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Molecular Insights in Psychiatry 2.0
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Molecular Insights in Psychiatry 2.0

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: closed (30 April 2023) | Viewed by 10092

Special Issue Editors

Prof. Dr. Jack A. Tuszynski

E-Mail Website
Guest Editor
Department of Oncology, University of Alberta, Edmonton, AB T6G 1Z2, Canada
Interests: computational drug design; systems biology of cancer and neurodegenerative diseases; tubulin
Special Issues, Collections and Topics in MDPI journals
Dr. Giovanna Traina

E-Mail Website
Guest Editor
Department of Pharmaceutical Sciences, University of Perugia, Via Romana, 06126 Perugia, Italy
Interests: inflammation; neuroinflammation; gut-brain axis; mast cells; learning and memory
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Massimo Cocchi

E-Mail Website
Guest Editor
Department of Veterinary Medical Science, University of Bologna, Via Tolora di Sopra, 50, 40064 Ozzano Emilia, Italy
Interests: lipid metabolism in humans and experimental animals with a particolar focus on cell membrane and organ function
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Psychiatric diagnosis has a rapidly growing need for a radical turning point. The present diagnostic methods cannot continue to be considered acceptable, because they are almost completely based on the psychiatrist’s opinion, which does not have an objective molecular approach.

Psychopathology is still characterised and defined by descriptive and non-biological criteria, but it will hopefully become possible to characterise it with the addition of new quantitative approaches resulting from molecular research in psychiatry. The error rate in clinical psychiatric diagnosis is very high—it ranges from 40% to 70% (Tenth World Day for the Prevention of Suicide, Rome, 2012), and this significantly affects the patient's life.

The biomolecular approach to psychopathology mainly involves cell membrane viscosity, Gsα protein, cytoskeleton and microtubules, ion channels modifications, genetic information, epigenetics, transcriptomics/proteomics, neuroimaging, and animal models. In-depth and integrated knowledge of these aspects can contribute significantly to the diagnostic framework of psychiatric pathology.

The aim of this Special Issue is dedicated to the recent insights and research progress in deciphering the molecular pathways mediating brain function in psychiatry, and to exploit such knowledge in the development of novel molecule-based therapies against psychopathological disorders.

Prof. Dr. Jack A. Tuszynski
Dr. Giovanna Traina
Prof. Dr. Massimo Cocchi
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

  • cell membrane mobility
  • Gs alpha protein
  • cytoskeleton
  • microtubules
  • ion channels
  • gut microbiota neurotransmitters
  • consciousness

Related Special Issue

Published Papers (3 papers)

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11 pages, 1664 KiB  
Article
Integrative Analyses of Transcriptomes to Explore Common Molecular Effects of Antipsychotic Drugs
by Trang T. T. Truong, Chiara C. Bortolasci, Srisaiyini Kidnapillai, Briana Spolding, Bruna Panizzutti, Zoe S. J. Liu, Jee Hyun Kim, Olivia M. Dean, Mark F. Richardson, Michael Berk and Ken Walder
Int. J. Mol. Sci. 2022, 23(14), 7508; https://doi.org/10.3390/ijms23147508 - 06 Jul 2022
Cited by 2 | Viewed by 2073
Abstract
There is little understanding of the underlying molecular mechanism(s) involved in the clinical efficacy of antipsychotics for schizophrenia. This study integrated schizophrenia-associated transcriptional perturbations with antipsychotic-induced gene expression profiles to detect potentially relevant therapeutic targets shared by multiple antipsychotics. Human neuronal-like cells (NT2-N) [...] Read more.
There is little understanding of the underlying molecular mechanism(s) involved in the clinical efficacy of antipsychotics for schizophrenia. This study integrated schizophrenia-associated transcriptional perturbations with antipsychotic-induced gene expression profiles to detect potentially relevant therapeutic targets shared by multiple antipsychotics. Human neuronal-like cells (NT2-N) were treated for 24 h with one of the following antipsychotic drugs: amisulpride, aripiprazole, clozapine, risperidone, or vehicle controls. Drug-induced gene expression patterns were compared to schizophrenia-associated transcriptional data in post-mortem brain tissues. Genes regulated by each of four antipsychotic drugs in the reverse direction to schizophrenia were identified as potential therapeutic-relevant genes. A total of 886 genes were reversely expressed between at least one drug treatment (versus vehicle) and schizophrenia (versus healthy control), in which 218 genes were commonly regulated by all four antipsychotic drugs. The most enriched biological pathways include Wnt signaling and action potential regulation. The protein-protein interaction (PPI) networks found two main clusters having schizophrenia expression quantitative trait loci (eQTL) genes such as PDCD10, ANK2, and AKT3, suggesting further investigation on these genes as potential novel treatment targets. Full article
(This article belongs to the Special Issue Molecular Insights in Psychiatry 2.0)
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Review

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14 pages, 1234 KiB  
Review
The Neurotransmission Basis of Post-Traumatic Stress Disorders by the Fear Conditioning Paradigm
by Giovanna Traina and Jack A. Tuszynski
Int. J. Mol. Sci. 2023, 24(22), 16327; https://doi.org/10.3390/ijms242216327 - 15 Nov 2023
Cited by 1 | Viewed by 1407
Abstract
Fear conditioning constitutes the best and most reproducible paradigm to study the neurobiological mechanisms underlying emotions. On the other hand, studies on the synaptic plasticity phenomena underlying fear conditioning present neural circuits enforcing this learning pattern related to post-traumatic stress disorder (PTSD). Notably, [...] Read more.
Fear conditioning constitutes the best and most reproducible paradigm to study the neurobiological mechanisms underlying emotions. On the other hand, studies on the synaptic plasticity phenomena underlying fear conditioning present neural circuits enforcing this learning pattern related to post-traumatic stress disorder (PTSD). Notably, in both humans and the rodent model, fear conditioning and context rely on dependent neurocircuitry in the amygdala and prefrontal cortex, cingulate gyrus, and hippocampus. In this review, an overview of the role that classical neurotransmitters play in the contextual conditioning model of fear, and therefore in PTSD, was reported. Full article
(This article belongs to the Special Issue Molecular Insights in Psychiatry 2.0)
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32 pages, 2260 KiB  
Review
MeCP2 Is an Epigenetic Factor That Links DNA Methylation with Brain Metabolism
by Yen My Vuu, Chris-Tiann Roberts and Mojgan Rastegar
Int. J. Mol. Sci. 2023, 24(4), 4218; https://doi.org/10.3390/ijms24044218 - 20 Feb 2023
Cited by 8 | Viewed by 6038
Abstract
DNA methylation, one of the most well-studied epigenetic modifications, is involved in a wide spectrum of biological processes. Epigenetic mechanisms control cellular morphology and function. Such regulatory mechanisms involve histone modifications, chromatin remodeling, DNA methylation, non-coding regulatory RNA molecules, and RNA modifications. One [...] Read more.
DNA methylation, one of the most well-studied epigenetic modifications, is involved in a wide spectrum of biological processes. Epigenetic mechanisms control cellular morphology and function. Such regulatory mechanisms involve histone modifications, chromatin remodeling, DNA methylation, non-coding regulatory RNA molecules, and RNA modifications. One of the most well-studied epigenetic modifications is DNA methylation that plays key roles in development, health, and disease. Our brain is probably the most complex part of our body, with a high level of DNA methylation. A key protein that binds to different types of methylated DNA in the brain is the methyl-CpG binding protein 2 (MeCP2). MeCP2 acts in a dose-dependent manner and its abnormally high or low expression level, deregulation, and/or genetic mutations lead to neurodevelopmental disorders and aberrant brain function. Recently, some of MeCP2-associated neurodevelopmental disorders have emerged as neurometabolic disorders, suggesting a role for MeCP2 in brain metabolism. Of note, MECP2 loss-of-function mutation in Rett Syndrome is reported to cause impairment of glucose and cholesterol metabolism in human patients and/or mouse models of disease. The purpose of this review is to outline the metabolic abnormalities in MeCP2-associated neurodevelopmental disorders that currently have no available cure. We aim to provide an updated overview into the role of metabolic defects associated with MeCP2-mediated cellular function for consideration of future therapeutic strategies. Full article
(This article belongs to the Special Issue Molecular Insights in Psychiatry 2.0)
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