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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 December 2025 | Viewed by 6595

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

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Keywords

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

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Published Papers (5 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 487
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 739
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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26 pages, 724 KiB  
Review
Molecular Basis of Anxiety: A Comprehensive Review of 2014–2024 Clinical and Preclinical Studies
by Ermis Merkouris, Alexandra Brasinika, Meropi Patsiavoura, Chrysanthi Siniosoglou, Dimitrios Tsiptsios, Andreas S. Triantafyllis, Christoph Mueller, Ioulia Mpikou, Myrto T. Samara, Nikolaos Christodoulou and Konstantinos Tsamakis
Int. J. Mol. Sci. 2025, 26(11), 5417; https://doi.org/10.3390/ijms26115417 - 5 Jun 2025
Viewed by 614
Abstract
Anxiety disorders are among the most common psychiatric conditions that significantly impair one’s quality of life and place a significant burden on healthcare systems. Conventional treatments have certain restraints, such as potential side effects and limited efficacy. Τhe underlying pathophysiological mechanisms of anxiety [...] Read more.
Anxiety disorders are among the most common psychiatric conditions that significantly impair one’s quality of life and place a significant burden on healthcare systems. Conventional treatments have certain restraints, such as potential side effects and limited efficacy. Τhe underlying pathophysiological mechanisms of anxiety are not fully understood. A comprehensive literature search was performed in MEDLINE and Scopus databases for original English-language articles published between January 2014 and December 2024. Study selection, data extraction, and screening were independently carried out by multiple investigators using predefined criteria. Our review aimed to help better comprehend the molecular basis of anxiety, focusing on the hypothalamic–pituitary–adrenal (HPA) axis, serotonergic signaling, and gamma-aminobutyric acid (GABA) neurotransmission. In addition, we addressed the role of epigenetics and pharmacogenomics in personalized treatment. Although novel anxiety treatments are promising, they are predominantly preclinical and highly heterogeneous, which poses a challenge to achieving reliable therapeutic efficacy. Our findings could potentially contribute to the development of new therapeutic interventions. Further research is warranted, especially in human subjects, with an aim to combine genetic and epigenetic profiles to refine treatment approaches and develop innovative therapeutics. Full article
(This article belongs to the Special Issue Molecular Basis of Neuropsychiatric Disorders: Recent and Future Developments)
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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 5 | Viewed by 3458
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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Other

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19 pages, 978 KiB  
Hypothesis
The Possible Role of Postnatal Biphasic Dysregulation of IGF-1 Tone in the Etiology of Idiopathic Autism Spectrum Disorder
by András Visegrády
Int. J. Mol. Sci. 2025, 26(10), 4483; https://doi.org/10.3390/ijms26104483 - 8 May 2025
Viewed by 619
Abstract
Autism spectrum disorder (ASD) is a pervasive condition of neurodevelopmental origin with an increasing burden on society. Idiopathic ASD is notorious for its heterogeneous behavioral manifestations, and despite substantial efforts, its etiopathology is still unclear. An increasing amount of data points to the [...] Read more.
Autism spectrum disorder (ASD) is a pervasive condition of neurodevelopmental origin with an increasing burden on society. Idiopathic ASD is notorious for its heterogeneous behavioral manifestations, and despite substantial efforts, its etiopathology is still unclear. An increasing amount of data points to the causative role of critical developmental alterations in the first year of life, although the contribution of fetal, environmental, and genetic factors cannot be clearly distinguished. This review attempts to propose a narrative starting from neuropathological findings in ASD, involving insulin-like growth factor 1 (IGF-1) as a key modulator and demonstrates how the most consistent gestational risk factors of ASD–maternal insulin resistance and fetal growth insufficiency–converge at the perinatal dysregulation of offspring anabolism in the critical period of early development. A unifying hypothesis is derived, stating that the co-occurrence of these gestational conditions leads to postnatal biphasic dysregulation of IGF-1 tone in the offspring, leading first to insulin-dependent accelerated development, then to subsequent arrest of growth and brain maturation in ASD as an etiologic process. This hypothesis is tested for its explanation of various widely reported risk factors and observations of idiopathic ASD, including early postnatal growth abnormalities, the pervasive spectrum of symptoms, familial predisposition, and male susceptibility. Finally, further directions of research are outlined. Full article
(This article belongs to the Special Issue Molecular Basis of Neuropsychiatric Disorders: Recent and Future Developments)
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