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Schizophrenia: From Molecular Mechanism to Therapy
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Schizophrenia: From Molecular Mechanism to Therapy

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 June 2024 | Viewed by 2822

Special Issue Editor

Dr. Yael Abreu-Villaça

E-Mail Website
Guest Editor
Laboratório de Neurofisiologia, Departamento de Ciências Fisiológicas, Instituto de Biologia Roberto Alcantara Gomes, Universidade do Estado do Rio de Janeiro (UERJ), Av. Prof. Manuel de Abreu 444, 5 andar – Vila Isabel, Rio de Janeiro, RJ 20550-170, Brazil
Interests: nicotine addiction; schizophrenia; comorbidity; animal models of disease; brain development; adolescence as a period of susceptibility; neurotransmission

Special Issue Information

Dear Colleagues,

Schizophrenia is a devastating chronic neuropsychiatric disorder that affects 0.9% of the population. It negatively impacts emotional responsiveness, cognition, and social interactions, leading to a broad range of adverse outcomes, including but not limited to unemployment, reduced prospects of finding a partner, stigma, and reduced life expectancy. Despite advances in the field, there is still no unifying hypothesis of schizophrenia, and the underlying pathogenic molecular mechanisms remain unclear. As a result, current treatments are symptomatic and only partially effective, mostly relieving positive symptoms and causing severe side effects.

Several factors add layers of complexity and hamper significant advances in the knowledge of molecular mechanisms and in the treatment of schizophrenia, such as: (1) the multiple genetic and environmental factors that contribute to its pathogenesis, (2) the fact the illness is sex-biased, (3) its comorbidity with addiction to drugs of abuse, and (4) its acceptance as a neurodevelopmental disorder, with its prodromal stage manifesting late during adolescence.

This Special Issue of the International Journal of Molecular Sciences intends to gather information aiming to help fill knowledge gaps and provide valuable insights into the complex nature of schizophrenia. Accordingly, the scope of the issue covers a broad range of topics, from the understanding of its molecular bases to the development of new therapeutic strategies.

Preclinical and clinical original research articles and short communications, reviews, and perspectives that cover these and related topics are welcome.

Dr. Yael Abreu-Villaça
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

  • schizophrenia
  • neurodevelopmental disorders
  • therapeutic approaches
  • drug of abuse
  • mental disorders

Published Papers (2 papers)

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Research

19 pages, 3873 KiB  
Article
Differential Effects of Aripiprazole on Electroencephalography-Recorded Gamma-Band Auditory Steady-State Response, Spontaneous Gamma Oscillations and Behavior in a Schizophrenia Rat Model
by Florian W. Adraoui, Kenza Hettak, Geoffrey Viardot, Magali Alix, Sabrina Guiffard, Benoît Meot, Philippe L’Hostis, Anne Maurin, Eric Delpy, Christophe Drieu La Rochelle and Kevin Carvalho
Int. J. Mol. Sci. 2024, 25(2), 1035; https://doi.org/10.3390/ijms25021035 - 14 Jan 2024
Viewed by 1405
Abstract
The available antipsychotics for schizophrenia (SZ) only reduce positive symptoms and do not significantly modify SZ neurobiology. This has raised the question of the robustness and translational value of methods employed during drug development. Electroencephalography (EEG)-based measures like evoked and spontaneous gamma oscillations [...] Read more.
The available antipsychotics for schizophrenia (SZ) only reduce positive symptoms and do not significantly modify SZ neurobiology. This has raised the question of the robustness and translational value of methods employed during drug development. Electroencephalography (EEG)-based measures like evoked and spontaneous gamma oscillations are considered robust translational biomarkers as they can be recorded in both patients and animal models to probe a key mechanism underlying all SZ symptoms: the excitation/inhibition imbalance mediated by N-methyl-D-aspartate receptor (NMDAr) hypofunction. Understanding the effects of commercialized atypical antipsychotics on such measures could therefore contribute to developing better therapies for SZ. Yet, the effects of such drugs on these EEG readouts are unknown. Here, we studied the effect of the atypical antipsychotic aripiprazole on the gamma-band auditory steady-state response (ASSR), spontaneous gamma oscillations and behavioral features in a SZ rat model induced by the NMDAr antagonist MK-801. Interestingly, we found that aripiprazole could not normalize MK-801-induced abnormalities in ASSR, spontaneous gamma oscillations or social interaction while it still improved MK-801-induced hyperactivity. Suggesting that aripiprazole is unable to normalize electrophysiological features underlying SZ symptoms, our results might explain aripiprazole’s inefficacy towards the social interaction deficit in our model but also its limited efficacy against social symptoms in patients. Full article
(This article belongs to the Special Issue Schizophrenia: From Molecular Mechanism to Therapy)
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30 pages, 6435 KiB  
Article
Nicotine Exposure in a Phencyclidine-Induced Mice Model of Schizophrenia: Sex-Selective Medial Prefrontal Cortex Protein Markers of the Combined Insults in Adolescent Mice
by Andrés Rodríguez-Vega, Ana Carolina Dutra-Tavares, Thainá P. Souza, Keila A. Semeão, Claudio C. Filgueiras, Anderson Ribeiro-Carvalho, Alex C. Manhães and Yael Abreu-Villaça
Int. J. Mol. Sci. 2023, 24(19), 14634; https://doi.org/10.3390/ijms241914634 - 27 Sep 2023
Viewed by 947
Abstract
Tobacco misuse as a comorbidity of schizophrenia is frequently established during adolescence. However, comorbidity markers are still missing. Here, the method of label-free proteomics was used to identify deregulated proteins in the medial prefrontal cortex (prelimbic and infralimbic) of male and female mice [...] Read more.
Tobacco misuse as a comorbidity of schizophrenia is frequently established during adolescence. However, comorbidity markers are still missing. Here, the method of label-free proteomics was used to identify deregulated proteins in the medial prefrontal cortex (prelimbic and infralimbic) of male and female mice modelled to schizophrenia with a history of nicotine exposure during adolescence. Phencyclidine (PCP), used to model schizophrenia (SCHZ), was combined with an established model of nicotine minipump infusions (NIC). The combined insults led to worse outcomes than each insult separately when considering the absolute number of deregulated proteins and that of exclusively deregulated ones. Partially shared Reactome pathways between sexes and between PCP, NIC and PCPNIC groups indicate functional overlaps. Distinctively, proteins differentially expressed exclusively in PCPNIC mice reveal unique effects associated with the comorbidity model. Interactome maps of these proteins identified sex-selective subnetworks, within which some proteins stood out: for females, peptidyl-prolyl cis-trans isomerase (Fkbp1a) and heat shock 70 kDa protein 1B (Hspa1b), both components of the oxidative stress subnetwork, and gamma-enolase (Eno2), a component of the energy metabolism subnetwork; and for males, amphiphysin (Amph), a component of the synaptic transmission subnetwork. These are proposed to be further investigated and validated as markers of the combined insult during adolescence. Full article
(This article belongs to the Special Issue Schizophrenia: From Molecular Mechanism to Therapy)
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