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Brain Sciences
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Drug Development for Schizophrenia
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Drug Development for Schizophrenia

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Neuropharmacology and Neuropathology".

Deadline for manuscript submissions: closed (30 November 2025) | Viewed by 7433

Special Issue Editor

Dr. Alessio Mosca

E-Mail Website
Guest Editor
Department of Neurosciences, Imaging and Clinical Sciences, Università degli Studi G. D’Annunzio Chieti-Pescara, 66100 Chieti, Italy
Interests: multiple chemical sensitivity; anxiety; depression; new psychoactive substances; NPS; suicide; suicidality; synthetic cannabinoids; synthetic cathinones; new synthetic opioids; ketamine; esketamine; s-ketamine; obsessive–compulsive disorder (OCD); substance use disorder; drug misuse; drug abuse; drug diversion; Psychosis; substance-induced-psychosis

Special Issue Information

Dear Colleagues,

Schizophrenia is a severe and complex psychiatric disorder that affects millions of individuals worldwide. Despite significant progress in understanding its pathophysiology, the development of effective pharmacological treatments remains a critical challenge. Current antipsychotic medications primarily target dopaminergic pathways and often fail to address the full spectrum of symptoms, including cognitive deficits and negative symptoms, while also being associated with significant side effects.

This Special Issue of Brain Sciences aims to present cutting-edge research on drug development for schizophrenia. We invite authors to contribute original research articles and reviews covering a broad range of topics, including but not limited to the following: novel pharmacological targets, advancements in antipsychotic drug mechanisms, personalized medicine approaches, drug repurposing strategies, biomarkers for treatment response, neuroinflammatory and neurodevelopmental perspectives, innovative drug delivery systems, computational drug discovery, and the role of emerging compounds in schizophrenia treatment. Special emphasis will be placed on translational research that bridges the gap between basic neuroscience and clinical applications.

By gathering the latest advancements in drug development for schizophrenia, this Special Issue aims to provide insights that will enhance future therapeutic strategies and improve patient outcomes.

Dr. Alessio Mosca
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 250 words) can be sent to the Editorial Office for assessment.

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. Brain Sciences 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 2200 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

  • antipsychotics
  • biomarkers
  • glutamatergic modulation
  • schizophrenia treatment
  • drug discovery

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Published Papers (2 papers)

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22 pages, 9556 KB  
Article
L-Borneolum Attenuates Ischemic Stroke Through Remodeling BBB Transporter Function via Regulating MFSD2A/Cav-1 Signaling Pathway
by Peiru Wang, Yilun Ma, Dazhong Lu, Li Wen, Fengyu Huang, Jianing Lian, Mengmeng Zhang and Taiwei Dong
Brain Sci. 2026, 16(1), 111; https://doi.org/10.3390/brainsci16010111 - 20 Jan 2026
Viewed by 799
Abstract
Objective: This study compares the brain protective effects of L-borneolum and its main components (a combined application of L-borneol and L-camphor) on the rat model of middle cerebral artery occlusion/reperfusion (MCAO/R). It also makes clear the intrinsic regulatory mechanisms that link the neuroprotective [...] Read more.
Objective: This study compares the brain protective effects of L-borneolum and its main components (a combined application of L-borneol and L-camphor) on the rat model of middle cerebral artery occlusion/reperfusion (MCAO/R). It also makes clear the intrinsic regulatory mechanisms that link the neuroprotective effects of these compounds on IS to the blood-brain barrier (BBB), based on network pharmacology predictions. Furthermore, the study investigates the relationship between these compounds and the Major Facilitator Superfamily Domain-containing Protein 2A (MFSD2A)/Caveolin-1 (Cav-1) signaling axis. Methods: The MCAO/R model in rats was established to evaluate the therapeutic effect of L-borneolum (200 mg/kg) and its main components combination of L-borneol and L-camphor (6:4 ratio, 200 mg/kg). Neurological scores, 2,3,5-triphenyl tetrazolium chloride (TTC) staining, hematoxylin-eosin (HE) staining, and Nissl staining were performed to evaluate the neurological damage in the rats. Cerebral blood flow Doppler was applied to monitor the cerebral blood flow changes. Immunofluorescence analysis of albumin leakage and transmission electron microscopy (TEM) were conducted to evaluate blood-brain barrier (BBB) integrity. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was used to determine the optimal drug concentration. Trans-epithelial electrical resistance (TEER) and horseradish peroxidase (HRP) assays were employed to confirm the successful establishment of an in vitro BBB co-culture model. Network pharmacology was utilized to predict the biological processes, molecular functions, and cellular components involved in the treatment of ischemic stroke (IS) by the main components of L-borneolum (L-borneol and L-camphor). Finally, immunofluorescence, real-time fluorescent quantitative PCR (RT-qPCR) and western blot analyses were performed to detect the expression of Major Facilitator Superfamily Domain Containing 2A (MFSD2A), caveolin-1 (CAV-1), sterol regulatory element-binding protein 1 (SREBP1) in brain tissue and hCMEC/D3 cells. Results: Network pharmacology prediction indicated that L-borneolum and its main components (L-borneol and L-camphor) in the treatment of IS are likely associated with vesicle transport and neuroprotection. Treatment of IS with L-borneolum and its main components significantly decreased neurological function scores and cerebral infarction area, while alleviating pathological morphological changes and increasing the number of Nissl bodies in the hippocampus. Additionally, it improved cerebral blood flow, reduced albumin leakage, and decreased vesicle counts in the brain. The trans-epithelial electrical resistance (TEER) of the co-culture model stabilized on the fifth day after co-culture, and the permeability to horseradish peroxidase (HRP) in the co-culture model was significantly lower than that of the blank chamber at this time. RT-qPCR and Western blot results demonstrated that, compared to the model group, the expression of SREBP1 and MFSD2A significantly increased, while the expression of Cav-1 decreased. Conclusions: L-borneolum and its main components combination (L-borneol/L-camphor, 6:4 ratio) may exert a protective effect in rats with IS by improving BBB transport function through modulation of the MFSD2A/Cav-1 signaling pathway. Full article
(This article belongs to the Special Issue Drug Development for Schizophrenia)
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33 pages, 1053 KB  
Systematic Review
Clinical Management of Synthetic-Cannabinoid-Induced Psychosis: A Systematic Review of Treatment Strategies and Outcomes
by Alessio Mosca, Stefania Chiappini, Andrea Miuli, Clara Cavallotto, Mauro Pettorruso, Giovanni Martinotti and Fabrizio Schifano
Brain Sci. 2025, 15(9), 1006; https://doi.org/10.3390/brainsci15091006 - 17 Sep 2025
Viewed by 6189
Abstract
Background: Synthetic cannabinoid receptor agonists (SCRAs, commercially known as “Spice”) have become a leading cause of substance-induced psychosis worldwide. These compounds show strong associations not only with acute psychotic episodes but also, in a subset of patients, with persistent or relapsing psychotic disorders, [...] Read more.
Background: Synthetic cannabinoid receptor agonists (SCRAs, commercially known as “Spice”) have become a leading cause of substance-induced psychosis worldwide. These compounds show strong associations not only with acute psychotic episodes but also, in a subset of patients, with persistent or relapsing psychotic disorders, patterns that raise concern about progression to schizophrenia. Yet clinicians still lack clear, evidence-based guidance, and the optimal management of SCRA-induced psychosis remains inadequately defined. Methods: We carried out a systematic search of PubMed, Scopus, and Web of Science on 2 April 2025, identifying 35 primary studies that together describe roughly 4600 clinical presentations (≈77% male; mean age: 24.7 years). Results: Across diverse settings a convergent three-step pharmacological strategy emerged. First, rapid tranquillization with parenteral benzodiazepines consistently controlled severe agitation and autonomic instability. Second, when florid psychosis persisted beyond 30–60 min, clinicians introduced a second-generation antipsychotic—most commonly olanzapine, risperidone, or aripiprazole—often at doses exceeding those used for primary psychoses. Third, for the minority of refractory or relapse-prone cases, escalation to long-acting injectable formulations or low-dose clozapine achieved symptom control, even at plasma levels below those required in treatment-resistant schizophrenia. Although the evidence base consists largely of uncontrolled clinical descriptions, across studies, a recurrent clinical pattern was observed: initial benzodiazepines for agitation, followed by antipsychotics when psychosis persisted and escalation to clozapine or long-acting injectables in refractory cases. This approach appears to be associated with symptom improvement, although the certainty of the evidence is low to very low. Conclusions. Prospective, comparative studies are urgently needed to refine dosing, directly compare antipsychotic classes, and evaluate emerging cannabinoid-modulating interventions. Full article
(This article belongs to the Special Issue Drug Development for Schizophrenia)
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