Molecular Research of Psychiatric Diseases

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: 15 May 2024 | Viewed by 6005

Special Issue Editor


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Guest Editor
Medical School, Institute of Physiology, University of Pécs, Szigeti Str. 12, P.O. Box 99, 7602 Pécs, Hungary
Interests: stress-related disorders; PTSD; neuropeptides; RFamide peptides; antidepressants; ASD
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Special Issue Information

Dear Colleagues,

Today, an increasing number of people are suffering from psychological disorders associated with stress and nutritional and metabolic problems. For better diagnosis and therapy, it would be important to reveal in detail the molecular background of psychiatric diseases such as anxiety disorders, depression, post-traumatic stress disorder (PTSD), and schizophrenia. At present, many molecular techniques are available to understand the pathomechanism of these diseases as precisely as possible, such as immunohistochemistry, Western blot, PCR, RNAscope, etc. The present Special Issue focuses on the molecular details of psychiatric diseases. Among other things, we are expecting results that can lead to the identification of novel diagnostic markers and drug targets, not only from animal but also from human studies. These data can serve as a basis for further translational and clinical studies.

The topic of the issue will cover but is not limited to:

  • Molecular background of psychiatric diseases;
  • Anxiety disorder, PTSD, schizophrenia, Alzheimer’s disease, autism spectrum disorder (ASD), depression;
  • Role of neurotransmitters in neuropsychiatric diseases;
  • Role of neuropeptides in neuropsychiatric diseases;
  • Role of interactions of neuropeptides and neurotransmitters in neuropsychiatric diseases;
  • Role of neuropeptides and their receptors in the treatment of neuropsychiatric diseases;
  • Use of techniques such as RNAscope technology and transcriptomicanalysis in psychiatric diseases;
  • Behavioral effects of neurotransmitters in psychiatric diseases;
  • Behavioral effects of neuropeptides in psychiatric diseases;
  • Psychiatric diseases and homeostasis.

Dr. Anita Kovács
Guest Editor

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Keywords

  • molecular background of psychiatric diseases
  • behavior
  • stress
  • anxiety
  • neuropeptides
  • neurotransmitters

Published Papers (4 papers)

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Research

16 pages, 1065 KiB  
Article
The Implications of Cytochrome P450 2D6/CYP2D6 Polymorphism in the Therapeutic Response of Atypical Antipsychotics in Adolescents with Psychosis—A Prospective Study
by Adriana Cojocaru, Adina Braha, Roxana Jeleriu, Nicoleta Ioana Andreescu, Maria Puiu, Luminita Ageu, Roxana Folescu, Carmen Lacramioara Zamfir and Laura Alexandra Nussbaum
Biomedicines 2024, 12(3), 494; https://doi.org/10.3390/biomedicines12030494 - 22 Feb 2024
Viewed by 1050
Abstract
Background: The plasma level of antipsychotics and their metabolites depends on the activity of the cytochrome P450 (CYP) system in the liver. This research aims to test the individual response variability to atypical antipsychotic drugs, depending on the activity of the CYP2D6 enzyme. [...] Read more.
Background: The plasma level of antipsychotics and their metabolites depends on the activity of the cytochrome P450 (CYP) system in the liver. This research aims to test the individual response variability to atypical antipsychotic drugs, depending on the activity of the CYP2D6 enzyme. Methods: In a prospective, noninterventional study, we included 56 adolescents, 51.79% male, diagnosed with schizophrenia. The patients underwent DNA sampling for genotyping SNP by RT-PCR and CYP* allelic variants using Applied Bio-systems™ TaqMan® Assays Foster City, CA, USA). and clinical and paraclinical assessments. The effectiveness of the therapy was evaluated with the PANSS scores at baseline and 3, 6, and 12 months after the initiation of an atypical antipsychotic treatment. Results: Based on the genotyping results, the patients were divided into slow metabolizers (Group 1), extensive metabolizers (Group 2), and intermediate metabolizers (Group 3). The PANSS score showed a significant decrease in Group 2, compared to Group 3 after 3 (p = 0.02), 6 (p = 0.0009), and 12 months (p < 0.0001). The patients in Group 1 showed high PANSS scores, and those in Group 2 had fewer adverse reactions than the other groups. Conclusions: Assessing the CYP2D6 polymorphism may be useful in clinical pediatric psychiatric practice towards improving clinical results and patients’ quality of life. Full article
(This article belongs to the Special Issue Molecular Research of Psychiatric Diseases)
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11 pages, 720 KiB  
Article
Influence of NUCB/Nesfatin-1 Polymorphism on Treatment Response to Naltrexone/Bupropion SR in Binge Eating Disorder and Obesity
by Elvira Anna Carbone, Mariarita Caroleo, Marianna Rania, Renato de Filippis, Francesca Condoleo, Federica Catalano, Matteo Aloi, Pasquale De Fazio, Franco Arturi, Marta Letizia Hribal, Teresa Vanessa Fiorentino and Cristina Segura-Garcia
Biomedicines 2024, 12(2), 451; https://doi.org/10.3390/biomedicines12020451 - 17 Feb 2024
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Abstract
Background and Objectives: The NUCB2 gene and its polymorphisms were identified as novel players in the regulation of food intake, potentially leading to obesity (OBE) and altered eating behaviors. Naltrexone/bupropion SR (NB) showed good efficacy and tolerability for treating OBE and altered [...] Read more.
Background and Objectives: The NUCB2 gene and its polymorphisms were identified as novel players in the regulation of food intake, potentially leading to obesity (OBE) and altered eating behaviors. Naltrexone/bupropion SR (NB) showed good efficacy and tolerability for treating OBE and altered eating behaviors associated with binge eating disorder (BED). This prospective study investigates the influence of NUCB2 gene polymorphism on NB treatment response in OBE and BED. Materials and Methods: Body mass index (BMI), eating (EDE-Q, BES, NEQ, GQ, Y-FAS 2.0) and general psychopathology (BDI, STAI-S) were evaluated at baseline (t0) and after 16 weeks (t1) of NB treatment in patients with OBE and BED (Group 1; N = 22) vs. patients with OBE without BED (Group 2; N = 20). Differences were evaluated according to the rs757081 NUCB2 gene polymorphism. Results: NUCB2 polymorphism was equally distributed between groups. Although weight at t0 was higher in Group 1, weight loss was similar at t1 in both groups. BMI was not influenced by NUCB2 polymorphism. In Group 1, the CG-genotype reported significant improvement in eating psychopathology while the GG-genotype reported improvement only for FA. No differences were observed in Group 2. Conclusions: Patients diagnosed with BED and treated with NB exhibited a more favorable treatment response within the CG-genotype of the NUCB2 polymorphism. Full article
(This article belongs to the Special Issue Molecular Research of Psychiatric Diseases)
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24 pages, 21709 KiB  
Article
The Effects of Antipsychotics in Experimental Models of Krabbe Disease
by Kapil Sharma and Kumlesh K. Dev
Biomedicines 2023, 11(5), 1313; https://doi.org/10.3390/biomedicines11051313 - 28 Apr 2023
Cited by 2 | Viewed by 1269
Abstract
The role of altered myelin in the onset and development of schizophrenia and changes in myelin due to antipsychotics remains unclear. Antipsychotics are D2 receptor antagonists, yet D2 receptor agonists increase oligodendrocyte progenitor numbers and limit oligodendrocyte injury. Conflicting studies suggest [...] Read more.
The role of altered myelin in the onset and development of schizophrenia and changes in myelin due to antipsychotics remains unclear. Antipsychotics are D2 receptor antagonists, yet D2 receptor agonists increase oligodendrocyte progenitor numbers and limit oligodendrocyte injury. Conflicting studies suggest these drugs promote the differentiation of neural progenitors to oligodendrocyte lineage, while others report antipsychotics inhibit the proliferation and differentiation of oligodendrocyte precursors. Here, we utilised in-vitro (human astrocytes), ex-vivo (organotypic slice cultures) and in-vivo (twitcher mouse model) experimental study designs of psychosine-induced demyelination, a toxin that accumulates in Krabbe disease (KD), to investigate direct effects of antipsychotics on glial cell dysfunction and demyelination. Typical and atypical antipsychotics, and selective D2 and 5HT2A receptor antagonists, attenuated psychosine-induced cell viability, toxicity, and morphological aberrations in human astrocyte cultures. Haloperidol and clozapine reduced psychosine-induced demyelination in mouse organotypic cerebellar slices. These drugs also attenuated the effects of psychosine on astrocytes and microglia and restored non-phosphorylated neurofilament levels, indicating neuroprotective effects. In the demyelinating twitcher mouse model of KD, haloperidol improved mobility and significantly increased the survival of these animals. Overall, this study suggests that antipsychotics directly regulate glial cell dysfunction and exert a protective effect on myelin loss. This work also points toward the potential use of these pharmacological agents in KD. Full article
(This article belongs to the Special Issue Molecular Research of Psychiatric Diseases)
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14 pages, 1510 KiB  
Article
The Interaction between Circulating Cell-Free Mitochondrial DNA and Inflammatory Cytokines in Predicting Human Mental Health Issue Risk in Adolescents: An Explorative Study
by Arto Alatalo, Izaque de Sousa Maciel, Nina Kucháriková, Sweelin Chew, Irene van Kamp, Maria Foraster, Jordi Julvez and Katja M. Kanninen
Biomedicines 2023, 11(3), 818; https://doi.org/10.3390/biomedicines11030818 - 7 Mar 2023
Cited by 1 | Viewed by 2164
Abstract
Adolescence is often a challenging time in which psychiatric issues have a strong connection to mental health disorders later in life. The early identification of the problems can reduce the burden of disease. To date, the effective identification of adolescents at risk of [...] Read more.
Adolescence is often a challenging time in which psychiatric issues have a strong connection to mental health disorders later in life. The early identification of the problems can reduce the burden of disease. To date, the effective identification of adolescents at risk of developing mental health problems remains understudied. Altogether, the interaction between circulating cell-free mtDNA (ccf-mtDNA) and inflammatory cytokines in adolescents is insufficiently understood regarding experienced mental health difficulties. Our study selected the participants based on the Strength and Difficulty Questionnaire (SDQ) score using the cut-off points of 3 and 18 for the low and the high score groups, respectively. The answers of the SDQ at the age of 12.2–15.7 years contributed to the investigation of (i) whether ccf-mtDNA units are associated with cytokines, and (ii) if an interaction model for predicting risk of mental health issues is observed. We discovered a sex-specific correlation between the screened markers associated with mental health problems in the low and high SDQ score groups among the male participants and in the low SDQ score group among the female participants. The mitochondrial MT-ND4 and MT-CO1 genes correlated significantly with interleukin-12p70 (IL-12p70) in males and with monocyte chemoattractant protein-1 (MCP-1) in females. Due to the nature of the explorative study, the studied markers alone did not indicate statistical significance for the prediction of mental health problems. Our analysis provided new insight into potential plasma-based biomarkers to predict mental health issues. Full article
(This article belongs to the Special Issue Molecular Research of Psychiatric Diseases)
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