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Translating Molecular Psychiatry: From Biomarkers to Personalized Therapies
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Translating Molecular Psychiatry: From Biomarkers to Personalized Therapies

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 May 2025 | Viewed by 14369

Special Issue Editor

Dr. Masaru Tanaka

E-Mail Website
Guest Editor
Danube Neuroscience Research Laboratory, HUN-REN-SZTE Neuroscience Research Group, Hungarian Research Network, University of Szeged (HUN-REN-SZTE), Tisza Lajos Krt. 113, H-6725 Szeged, Hungary
Interests: depression; anxiety; dementia pain; their comorbidities nature; translational research in neurological diseases; psychiatric disorders
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We invite submissions for a Special Issue dedicated to the transformative potential of translational research in molecular psychiatry. This issue seeks to bridge the gap between cutting-edge molecular insights and their practical application in clinical settings, focusing on key areas that promise to revolutionize psychiatric care. We welcome contributions that investigate the identification and validation of molecular biomarkers, such as genetic markers and metabolites, which are critical for improving diagnostic precision and tailoring personalized treatment plans in psychiatric disorders. These advancements are fundamental to the development of precision medicine in mental health.

The Special Issue also welcomes papers on pharmacogenomics, emphasizing how genetic variations influence individual responses to psychiatric medications. Research in this area can significantly reduce adverse effects and optimize therapeutic outcomes by guiding personalized drug regimens. Furthermore, we are looking for studies on gene-environment interactions in psychiatric disorders that will help us understand the complex interplay between genetic predispositions and environmental triggers, with the goal of informing the design of targeted prevention and intervention strategies.

Further, we highlight the importance of neuroinflammation and immune modulation in understanding and treating psychiatric conditions, alongside the role of neuroimaging and molecular imaging in correlating molecular changes with clinical symptoms. This issue aims to advance the field by accelerating the translation of molecular research into effective clinical innovations, ultimately improving patient care and outcomes in psychiatry.

Dr. Masaru Tanaka
Guest Editor

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Keywords

  • molecular psychiatry
  • biomarkers
  • pharmacogenomics
  • precision medicine
  • gene-environment Interaction
  • neuroinflammation
  • immune modulation
  • neuroimaging
  • molecular imaging
  • psychiatric disorders

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Published Papers (6 papers)

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Research

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18 pages, 465 KiB  
Article
Optimising Aripiprazole Long-Acting Injectable: A Comparative Study of One- and Two-Injection Start Regimens in Schizophrenia with and Without Substance Use Disorders and Relationship to Early Serum Levels
by Giada Trovini, Ginevra Lombardozzi, Georgios D. Kotzalidis, Luana Lionetto, Felicia Russo, Angela Sabatino, Elio Serra, Simone Castorina, Giorgia Civita, Sara Frezza, Donatella De Bernardini, Giuseppe Costanzi, Marika Alborghetti, Maurizio Simmaco, Ferdinando Nicoletti and Sergio De Filippis
Int. J. Mol. Sci. 2025, 26(3), 1394; https://doi.org/10.3390/ijms26031394 - 6 Feb 2025
Viewed by 2016
Abstract
Aripiprazole as a long-acting injectable (LAI) is initiated in oral aripiprazole-stabilised patients and needs, after first injection, 14 days supplementation of oral aripiprazole (one-injection start, OIS). Recently, an alternative two-injection start (TIS) was advanced, involving two 400 mg injections with a single 20 [...] Read more.
Aripiprazole as a long-acting injectable (LAI) is initiated in oral aripiprazole-stabilised patients and needs, after first injection, 14 days supplementation of oral aripiprazole (one-injection start, OIS). Recently, an alternative two-injection start (TIS) was advanced, involving two 400 mg injections with a single 20 mg oral supplementation of aripiprazole. We tested the two regimens in patients with schizophrenia (SCZ, n = 152, 90 men and 62 women) with (SUD+; n = 93) or without (SUD–; n = 59) substance use disorders (SUDs), comparing OIS (n = 66) with TIS (n = 86) and SUD+ vs. SUD–. For 26 patients, we measured weekly for one month, aripiprazole + dehydroaripiprazole (active moiety) levels. Patients were followed for three months after LAI with psychopathology and quality-of-life scales (BPRS, CGI-S, ACES, BIS-11, and WHOQOL). All groups improved in psychopathology with no differences between OSI and TIS and between SCZ–SUD+ and SCZ–SUD–. The TIS group was associated with serum blood levels of the active moiety within the therapeutic window, while the OIS group showed peaks above the window, possibly exposing patients to toxicity. Treatments were well-tolerated. Here we showed no disadvantages for TIS vs. OIS and possibly increased safety. Shifting the initiation of aripiprazole LAIs to the TIS modality may be safe and pharmacokinetically advantageous. Full article
(This article belongs to the Special Issue Translating Molecular Psychiatry: From Biomarkers to Personalized Therapies)
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Review

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34 pages, 1835 KiB  
Review
Rethinking Depression—Beyond Neurotransmitters: An Integrated Psychoneuroendocrineimmunology Framework for Depression’s Pathophysiology and Tailored Treatment
by Anna Giulia Bottaccioli, Mauro Bologna and Francesco Bottaccioli
Int. J. Mol. Sci. 2025, 26(6), 2759; https://doi.org/10.3390/ijms26062759 - 19 Mar 2025
Viewed by 1409
Abstract
It is known that the effectiveness of drug treatment for depression, ammine deficit based, is largely unsatisfactory. In this review, we examine the proposal of a precision therapy has emerged and has received a strong push by the identification of the role of [...] Read more.
It is known that the effectiveness of drug treatment for depression, ammine deficit based, is largely unsatisfactory. In this review, we examine the proposal of a precision therapy has emerged and has received a strong push by the identification of the role of inflammation in depression. However, precision psychiatry risks being caught in the reductionist trap of searching for the molecular switch that resets the whole system and switches off the disease. This is an illusion since the human being is complex and depression is a systemic and variable disorder. In this study, we show the inadequacy of the reductionist paradigm, and, at the same time, illustrate the superiority of the systemic paradigm centered on psychoneuroendocrineimmunology (PNEI). According to the PNEI paradigm, depression is a disease of the whole human being, caused by different sources working together: psychological, biological, and behavioral. This means knowing the biological and psychological history of the subject, identifying relational and biological crisis factors, and building personalized treatments targeting those factors with the tools of medicine and psychology, which are not reducible to the combination of drugs and psychotherapy. Our proposal presents a paradigm shift that is both theoretical and practical, which enables clinicians to assess patients experiencing depression in a unified way and treat them in an integrated manner. Full article
(This article belongs to the Special Issue Translating Molecular Psychiatry: From Biomarkers to Personalized Therapies)
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24 pages, 713 KiB  
Review
Blood–Brain Barrier Disruption in Schizophrenia: Insights, Mechanisms, and Future Directions
by Fangsong Zhang, Jianye Zhang, Xuexue Wang, Mengyang Han, Yi Fei and Jinhong Wang
Int. J. Mol. Sci. 2025, 26(3), 873; https://doi.org/10.3390/ijms26030873 - 21 Jan 2025
Cited by 1 | Viewed by 2382
Abstract
The blood–brain barrier (BBB) plays a crucial role in maintaining the homeostasis of the central nervous system by regulating solute transport and preventing neurotoxic substances from infiltrating brain tissue. In schizophrenia, emerging evidence identifies BBB dysfunction as a key pathophysiological factor associated with [...] Read more.
The blood–brain barrier (BBB) plays a crucial role in maintaining the homeostasis of the central nervous system by regulating solute transport and preventing neurotoxic substances from infiltrating brain tissue. In schizophrenia, emerging evidence identifies BBB dysfunction as a key pathophysiological factor associated with neuroinflammation, tight junction abnormalities, and endothelial dysfunction. Recent advancements in neuroimaging techniques, such as arterial spin labeling (ASL), have provided valuable tools for investigating BBB permeability and its role in disease progression. This review synthesizes findings from postmortem studies, serum and cerebrospinal fluid biomarker analyses, and advanced neuroimaging research to elucidate BBB alterations in schizophrenia. It highlights the mechanistic roles of tight junction protein dysregulation, neurovascular unit dysfunction, and immune responses in disrupting BBB integrity. Furthermore, the review examines the bidirectional effects of antipsychotic medications on BBB, addressing both therapeutic opportunities and potential challenges. By emphasizing the pivotal role of BBB dysfunction in schizophrenia pathogenesis, this review underscores its translational potential. Through the integration of multidisciplinary evidence, it lays the foundation for innovative diagnostic approaches and therapeutic strategies, enhancing our understanding of schizophrenia’s complex pathophysiology. Full article
(This article belongs to the Special Issue Translating Molecular Psychiatry: From Biomarkers to Personalized Therapies)
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23 pages, 3711 KiB  
Review
AdipoRon’s Impact on Alzheimer’s Disease—A Systematic Review and Meta-Analysis
by Sandra Maria Barbalho, Lucas Fornari Laurindo, Bárbara de Oliveira Zanuso, Rebeca Maria Siqueira da Silva, Lívia Gallerani Caglioni, Victor Bruno Fonseca Nunes Junqueira de Moraes, Lívia Fornari Laurindo, Victória Dogani Rodrigues, Jéssica da Silva Camarinha Oliveira, Maria Eduarda Beluce, Cláudia Rucco Penteado Detregiachi, Caroline Barbalho Lamas, Jesselina Francisco dos Santos Haber, Virgínia Maria Cavallari Strozze Catharin, Karina Quesada, Masaru Tanaka and Vitor Engrácia Valenti
Int. J. Mol. Sci. 2025, 26(2), 484; https://doi.org/10.3390/ijms26020484 - 8 Jan 2025
Cited by 1 | Viewed by 3529
Abstract
Alzheimer’s disease (AD) remains a leading cause of cognitive decline and mortality worldwide, characterized by neurodegeneration, synaptic deficiencies, and neuroinflammation. Despite advancements in early detection, diagnosis, and treatment, AD presents substantial challenges due to its complex pathology, heterogeneity, and the limited efficacy of [...] Read more.
Alzheimer’s disease (AD) remains a leading cause of cognitive decline and mortality worldwide, characterized by neurodegeneration, synaptic deficiencies, and neuroinflammation. Despite advancements in early detection, diagnosis, and treatment, AD presents substantial challenges due to its complex pathology, heterogeneity, and the limited efficacy of current therapies. Consequently, there is a pressing need for novel therapeutic agents to target the multifaceted aspects of AD pathology, enhance current treatments, and minimize adverse effects. AdipoRon, an adiponectin receptor agonist, has garnered interest for its potential neuroprotective effects, including reducing neuroinflammation, improving mitochondrial function, and mitigating tau hyperphosphorylation. This review aimed to evaluate the effects of AdipoRon-based adiponectin replacement therapy against AD, using a comprehensive approach grounded in the PICO framework—Population, Intervention, Comparison, and Outcomes. A total of six studies were reviewed, including in vitro and in vivo investigations examining AdipoRon’s impact on various AD models. These studies involved different cell lines and transgenic mouse models, assessing various outcomes such as cognitive function, neuroinflammation, tau phosphorylation, synaptic deficiencies, and relevant molecular pathways. By synthesizing data from these studies, our review thoroughly explains AdipoRon’s neuroprotective effects, mechanisms of action, and potential as a therapeutic agent for AD. This analysis aims to highlight the current state of knowledge, identify gaps in the research, and suggest directions for future studies and clinical applications. Full article
(This article belongs to the Special Issue Translating Molecular Psychiatry: From Biomarkers to Personalized Therapies)
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Other

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14 pages, 1544 KiB  
Brief Report
RNA Editing Signatures Powered by Artificial Intelligence: A New Frontier in Differentiating Schizophrenia, Bipolar, and Schizoaffective Disorders
by Francisco J. Checa-Robles, Nicolas Salvetat, Christopher Cayzac, Mary Menhem, Mathieu Favier, Diana Vetter, Ilhème Ouna, João V. Nani, Mirian A. F. Hayashi, Elisa Brietzke and Dinah Weissmann
Int. J. Mol. Sci. 2024, 25(23), 12981; https://doi.org/10.3390/ijms252312981 - 3 Dec 2024
Viewed by 1890
Abstract
Mental health disorders are devastating illnesses, often misdiagnosed due to overlapping clinical symptoms. Among these conditions, bipolar disorder, schizophrenia, and schizoaffective disorder are particularly difficult to distinguish, as they share alternating positive and negative mood symptoms. Accurate and timely diagnosis of these diseases [...] Read more.
Mental health disorders are devastating illnesses, often misdiagnosed due to overlapping clinical symptoms. Among these conditions, bipolar disorder, schizophrenia, and schizoaffective disorder are particularly difficult to distinguish, as they share alternating positive and negative mood symptoms. Accurate and timely diagnosis of these diseases is crucial to ensure effective treatment and to tailor therapeutic management to each individual patient. In this context, it is essential to move beyond standard clinical assessment and employ innovative approaches to identify new biomarkers that can be reliably quantified. We previously identified a panel of RNA editing biomarkers capable of differentiating healthy controls from depressed patients and, among depressed patients, those with major depressive disorder and those with bipolar disorder. In this study, we integrated Adenosine-to-Inosine RNA editing blood biomarkers with clinical data through machine learning algorithms to establish specific signatures for bipolar disorder and schizophrenia spectrum disorders. This groundbreaking study paves the way for the application of RNA editing in other psychiatric disorders, such as schizophrenia and schizoaffective disorder. It represents a first proof-of-concept and provides compelling evidence for the establishment of an RNA editing signature for the diagnosis of these psychiatric conditions. Full article
(This article belongs to the Special Issue Translating Molecular Psychiatry: From Biomarkers to Personalized Therapies)
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9 pages, 1222 KiB  
Brief Report
IL-1 Blockade Mitigates Autism and Cerebral Palsy Traits in Offspring In-Utero Exposed to Group B Streptococcus Chorioamnionitis
by Taghreed A. Ayash, Marie-Julie Allard, Mathilde Chevin and Guillaume Sébire
Int. J. Mol. Sci. 2024, 25(21), 11393; https://doi.org/10.3390/ijms252111393 - 23 Oct 2024
Cited by 1 | Viewed by 1809
Abstract
Group B Streptococcus (GBS) is one of the most common bacteria responsible for placental and neonatal infection and inflammation resulting in lifelong neurobehavioral impairments. In particular, GBS-induced chorioamnionitis is known in preclinical models to upregulate inflammatory pathways, primarily through the activation of the [...] Read more.
Group B Streptococcus (GBS) is one of the most common bacteria responsible for placental and neonatal infection and inflammation resulting in lifelong neurobehavioral impairments. In particular, GBS-induced chorioamnionitis is known in preclinical models to upregulate inflammatory pathways, primarily through the activation of the interleukin-1 (IL-1) pathway, leading to brain injury and subsequent neurodevelopmental issues. Previous studies from our laboratory using Lewis rat pups have shown that male offspring exposed in utero to GBS chorioamnionitis develop brain injuries leading to neurobehavioral impairments such as autistic traits. In the present study, we aimed to explore whether blocking the IL-1 pathway could prevent or mitigate these neurodevelopmental impairments in adulthood. Using our established preclinical model, we administered IL-1 receptor antagonist (IL-1Ra) to dams with GBS-induced chorioamnionitis. Here, we show that IL-1Ra administration to dams reversed autistic and cerebral palsy traits in male adult offspring exposed in utero to GBS. Hence, IL-1 blockade could serve as a therapeutic intervention against pathogen-induced neurodevelopmental disorders. This research supports the need for future human randomized controlled trials to assess IL-1 blockade administered during pregnancy or in newborns as a strategy to reduce the long-term neurobehavioral consequences of prenatal infections, such as autism, cerebral palsy, learning disabilities, and other neurodevelopmental disorders. Full article
(This article belongs to the Special Issue Translating Molecular Psychiatry: From Biomarkers to Personalized Therapies)
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