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Molecular Basis of Neuropsychiatric Disorders: Recent and Future Developments
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Molecular Basis of Neuropsychiatric Disorders: Recent and Future Developments

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 June 2025 | Viewed by 2803

Special Issue Editor

Dr. Konstantinos Tsamakis

E-Mail Website
Guest Editor
Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK
Interests: mental health; depression; anxiety; gut microbiome; dementia; psychosis; psychopharmacology; covid-19
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neuropsychiatric disorders, such as schizophrenia, bipolar disorder, and autism, significantly affect the lives of individuals with these conditions as well as their families. The probability of developing these disorders may be influenced by a range of genetic, developmental, and environmental factors. However, despite recent advances in understanding the genetic risk factors and molecular and cellular mechanisms behind neuropsychiatric disorders, their pathogenesis is still not fully understood. In addition, while various psychotropic drugs are available, they primarily target symptom relief and associated comorbidities. Therefore, it is crucial to focus on the biology of these diseases and analyze the specific molecular circuits and pathways involved. Understanding the molecular mechanisms of such diseases will enhance our knowledge of their underlying pathophysiology and enable the design of targeted treatments.

The aim of this research topic is to offer an update on the current understanding of the molecular mechanisms underlying neuropsychiatric disorders and explore the future directions in terms of therapeutic agents and areas of research.

Dr. Konstantinos Tsamakis
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

  • molecular
  • schizophrenia
  • depression
  • genetic
  • autism
  • mechanisms
  • genetic

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Published Papers (3 papers)

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Research

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16 pages, 2760 KiB  
Article
Transcriptional Regulators in the Cerebellum in Chronic Schizophrenia: Novel Possible Targets for Pharmacological Interventions
by América Vera-Montecinos and Belén Ramos
Int. J. Mol. Sci. 2025, 26(8), 3653; https://doi.org/10.3390/ijms26083653 - 12 Apr 2025
Viewed by 230
Abstract
Despite the emerging evidence of the role of transcriptional regulators in schizophrenia as key molecular effectors responsible for the dysregulation of multiple biological processes, limited information is available for brain areas that control higher cognitive functions, such as the cerebellum. To identify transcription [...] Read more.
Despite the emerging evidence of the role of transcriptional regulators in schizophrenia as key molecular effectors responsible for the dysregulation of multiple biological processes, limited information is available for brain areas that control higher cognitive functions, such as the cerebellum. To identify transcription factors that could control a wide panel of altered proteins in the cerebellar cortex in schizophrenia, we analyzed a dataset obtained using one-shot liquid chromatography–tandem mass spectrometry on the postmortem human cerebellar cortex in chronic schizophrenia (PXD024937 identifier in the ProteomeXchange repository). Our analysis revealed a panel of 11 enriched transcription factors (SP1, KLF7, SP4, EGR1, HNF4A, CTCF, GABPA, NRF1, NFYA, YY1, and MEF2A) that could be controlling 250 altered proteins. The top three significantly enriched transcription factors were SP1, YY1, and EGR1, and the transcription factors with the largest number of targets were SP1, KLF7, and SP4 which belong to the Krüppel superfamily. An enrichment in vesicle-mediated transport was found for SP1, KLF7, EGR1, HNF4A, CTCF, and MEF2A targets, while pathways related to signaling, inflammation/immune responses, apoptosis, and energy were found for SP1 and KLF7 targets. EGR1 targets were enriched in RNA processing, and GABPA and YY1 targets were mainly involved in organelle organization and assembly. This study provides a reduced panel of transcriptional regulators that could impact multiple pathways through the control of a number of targets in the cerebellum in chronic schizophrenia. These findings suggest that this panel of transcription factors could represent key targets for pharmacological interventions in schizophrenia. Full article
(This article belongs to the Special Issue Molecular Basis of Neuropsychiatric Disorders: Recent and Future Developments)
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23 pages, 998 KiB  
Article
Purinergic System Transcript Changes in the Dorsolateral Prefrontal Cortex in Suicide and Major Depressive Disorder
by Smita Sahay, Anna E. Lundh, Roshan P. Sirole, Robert E. McCullumsmith and Sinead M. O’Donovan
Int. J. Mol. Sci. 2025, 26(5), 1826; https://doi.org/10.3390/ijms26051826 - 20 Feb 2025
Viewed by 504
Abstract
Suicide is a major public health priority, and its molecular mechanisms appear to be related to imbalanced purine metabolism in the brain. This exploratory study investigates purinergic gene expression in the postmortem dorsolateral prefrontal cortex (DLPFC) tissue isolated from subjects with major depressive [...] Read more.
Suicide is a major public health priority, and its molecular mechanisms appear to be related to imbalanced purine metabolism in the brain. This exploratory study investigates purinergic gene expression in the postmortem dorsolateral prefrontal cortex (DLPFC) tissue isolated from subjects with major depressive disorder (MDD) who died by suicide (MDD-S, n = 10), MDD subjects who did not die by suicide (MDD-NS, n = 6) and non-psychiatrically ill controls (CTL, n = 9–10). Purinergic system transcripts were assayed by quantitative polymerase chain reactions (qPCR) in superficial and deep gray matter as well as white matter DLPFC cortical layers using laser microdissection (LMD). Across all subjects, regardless of sex, P2RY12 (F(2,23) = 5.40, p = 0.004) and P2RY13 (KW statistic = 11.82, p = 0.001) transcript levels were significantly greater in MDD-S compared to MDD-NS subjects. Several other perturbations were observed in the white matter tissue isolated from females: NT5E (F(2,10) = 13.37, p = 0.001) and P2RY13 (F(2,9) = 3.99, p = 0.011, controlled for age) transcript expression was significantly greater in MDD-S vs. MDD-NS female groups. ENTPD2 (F(2,10) = 5.20, p = 0.03), ENTPD3 (F(2,10) = 28.99, p < 0.0001), and NT5E (F(2,10) = 13.37, p = 0.001) were among the transcripts whose expression was significantly elevated in MDD-S vs. CTL female groups. Transcripts that exhibited significantly altered expression in the superficial and deep gray matter included ENTPD2, NT5E, PANX1, and P2RY13 (p ≤ 0.05). Our medication analysis revealed that the expression of these transcripts was not significantly altered by antidepressants. This is the first study to holistically quantify the purinergic metabolic pathway transcripts in suicide and MDD utilizing human postmortem brain tissue. Our preliminary findings support evidence implicating changes in purinergic P2 receptors in the brain in suicide and provide support for broader purinergic system dysregulation in mood disorders. Full article
(This article belongs to the Special Issue Molecular Basis of Neuropsychiatric Disorders: Recent and Future Developments)
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Review

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30 pages, 2412 KiB  
Review
Unraveling the Complex Interplay Between Neuroinflammation and Depression: A Comprehensive Review
by Andreea Sălcudean, Ramona-Amina Popovici, Dana Emanuela Pitic, Diana Sârbu, Adela Boroghina, Mohammad Jomaa, Matin Asad Salehi, Alsayed Ahmad Mhd Kher, Maria Melania Lica, Cristina Raluca Bodo and Virgil Radu Enatescu
Int. J. Mol. Sci. 2025, 26(4), 1645; https://doi.org/10.3390/ijms26041645 - 14 Feb 2025
Cited by 2 | Viewed by 1561
Abstract
The relationship between neuroinflammation and depression is a complex area of research that has garnered significant attention in recent years. Neuroinflammation, characterized by the activation of glial cells and the release of pro-inflammatory cytokines, has been implicated in the pathophysiology of depression. The [...] Read more.
The relationship between neuroinflammation and depression is a complex area of research that has garnered significant attention in recent years. Neuroinflammation, characterized by the activation of glial cells and the release of pro-inflammatory cytokines, has been implicated in the pathophysiology of depression. The relationship between neuroinflammation and depression is bidirectional; not only can inflammation contribute to the onset of depressive symptoms, but depression itself can also exacerbate inflammatory responses, creating a vicious cycle that complicates treatment and recovery. The present comprehensive review aimed to explore the current findings on the interplay between neuroinflammation and depression, as well as the mechanisms, risk factors, and therapeutic implications. The mechanisms by which neuroinflammation induces depressive-like behaviors are diverse. Neuroinflammation can increase pro-inflammatory cytokines, activate the hypothalamus–pituitary–adrenal (HPA) axis, and impair serotonin synthesis, all of which contribute to depressive symptoms. Furthermore, the activation of microglia has been linked to the release of inflammatory mediators that can disrupt neuronal function and contribute to mood disorders. Stress-induced neuroinflammatory responses can lead to the release of pro-inflammatory cytokines that not only affect brain function but also influence behavior and mood. Understanding these mechanisms is crucial for developing targeted therapies that can mitigate the effects of neuroinflammation on mood disorders. Full article
(This article belongs to the Special Issue Molecular Basis of Neuropsychiatric Disorders: Recent and Future Developments)
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