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Life
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Biology, Pathophysiology and Pharmacotherapy for Schizophrenia
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Biology, Pathophysiology and Pharmacotherapy for Schizophrenia

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Physiology and Pathology".

Deadline for manuscript submissions: closed (29 March 2024) | Viewed by 195

Special Issue Editors

Prof. Dr. Felix Martin Werner

E-Mail Website
Guest Editor
Institute of Neurosciences Human Medicine, University of Bonn, Bonn, Germany
Interests: psycho- and neuropharmacology
Prof. Dr. Rafael Coveñas Rodríguez

E-Mail Website
Guest Editor
Laboratory of Neuroanatomy of the Peptidergic Systems, Institute of Neuroscience of Castilla and León (INCYL), University of Salamanca, c/ Pintor Fernando Gallego 1, 37007 Salamanca, Spain
Interests: cancer and anticancer peptides; substance P/neurokinin-1 receptor system; neurokinin-1 receptor antagonists
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Schizophrenia and schizoaffective disorder are disabling mental diseases, which can possibly remanifest as a recurrent psychosis. Therefore, treatment with antipsychotic drugs is essential. Adverse effects, such as movement disturbances as well as metabolic and cardiac adverse effects reduce patients’ adherence to medical treatment. In recent years, new antipsychotic drugs, which interact with new specific receptors, have been found and admitted for the treatment of this disease. Have these new antipsychotic drugs made progress in the treatment of schizophrenic symptoms, have they caused less adverse effects, and have they had a secure therapeutic effect? Has patients’ adherence become more reliable and have schizophrenic symptoms been treated better? Have therapeutic measures beside pharmacological treatment made progress in medical treatment? Clinical trials and case reports show the development of the successful treatment of disease symptoms.

Prof. Dr. Felix Martin Werner
Prof. Dr. Rafael Coveñas Rodríguez
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. Life 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 2600 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

  • antipsychotic drug
  • schizophrenia
  • schizoaffective disorder

Published Papers (1 paper)

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Research

16 pages, 681 KiB  
Article
Prenatal Immune Challenge Differentiates the Effect of Aripiprazole and Risperidone on CD200–CD200R and CX3CL1–CX3CR1 Dyads and Microglial Polarization: A Study in Organotypic Cortical Cultures
by Katarzyna Chamera, Katarzyna Curzytek, Kinga Kamińska, Monika Leśkiewicz and Agnieszka Basta-Kaim
Life 2024, 14(6), 721; https://doi.org/10.3390/life14060721 (registering DOI) - 2 Jun 2024
Abstract
Microglia are the primary innate immune cells of the central nervous system and extensively contribute to brain homeostasis. Dysfunctional or excessive activity of microglia may be associated with several neuropsychiatric disorders, including schizophrenia. Therefore, we examined whether aripiprazole and risperidone could influence the [...] Read more.
Microglia are the primary innate immune cells of the central nervous system and extensively contribute to brain homeostasis. Dysfunctional or excessive activity of microglia may be associated with several neuropsychiatric disorders, including schizophrenia. Therefore, we examined whether aripiprazole and risperidone could influence the expression of the Cd200–Cd200r and Cx3cl1–Cx3cr1 axes, which are crucial for the regulation of microglial activity and interactions of these cells with neurons. Additionally, we evaluated the impact of these drugs on microglial pro- and anti-inflammatory markers (Cd40, Il-1β, Il-6, Cebpb, Cd206, Arg1, Il-10 and Tgf-β) and cytokine release (IL-6, IL-10). The research was executed in organotypic cortical cultures (OCCs) prepared from the offspring of control rats (control OCCs) or those exposed to maternal immune activation (MIA OCCs), which allows for the exploration of schizophrenia-like disturbances in animals. All experiments were performed under basal conditions and after additional stimulation with lipopolysaccharide (LPS), following the “two-hit” hypothesis of schizophrenia. We found that MIA diminished the mRNA level of Cd200r and affected the OCCs’ response to additional LPS exposure in terms of this parameter. LPS downregulated the Cx3cr1 expression and profoundly changed the mRNA levels of pro- and anti-inflammatory microglial markers in both types of OCCs. Risperidone increased Cd200 expression in MIA OCCs, while aripiprazole treatment elevated the gene levels of the Cx3cl1–Cx3cr1 dyad in control OCCs. The antipsychotics limited the LPS-generated increase in the expression of proinflammatory factors (Il-1β and Il-6) and enhanced the mRNA levels of anti-inflammatory components (Cd206 and Tgf-β) of microglial polarization, mostly in the absence of the MIA procedure. Finally, we observed a more pronounced modulating impact of aripiprazole on the expression of pro- and anti-inflammatory cytokines when compared to risperidone in MIA OCCs. In conclusion, our data suggest that MIA might influence microglial activation and crosstalk of microglial cells with neurons, whereas aripiprazole and risperidone could beneficially affect these changes in OCCs. Full article
(This article belongs to the Special Issue Biology, Pathophysiology and Pharmacotherapy for Schizophrenia)
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