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Advances in Genetics of Psychiatric Disorder
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Advances in Genetics of Psychiatric Disorder

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: closed (20 January 2023) | Viewed by 6741

Special Issue Editor

Dr. Olga Fedorenko

E-Mail Website
Guest Editor
1. Laboratory of Molecular Genetics and Biochemistry, Tomsk National Research Medical Center, Mental Health Research Institute, Russian Academy of Sciences, 4 Aleutskaya Ul, Tomsk 634014, Russia
2. Division for Testing and Diagnostics, National Research Tomsk Polytechnic University, 30 Lenina Prosp, Tomsk 634050, Russia
Interests: psychiatric disorders; schizophrenia; cognitive deficit; molecular genetic markers; genetic polymorphism; pharmacogenetics; epigenetics

Special Issue Information

Dear Colleagues,

Psychiatric disorders have high levels of heterogeneity at the phenotypic and genetic levels. The challenges of genetic research in psychiatry are well-known, i.e., the weak effects of multiple genes with an additive and interactive impact; the ambiguity of hypotheses about pathogenesis; psychiatric and somatic comorbidity; the lack of reliable and verified laboratory tests; ethnic stratification; and blurred and overlapping diagnostic categories. Studies have been conducted with the aim of detecting the common genetic variations linked with neuropsychiatric disorders, involving a psychiatric genetics consortium and next-generation sequencing technologies, such as targeted sequencing, exome or genome sequencing, and more recently, third-generation sequencing technologies (i.e. long-read sequencing). These genome-wide association studies (GWASs) have been hugely successful, and hundreds of high-confidence risk genes involved in psychiatric disorders and their underlying mechanisms have been identified through detailed genotype–phenotype correlations. However, many causative genes related to psychiatric disorders, as well as their mechanisms, remain undiscovered.

This Special Issue aims highlight the progress of the genetic and functional studies related to psychiatric disorders, focusing on omics-based findings and their basic and clinical applications in psychiatric disorders. We welcome submissions detailing novel gene discoveries and genetic mechanisms, treatment studies using animal or cellular models (or others), new diagnostic approaches, integrated databases, and genetic resources, and papers dissecting phenotypic clinical and genetic heterogenicity in psychiatric disorders. Original research papers, brief research reports, and reviews covering the topics above are all welcome.

Dr. Olga Fedorenko
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. Genes 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

  • psychiatric disorders
  • schizophrenia
  • bipolar disorders
  • alcoholism
  • genetic factors
  • epigenetic factors
  • polymorphisms
  • genotype–phenotype correlations

Published Papers (4 papers)

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Research

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16 pages, 389 KiB  
Article
Taste Preference-Related Genetic Polymorphisms Modify Alcohol Consumption Behavior of the Hungarian General and Roma Populations
by Ali Abbas Mohammad Kurshed, Ferenc Vincze, Péter Pikó, Zsigmond Kósa, János Sándor, Róza Ádány and Judit Diószegi
Genes 2023, 14(3), 666; https://doi.org/10.3390/genes14030666 - 7 Mar 2023
Cited by 2 | Viewed by 1375
Abstract
Harmful alcohol consumption has been considered a major public health issue globally, with the amounts of alcohol drunk being highest in the WHO European Region including Hungary. Alcohol consumption behaviors are complex human traits influenced by environmental factors and numerous genes. Beyond alcohol [...] Read more.
Harmful alcohol consumption has been considered a major public health issue globally, with the amounts of alcohol drunk being highest in the WHO European Region including Hungary. Alcohol consumption behaviors are complex human traits influenced by environmental factors and numerous genes. Beyond alcohol metabolization and neurotransmitter gene polymorphisms, taste preference-related genetic variants may also mediate alcohol consumption behaviors. Applying the Alcohol Use Disorders Identification Test (AUDIT) we aimed to elucidate the underlying genetic determinants of alcohol consumption patterns considering taste preference gene polymorphisms (TAS1R3 rs307355, TAS2R38 rs713598, TAS2R19 rs10772420 and CA6 rs2274333) in the Hungarian general (HG) and Roma (HR) populations. Alcohol consumption assessment was available for 410 HG and 387 HR individuals with 405 HG and 364 HR DNA samples being obtained for genotyping. No significant associations were found between TAS1R3 rs307355, TAS2R19 rs10772420, and CA6 rs2274333 polymorphisms and alcohol consumption phenotypes. Significant associations were identified between TAS2R38 rs713598 and the number of standard drinks consumed in the HG sample (genotype GG negatively correlated with the number of standard drinks; coef: −0.136, p = 0.028) and the prevalence of having six or more drinks among Roma (a negative correlation was identified in the recessive model; genotype GG, coef: −0.170, p = 0.049), although, none of these findings passed the Bonferroni-corrected probability criterion (p > 0.05). Nevertheless, our findings may suggest that alcohol consumption is partially driven by genetically determined taste preferences in our study populations. Further studies are required to strengthen the findings and to understand the drivers of alcohol consumption behavior in more depth. Full article
(This article belongs to the Special Issue Advances in Genetics of Psychiatric Disorder)
10 pages, 443 KiB  
Article
The Role of Glutamatergic Gene Polymorphisms in the Clinical Phenotypes of Schizophrenia
by Evgeniya G. Poltavskaya, Elena G. Kornetova, Maxim B. Freidin, Ivan V. Pozhidaev, Diana Z. Paderina, Anna V. Bocharova, Arkadiy V. Semke, Nikolay A. Bokhan, Svetlana A. Ivanova and Olga Y. Fedorenko
Genes 2023, 14(3), 575; https://doi.org/10.3390/genes14030575 - 24 Feb 2023
Cited by 1 | Viewed by 1414
Abstract
Background: Personal variations in genetic risk for schizophrenia relate to its phenotypic heterogeneity—both in disorder development and clinical manifestations. Abnormal glutamatergic neurotransmitter system functioning is integrated in the pathogenesis of schizophrenia. Methods: A sample of 805 Russian schizophrenia patients from the Siberian Federal [...] Read more.
Background: Personal variations in genetic risk for schizophrenia relate to its phenotypic heterogeneity—both in disorder development and clinical manifestations. Abnormal glutamatergic neurotransmitter system functioning is integrated in the pathogenesis of schizophrenia. Methods: A sample of 805 Russian schizophrenia patients from the Siberian Federal region was investigated. We examined the association of 39 single nucleotide polymorphisms in eight genes (GRIN2A, GRIN2B, SLC1A2, SLC1A3, SLC17A7, GRM3, GRM7, and GRM8) involved in the glutamatergic system with the development of clinical heterogeneity of schizophrenia. The MassARRAY Analyzer 4 was used for genotyping. Results: GRIN2A rs11644461, rs8057394 and GRIN2B rs7313149 are associated with the continuous type of schizophrenia. The GRIN2A rs8057394*G allele is a relative risk factor (p = 0.019) for developing the continuous type of schizophrenia. We found a nominally significant association between negative symptoms of schizophrenia and SLC17A7 rs62126236. The SLC17A7 rs62126236*T allele has a protective effect (p = 0.039) against predominant negative symptoms in schizophrenia. The total Positive and Negative Syndrome Scale (PANSS) scores were significantly associated with GRIN2A rs9788936 after adjusting for multiple testing (p = 0.001). Conclusions: In this study the contribution of the glutamatergic gene polymorphisms to the clinical heterogeneity of schizophrenia has been demonstrated. Full article
(This article belongs to the Special Issue Advances in Genetics of Psychiatric Disorder)
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16 pages, 4003 KiB  
Article
Exposure to Juvenile Stress Induces Epigenetic Alterations in the GABAergic System in Rats
by Gil Ben David, Yam Amir, Kuldeep Tripathi, Lital Sharvit, Amir Benhos, Rachel Anunu, Gal Richter-Levin and Gil Atzmon
Genes 2023, 14(3), 565; https://doi.org/10.3390/genes14030565 - 23 Feb 2023
Viewed by 1440
Abstract
Epigenetics is a gene–environment interaction mechanism, manifested mostly through changes in regulatory gene expression. Stress is an established environmental factor known to induce epigenetic changes. This study aimed to assess the long-term effect of stress as juveniles, or juvenile and adult stress, on [...] Read more.
Epigenetics is a gene–environment interaction mechanism, manifested mostly through changes in regulatory gene expression. Stress is an established environmental factor known to induce epigenetic changes. This study aimed to assess the long-term effect of stress as juveniles, or juvenile and adult stress, on alterations in glutamic acid decarboxylase genes (GAD65, GAD67). We assessed DNA methylation and RNA expression in four rat groups: (1) control group, (2) juvenile stress group sacrificed two days following stress exposure (JSe) (RNA only), (3) juvenile stress group sacrificed as adults (JS), and (4) juvenile and adult stress group (JS + AS). Three different areas of the brain were examined in each group: the dorsal dentate gyrus (dDG), the dorsal CA1 (dCA1), and the basolateral amygdala (BLA). A significantly low methylation level of GAD65 in the BLA was observed among the JS group, followed by almost complete recovery among the JS + AS group. However, in dDG, an opposite trend was captured, and higher GAD65 methylation was found in JS. In addition, RNA levels were found to be decreased in JS compared to JSe and JS + AS. These findings can point to a possible mechanism: while juvenile stress may enhance a better coping strategy with life challenges, additional stress in adulthood may trigger a contradictory response, either beneficial or harmful. Full article
(This article belongs to the Special Issue Advances in Genetics of Psychiatric Disorder)
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Review

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22 pages, 3494 KiB  
Review
Single-Nucleotide Polymorphisms as Biomarkers of Antipsychotic-Induced Akathisia: Systematic Review
by Regina F. Nasyrova, Elena E. Vaiman, Vera V. Repkina, Aiperi K. Khasanova, Azat R. Asadullin, German A. Shipulin, Kuanysh S. Altynbekov, Mustafa Al-Zamil, Marina M. Petrova and Natalia A. Shnayder
Genes 2023, 14(3), 616; https://doi.org/10.3390/genes14030616 - 28 Feb 2023
Viewed by 2097
Abstract
Antipsychotic-induced akathisia (AIA) is a movement disorder characterized by a subjective feeling of inner restlessness or nervousness with an irresistible urge to move, resulting in repetitive movements of the limbs and torso, while taking antipsychotics (APs). In recent years, there have been some [...] Read more.
Antipsychotic-induced akathisia (AIA) is a movement disorder characterized by a subjective feeling of inner restlessness or nervousness with an irresistible urge to move, resulting in repetitive movements of the limbs and torso, while taking antipsychotics (APs). In recent years, there have been some associative genetic studies of the predisposition to the development of AIA. Objective: The goal of our study was to review the results of associative genetic and genome-wide studies and to systematize and update the knowledge on the genetic predictors of AIA in patients with schizophrenia (Sch). Methods: We searched full-text publications in PubMed, Web of Science, Springer, Google Scholar, and e-Library databases from 1977 to 2022. The Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) quality scale was used for the critical selection of the studies. Results: We identified 37 articles, of which 3 were included in the review. Thus, the C allele of rs1800498 (59414 C>T) and the A allele of rs1800497 (17316 G>A) (TaqIA) from the DRD2 gene as well as the TT genotype rs13212041 (77461407 C>T) from the HTR1B gene were found to be associated with AIA. Conclusions: Uncovering the genetic biomarkers of AIA may provide a key to developing a strategy for the personalized prevention and treatment of this adverse neurological drug reaction of APs in patients with Sch in real clinical practice. Full article
(This article belongs to the Special Issue Advances in Genetics of Psychiatric Disorder)
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