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Gene-Exposome Interactions in Mental Illness
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Gene-Exposome Interactions in Mental Illness

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Genes & Environments".

Deadline for manuscript submissions: closed (15 November 2022) | Viewed by 18355

Special Issue Editor

Dr. Per Qvist

E-Mail Website
Guest Editor
Department of Biomedicine, Aarhus University, 8000 Aarhus C, Denmark
Interests: psychiatric genetics; neuro-endocrinology; precision medicine; systems biology; nuclear receptors, epigenetics

Special Issue Information

Dear Colleagues,

Recent years have seen an explosion of discoveries concerning the risk landscape of mental illness. Thousands of genetic variants are likely to contribute with risk and their effect is further conditional on both biological and environmental factors. Intriguingly, identified risks are typically non-specifically associated with a range of disorders. This implies that the clinical manifestation of distinct diagnostic entities is determined by a complex and concerted interplay between a shared set of intrinsic and extrinsic factors. Understanding how hereditary risk and various exposures collectively shape the developing brain and mind is thus key to comprehending the pathobiology of mental illness and to the implementation of precision medicine in psychiatry.

In this Special Issue, we welcome reviews, communications, new methods, and original research articles covering aspects of gene–exposome interactions in mental illness. These include, but are not limited to, studies of molecular genetics/epigenetics; genomics/epigenomics; computational biology; and cell and animal models within the disorder schizophrenia; bipolar disorder; major depressive disorder; attention deficit hyperactivity disorders; and autism spectrum disorder. We look forward to your contributions.

Dr. Per Qvist
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

  • gene–exposome interactions
  • schizophrenia
  • bipolar disorder
  • major depressive disorder
  • attention deficit hyperactivity disorder
  • autism spectrum disorder
  • stress
  • deficiency, vitamin D
  • sex
  • substance use
  • malnutrition

Published Papers (6 papers)

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Research

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21 pages, 3592 KiB  
Article
Circulating miRNAs as Potential Biomarkers for Patient Stratification in Bipolar Disorder: A Combined Review and Data Mining Approach
by Alexandra R. Clausen, Simon Durand, Rasmus L. Petersen, Nicklas H. Staunstrup and Per Qvist
Genes 2022, 13(6), 1038; https://doi.org/10.3390/genes13061038 - 10 Jun 2022
Cited by 7 | Viewed by 2822
Abstract
Bipolar disorder is a debilitating psychiatric condition that is shaped in a concerted interplay between hereditary and triggering risk factors. Profound depression and mania define the disorder, but high clinical heterogeneity among patients complicates diagnosis as well as pharmacological intervention. Identification of peripheral [...] Read more.
Bipolar disorder is a debilitating psychiatric condition that is shaped in a concerted interplay between hereditary and triggering risk factors. Profound depression and mania define the disorder, but high clinical heterogeneity among patients complicates diagnosis as well as pharmacological intervention. Identification of peripheral biomarkers that capture the genomic response to the exposome may thus progress the development of personalized treatment. MicroRNAs (miRNAs) play a prominent role in of post-transcriptional gene regulation in the context of brain development and mental health. They are coordinately modulated by multifarious effectors, and alteration in their expression profile has been reported in a variety of psychiatric conditions. Intriguingly, miRNAs can be released from CNS cells and enter circulatory bio-fluids where they remain remarkably stable. Hence, peripheral circulatory miRNAs may act as bio-indicators for the combination of genetic risk, environmental exposure, and/or treatment response. Here we provide a comprehensive literature search and data mining approach that summarize current experimental evidence supporting the applicability of miRNAs for patient stratification in bipolar disorder. Full article
(This article belongs to the Special Issue Gene-Exposome Interactions in Mental Illness)
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14 pages, 1926 KiB  
Article
Identification of Key Modules and Genes Associated with Major Depressive Disorder in Adolescents
by Bao Zhao, Qingyue Fan, Jintong Liu, Aihua Yin, Pingping Wang and Wenxin Zhang
Genes 2022, 13(3), 464; https://doi.org/10.3390/genes13030464 - 5 Mar 2022
Cited by 5 | Viewed by 2788
Abstract
Major depressive disorder (MDD) is a leading cause of disability worldwide. Adolescence is a crucial period for the occurrence and development of depression. There are essential distinctions between adolescent and adult depression patients, and the etiology of depressive disorder is unclear. The interactions [...] Read more.
Major depressive disorder (MDD) is a leading cause of disability worldwide. Adolescence is a crucial period for the occurrence and development of depression. There are essential distinctions between adolescent and adult depression patients, and the etiology of depressive disorder is unclear. The interactions of multiple genes in a co-expression network are likely to be involved in the physiopathology of MDD. In the present study, RNA-Seq data of mRNA were acquired from the peripheral blood of MDD in adolescents and healthy control (HC) subjects. Co-expression modules were constructed via weighted gene co-expression network analysis (WGCNA) to investigate the relationships between the underlying modules and MDD in adolescents. In the combined MDD and HC groups, the dynamic tree cutting method was utilized to assign genes to modules through hierarchical clustering. Moreover, functional enrichment analysis was conducted on those co-expression genes from interested modules. The results showed that eight modules were constructed by WGCNA. The blue module was significantly associated with MDD after multiple comparison adjustment. Several Gene Ontology (GO) terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways associated with stress and inflammation were identified in this module, including histone methylation, apoptosis, NF-kappa β signaling pathway, and TNF signaling pathway. Five genes related to inflammation, immunity, and the nervous system were identified as hub genes: CNTNAP3, IL1RAP, MEGF9, UBE2W, and UBE2D1. All of these findings supported that MDD was associated with stress, inflammation, and immune responses, helping us to obtain a better understanding of the internal molecular mechanism and to explore biomarkers for the diagnosis or treatment of depression in adolescents. Full article
(This article belongs to the Special Issue Gene-Exposome Interactions in Mental Illness)
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16 pages, 1477 KiB  
Article
Interaction Effects of DRD2 Genetic Polymorphism and Interpersonal Stress on Problematic Gaming in College Students
by Esther Kim, Dojin Lee, KyuMi Do and Jueun Kim
Genes 2022, 13(3), 449; https://doi.org/10.3390/genes13030449 - 28 Feb 2022
Cited by 4 | Viewed by 2709
Abstract
Problematic gaming has become a public concern, influenced both by genetic factors and stressful environments. Studies have reported the effects of dopamine-related genes and interpersonal stressors on problematic gaming, but gene and environment interaction (G × E) studies have not been conducted. In [...] Read more.
Problematic gaming has become a public concern, influenced both by genetic factors and stressful environments. Studies have reported the effects of dopamine-related genes and interpersonal stressors on problematic gaming, but gene and environment interaction (G × E) studies have not been conducted. In this study, we investigated the interaction effects of dopamine receptor D2 (DRD2) polymorphisms and interpersonal stress on problematic gaming and the mediating effect of avoidant coping to reveal the mechanism of the G × E process. We recruited 168 college students (mean age = 22; male 63.1%) and genotyped their DRD2 C957T (rs6277) and Taq1 (rs1800497) polymorphisms. The results of the mediated moderation analysis showed that, when experiencing interpersonal stressors, individuals with both the C957T T allele and the Taq1 A1 allele showed more elevated problematic gaming scores than non-carriers. Moreover, the interaction effect of the combined DRD2 polymorphisms and interpersonal stress was significantly mediated by avoidant coping. These findings suggest that the influence of interpersonal stress on problematic gaming can be changed as a function of DRD2 genotypes, which may be because of the avoidant coping styles of C957T T allele and Taq1 A1 allele carriers in response to stress. Full article
(This article belongs to the Special Issue Gene-Exposome Interactions in Mental Illness)
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Review

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20 pages, 3190 KiB  
Review
Regulation of DNA Methylation by Cannabidiol and Its Implications for Psychiatry: New Insights from In Vivo and In Silico Models
by Luana B. Domingos, Nicole R. Silva, Adriano J. M. Chaves Filho, Amanda J. Sales, Anna Starnawska and Sâmia Joca
Genes 2022, 13(11), 2165; https://doi.org/10.3390/genes13112165 - 20 Nov 2022
Cited by 5 | Viewed by 2795
Abstract
Cannabidiol (CBD) is a non-psychotomimetic compound present in cannabis sativa. Many recent studies have indicated that CBD has a promising therapeutic profile for stress-related psychiatric disorders, such as anxiety, schizophrenia and depression. Such a diverse profile has been associated with its complex pharmacology, [...] Read more.
Cannabidiol (CBD) is a non-psychotomimetic compound present in cannabis sativa. Many recent studies have indicated that CBD has a promising therapeutic profile for stress-related psychiatric disorders, such as anxiety, schizophrenia and depression. Such a diverse profile has been associated with its complex pharmacology, since CBD can target different neurotransmitter receptors, enzymes, transporters and ion channels. However, the precise contribution of each of those mechanisms for CBD effects is still not yet completely understood. Considering that epigenetic changes make the bridge between gene expression and environment interactions, we review and discuss herein how CBD affects one of the main epigenetic mechanisms associated with the development of stress-related psychiatric disorders: DNA methylation (DNAm). Evidence from in vivo and in silico studies indicate that CBD can regulate the activity of the enzymes responsible for DNAm, due to directly binding to the enzymes and/or by indirectly regulating their activities as a consequence of neurotransmitter-mediated signaling. The implications of this new potential pharmacological target for CBD are discussed in light of its therapeutic and neurodevelopmental effects. Full article
(This article belongs to the Special Issue Gene-Exposome Interactions in Mental Illness)
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15 pages, 995 KiB  
Review
The Cannabis-Induced Epigenetic Regulation of Genes Associated with Major Depressive Disorder
by Guldar Sayed Mohammad, Sâmia Joca and Anna Starnawska
Genes 2022, 13(8), 1435; https://doi.org/10.3390/genes13081435 - 12 Aug 2022
Cited by 4 | Viewed by 3771
Abstract
The prevalence of depression is increasing worldwide, as is the number of people suffering from treatment-resistant depression; these patients constitute 30% of those treated. Unfortunately, there have not been significant advances in the treatment of this disorder in the past few decades. Exposure [...] Read more.
The prevalence of depression is increasing worldwide, as is the number of people suffering from treatment-resistant depression; these patients constitute 30% of those treated. Unfortunately, there have not been significant advances in the treatment of this disorder in the past few decades. Exposure to cannabis and cannabis-derived compounds impacts depression symptomatology in different ways, with evidence indicating that cannabidiol has antidepressant effects; there have been mixed results with medical cannabis. Even though the exact molecular mechanisms of the action underlying changes in depression symptomatology upon exposure to cannabis and cannabis-derived compounds are still unknown, there is strong evidence that these agents have a widespread impact on epigenetic regulation. We hypothesized that exposure to cannabis or cannabis-derived compounds changes the DNA methylation levels of genes associated with depression. To test this hypothesis, we first performed a literature search to identify genes that are differentially methylated upon exposure to cannabis and cannabis-derived compounds, as reported in methylome-wide association studies. We next checked whether genes residing in loci associated with depression, as identified in the largest currently available genome-wide association study of depression, were reported to be epigenetically regulated by cannabis or cannabis-related compounds. Multiple genes residing in loci associated with depression were found to be epigenetically regulated by exposure to cannabis or cannabis-derived compounds. This epigenomic regulation of depression-associated genes by cannabis or cannabis-derived compounds was reported across diverse organisms, tissues, and developmental stages and occurred in genes crucial for neuronal development, functioning, survival, and synapse functioning, as well as in genes previously implicated in other mental disorders. Full article
(This article belongs to the Special Issue Gene-Exposome Interactions in Mental Illness)
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Other

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8 pages, 243 KiB  
Commentary
Phenotypic Variability in Phelan–McDermid Syndrome and Its Putative Link to Environmental Factors
by Luigi Boccuto, Andrew Mitz, Ludovico Abenavoli, Sara M. Sarasua, William Bennett, Curtis Rogers, Barbara DuPont and Katy Phelan
Genes 2022, 13(3), 528; https://doi.org/10.3390/genes13030528 - 17 Mar 2022
Cited by 4 | Viewed by 2173
Abstract
Phelan–McDermid syndrome (PMS) is a multi-systemic disorder characterized by both genetic and phenotypic variability. Genetic abnormalities causing PMS span from pathogenic variants of the SHANK3 gene to chromosomal rearrangements affecting the 22q13 region and leading to the loss of up to over nine [...] Read more.
Phelan–McDermid syndrome (PMS) is a multi-systemic disorder characterized by both genetic and phenotypic variability. Genetic abnormalities causing PMS span from pathogenic variants of the SHANK3 gene to chromosomal rearrangements affecting the 22q13 region and leading to the loss of up to over nine megabases. The clinical presentation of individuals with PMS includes intellectual disability, neonatal hypotonia, delayed or absent speech, developmental delay, and minor dysmorphic facial features. Several other features may present with differences in age of onset and/or severity: seizures, autism, regression, sleep disorders, gastrointestinal problems, renal disorders, dysplastic toenails, and disrupted thermoregulation. Among the causes of this phenotypic variability, the size of the 22q13 deletion has effects that may be influenced by environmental factors interacting with haploinsufficiency or hemizygous variants of certain genes. Another mechanism linking environmental factors and phenotypic variability in PMS involves the loss of one copy of genes like BRD1 or CYP2D6, located at 22q13 and involved in the regulation of genomic methylation or pharmacokinetics, which are also influenced by external agents, such as diet and drugs. Overall, several non-mutually exclusive genetic and epigenetic mechanisms interact with environmental factors and may contribute to the clinical variability observed in individuals with PMS. Characterization of such factors will help to better manage this disorder. Full article
(This article belongs to the Special Issue Gene-Exposome Interactions in Mental Illness)
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