4), 425; https://doi.org/10.3390/cimb48040425 - 21 Apr 2026
Cited by 1 | Viewed by 1972
Abstract
Background: Cognitive and psychiatric disorders are caused by a complex interplay between genetic predisposition, environmental exposures, and dynamic molecular regulation in the brain. Animal models provide a controlled environment for examining these mechanisms, and advances in transcriptome and epigenomic technologies have greatly expanded [...] Read more.
Background: Cognitive and psychiatric disorders are caused by a complex interplay between genetic predisposition, environmental exposures, and dynamic molecular regulation in the brain. Animal models provide a controlled environment for examining these mechanisms, and advances in transcriptome and epigenomic technologies have greatly expanded our knowledge of disease-relevant pathways. Objective: This scoping review systematically maps and synthesizes the epigenetic and transcriptomic findings from the established animal models of four neuropsychiatric conditions—autism spectrum disorder (ASD), schizophrenia, depression, and Rett syndrome—drawing on a PRISMA-ScR-guided literature search. The review characterizes the breadth of evidence, identifies convergent and divergent molecular pathways, and highlights the translational gaps and therapeutic implications. Methods: Research employing chromatin accessibility testing, genome-wide DNA methylation mapping, single-cell and bulk RNA sequencing, histone modification profiling, and multi-omics integration in mouse and other validated animal models was thoroughly reviewed. A quality appraisal of the primary experimental studies (n = 63) was performed using a modified CAMARADES checklist. Results: Beyond generalized cellular stress responses, multi-omics analysis emphasizes the cell-type- and context-dependent nature of epigenetic changes in animal models, including isoform-specific histone modifications and model-dependent binding of HDAC/MeCP2 complexes to genes involved in synaptic plasticity. Single-cell RNA sequencing analyses have uniformly shown transcriptional changes in parvalbumin-positive (PV+) interneurons. Conclusions: The specific convergence of epigenetic disruptions in neural circuits involved in synaptic structure and inhibitory function could play a role in the generation of neuropsychiatric phenotypes in animal models, highlighting the importance of circuit- and cell-type-specific epigenetics while pointing to potential therapeutic avenues. Full article
(This article belongs to the Special Issue Molecular Neuropsychiatry: Target Discovery for Mental Disorders)
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Other

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12 pages, 1136 KB  
Case Report
WWOX-Related Epileptic Encephalopathy (WOREE Syndrome): Clinical Case Study and Literature Review
by Annamaria Sapuppo, Roberta Rizzo, Gaia Fusto, Roberta Rocca, Vincenzo Sortino, Xena Giada Pappalardo, Martino Ruggieri and Raffaele Falsaperla
Curr. Issues Mol. Biol. 2026, 48(5), 449; https://doi.org/10.3390/cimb48050449 - 25 Apr 2026
Cited by 1 | Viewed by 940
Abstract
The WW domain-containing oxidoreductase (WWOX) gene, well-known as a tumor suppressor, also has a crucial role as a transcription factor in the developing brain. The bi-allelic loss of the WWOX gene causes a condition characterized by drug-resistant epilepsy, developmental delay, and [...] Read more.
The WW domain-containing oxidoreductase (WWOX) gene, well-known as a tumor suppressor, also has a crucial role as a transcription factor in the developing brain. The bi-allelic loss of the WWOX gene causes a condition characterized by drug-resistant epilepsy, developmental delay, and neurological impairments, often resulting in mortality within the first year of life, known as WWOX-related epileptic encephalopathy (WOREE) syndrome (MIM: 616211). Whole Exome Sequencing (WES) analysis was performed on a female patient who died within three months of birth and was diagnosed with microcephaly, severe early-onset refractory seizures, and drug-resistant epileptic encephalopathy. WES revealed a 38 kb CNV deletion spanning WWOX exons 6–7, and a known frameshift variant in exon 8, impairing a highly clinically significant region of the encoded protein. Clinical and genetic features of reported WOREE patients with WWOX gene deletions similar to our patient were analyzed. Our case highlights the clinical heterogeneity of WWOX variants in WOREE syndrome and expands the spectrum of reported compound heterozygous deletions. Further research needs to elucidate WWOX pathophysiology and improve diagnostic and therapeutic strategies. Full article
(This article belongs to the Special Issue Molecular Neuropsychiatry: Target Discovery for Mental Disorders)
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