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Advances in Genetics of Psychiatric Disorders

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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 March 2024) | Viewed by 32037

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Prof. Dr. Margarita Rivera

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Guest Editor

Department of Biochemistry and Molecular Biology II, Faculty of Pharmacy and Institute of Neurosciences, Biomedical Research Centre (CIBM), University of Granada, Granada, Spain
Interests: psychiatric disorders; genetics; GWAS studies; comorbid physical disorders

Dr. Esther Molina

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Department of Nursing, Faculty of Health Sciences and Institute of Neurosciences, Biomedical Research Centre (CIBM), University of Granada, Granada, Spain
Interests: psychiatric disorders; genetics; epidemiology; health sciences

Special Issue Information

Dear Colleagues,

Psychiatric disorders are very common and a leading cause of worldwide disability. They have significant impacts on health and major social, human rights and economic consequences in all countries around the world.

They are highly polygenic, and multifactorial disorders with both genetic and environmental factors contribute to their development. Since the beginning of genome-wide association studies (GWAS), a large number of genetic risk variants has been linked to the presence of psychiatric disorders and has provided insights into the biological pathways involved in their susceptibility. Despite the increased availability of innovative techniques and new approaches for genetic studies, the complex genetic architecture of the psychiatric disorders has not yet been fully elucidated.

Nowadays, multiple studies and research projects are being carried out worldwide on the implications of genetic aspects in the development of psychiatric disorders. All this effort could improve the diagnosis and prediction of the disorder risk and help to identify new specific drug targets, as well as enhance the prediction of individual response to drugs.

This Special Issue “Advances in Genetics of Psychiatric Disorders” in Genes will present recent advances in the study of the genetic underpinnings of different psychiatric disorders and a general overview of new challenges in this field.

Prof. Dr. Margarita Rivera
Dr. Esther Molina
Guest Editors

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Keywords

Psychiatric disorders
Genetic variants
GWAS studies
Candidate genes studies

Published Papers (11 papers)

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15 pages, 2837 KiB

Open AccessArticle

UNC5C: Novel Gene Associated with Psychiatric Disorders Impacts Dysregulation of Axon Guidance Pathways

by Simone Treccarichi, Pinella Failla, Mirella Vinci, Antonino Musumeci, Angelo Gloria, Anna Vasta, Giuseppe Calabrese, Carla Papa, Concetta Federico, Salvatore Saccone and Francesco Calì

Genes 2024, 15(3), 306; https://0-doi-org.brum.beds.ac.uk/10.3390/genes15030306 - 27 Feb 2024

Viewed by 742

Abstract

The UNC-5 family of netrin receptor genes, predominantly expressed in brain tissues, plays a pivotal role in various neuronal processes. Mutations in genes involved in axon development contribute to a wide spectrum of human diseases, including developmental, neuropsychiatric, and neurodegenerative disorders. The NTN1/DCC signaling pathway, interacting with UNC5C, plays a crucial role in central nervous system axon guidance and has been associated with psychiatric disorders during adolescence in humans. Whole-exome sequencing analysis unveiled two compound heterozygous causative mutations within the UNC5C gene in a patient diagnosed with psychiatric disorders. In silico analysis demonstrated that neither of the observed variants affected the allosteric linkage between UNC5C and NTN1. In fact, these mutations are located within crucial cytoplasmic domains, specifically ZU5 and the region required for the netrin-mediated axon repulsion of neuronal growth cones. These domains play a critical role in forming the supramodular protein structure and directly interact with microtubules, thereby ensuring the functionality of the axon repulsion process. We emphasize that these mutations disrupt the aforementioned processes, thereby associating the UNC5C gene with psychiatric disorders for the first time and expanding the number of genes related to psychiatric disorders. Further research is required to validate the correlation of the UNC5C gene with psychiatric disorders, but we suggest including it in the genetic analysis of patients with psychiatric disorders. Full article

(This article belongs to the Special Issue Advances in Genetics of Psychiatric Disorders)

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12 pages, 1380 KiB

Open AccessArticle

Differences and Similarities in Adaptive Functioning between Children with Autism Spectrum Disorder and Williams–Beuren Syndrome: A Longitudinal Study

by Paolo Alfieri, Francesco Scibelli, Federica Alice Maria Montanaro, Maria Cristina Digilio, Lucilla Ravà, Giovanni Valeri and Stefano Vicari

Genes 2022, 13(7), 1266; https://0-doi-org.brum.beds.ac.uk/10.3390/genes13071266 - 16 Jul 2022

Cited by 3 | Viewed by 2253

Abstract

Background: The last decade has seen a growing number of comparative studies on adaptive profiles between individuals with autism spectrum disorder (ASD) and Williams–Beuren syndrome (WBS), showing shared and syndrome-specific adaptive trajectories. Studies have revealed similarities in global adaptive profiles across conditions, while some differences have been found in preschoolers on the specific sub-domains of communication and socialization. However, the majority of studies that have focused on the differences in adaptive functioning across these two conditions used a cross-sectional design. To the best of our knowledge, there are no studies exploring the differences and similarities of adaptive functioning over time. Methods: We compared longitudinal data of adaptive functioning measured by Vineland Adaptive Behavior Scales (VABS) between two samples of children and adolescents with ASD and WBS, matched for chronological age and cognitive/developmental level at the time of the first evaluation. Results and Conclusions: We did not find any difference on the global adaptive level, both at the first evaluation and over time. However, significant differences emerged on the socialization and communication levels at the time of recruitment. Longitudinal data show that only the socialization domain remains different over time, with individuals with WBS having better functioning than those with ASD. The results on shared and distinct patterns of adaptive functioning between disorders are discussed from a developmental perspective, thus contributing to the implementation of age-specific interventions. Full article

(This article belongs to the Special Issue Advances in Genetics of Psychiatric Disorders)

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16 pages, 1603 KiB

Open AccessArticle

Functional Genomics Analysis to Disentangle the Role of Genetic Variants in Major Depression

by Judith Pérez-Granado, Janet Piñero, Alejandra Medina-Rivera and Laura I. Furlong

Genes 2022, 13(7), 1259; https://0-doi-org.brum.beds.ac.uk/10.3390/genes13071259 - 15 Jul 2022

Cited by 1 | Viewed by 2855

Abstract

Understanding the molecular basis of major depression is critical for identifying new potential biomarkers and drug targets to alleviate its burden on society. Leveraging available GWAS data and functional genomic tools to assess regulatory variation could help explain the role of major depression-associated genetic variants in disease pathogenesis. We have conducted a fine-mapping analysis of genetic variants associated with major depression and applied a pipeline focused on gene expression regulation by using two complementary approaches: cis-eQTL colocalization analysis and alteration of transcription factor binding sites. The fine-mapping process uncovered putative causally associated variants whose proximal genes were linked with major depression pathophysiology. Four colocalizing genetic variants altered the expression of five genes, highlighting the role of SLC12A5 in neuronal chlorine homeostasis and MYRF in nervous system myelination and oligodendrocyte differentiation. The transcription factor binding analysis revealed the potential role of rs62259947 in modulating P4HTM expression by altering the YY1 binding site, altogether regulating hypoxia response. Overall, our pipeline could prioritize putative causal genetic variants in major depression. More importantly, it can be applied when only index genetic variants are available. Finally, the presented approach enabled the proposal of mechanistic hypotheses of these genetic variants and their role in disease pathogenesis. Full article

(This article belongs to the Special Issue Advances in Genetics of Psychiatric Disorders)

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10 pages, 753 KiB

Open AccessArticle

Toxoplasma gondii Seropositivity Interacts with Catechol-O-methyltransferase Val105/158Met Variation Increasing the Risk of Schizophrenia

by Paula Rovira, Blanca Gutiérrez, Antonio Sorlózano-Puerto, José Gutiérrez-Fernández, Esther Molina, Margarita Rivera, Rafael Martínez-Leal, Inmaculada Ibanez-Casas, María Victoria Martín-Laguna, Araceli Rosa, Francisco Torres-González and Jorge A. Cervilla

Genes 2022, 13(6), 1088; https://0-doi-org.brum.beds.ac.uk/10.3390/genes13061088 - 18 Jun 2022

Cited by 4 | Viewed by 2305

Abstract

Schizophrenia is a heterogeneous and severe psychotic disorder. Epidemiological findings have suggested that the exposure to infectious agents such as Toxoplasma gondii (T. gondii) is associated with an increased risk for schizophrenia. On the other hand, there is evidence involving the catechol-O-methyltransferase (COMT) Val105/158Met polymorphism in the aetiology of schizophrenia since it alters the dopamine metabolism. A case–control study of 141 patients and 142 controls was conducted to analyse the polymorphism, the prevalence of anti-T. gondii IgG, and their interaction on the risk for schizophrenia. IgG were detected by ELISA, and genotyping was performed with TaqMan Real-Time PCR. Although no association was found between any COMT genotype and schizophrenia, we found a significant association between T. gondii seropositivity and the disorder (χ² = 11.71; p-value < 0.001). Furthermore, the risk for schizophrenia conferred by T. gondii was modified by the COMT genotype, with those who had been exposed to the infection showing a different risk compared to that of nonexposed ones depending on the COMT genotype (χ² for the interaction = 7.28, p-value = 0.007). This study provides evidence that the COMT genotype modifies the risk for schizophrenia conferred by T. gondii infection, with it being higher in those individuals with the Met/Met phenotype, intermediate in heterozygous, and lower in those with the Val/Val phenotype. Full article

(This article belongs to the Special Issue Advances in Genetics of Psychiatric Disorders)

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15 pages, 1362 KiB

Open AccessArticle

Adolescent Verbal Memory as a Psychosis Endophenotype: A Genome-Wide Association Study in an Ancestrally Diverse Sample

by Baihan Wang, Olga Giannakopoulou, Isabelle Austin-Zimmerman, Haritz Irizar, Jasmine Harju-Seppänen, Eirini Zartaloudi, Anjali Bhat, Andrew McQuillin, Karoline Kuchenbäcker and Elvira Bramon

Genes 2022, 13(1), 106; https://0-doi-org.brum.beds.ac.uk/10.3390/genes13010106 - 03 Jan 2022

Cited by 2 | Viewed by 2121

Abstract

Verbal memory impairment is one of the most prominent cognitive deficits in psychosis. However, few studies have investigated the genetic basis of verbal memory in a neurodevelopmental context, and most genome-wide association studies (GWASs) have been conducted in European-ancestry populations. We conducted a GWAS on verbal memory in a maximum of 11,017 participants aged 8.9 to 11.1 years in the Adolescent Brain Cognitive Development Study^®, recruited from a diverse population in the United States. Verbal memory was assessed by the Rey Auditory Verbal Learning Test, which included three measures of verbal memory: immediate recall, short-delay recall, and long-delay recall. We adopted a mixed-model approach to perform a joint GWAS of all participants, adjusting for ancestral background and familial relatedness. The inclusion of participants from all ancestries increased the power of the GWAS. Two novel genome-wide significant associations were found for short-delay and long-delay recall verbal memory. In particular, one locus (rs9896243) associated with long-delay recall was mapped to the NSF (N-Ethylmaleimide Sensitive Factor, Vesicle Fusing ATPase) gene, indicating the role of membrane fusion in adolescent verbal memory. Based on the GWAS in the European subset, we estimated the SNP-heritability to be 15% to 29% for the three verbal memory traits. We found that verbal memory was genetically correlated with schizophrenia, providing further evidence supporting verbal memory as an endophenotype for psychosis. Full article

(This article belongs to the Special Issue Advances in Genetics of Psychiatric Disorders)

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12 pages, 620 KiB

Open AccessArticle

Exploring the Contribution to ADHD of Genes Involved in Mendelian Disorders Presenting with Hyperactivity and/or Inattention

by Noèlia Fernàndez-Castillo, Judit Cabana-Domínguez, Djenifer B. Kappel, Bàrbara Torrico, Heike Weber, Klaus-Peter Lesch, Oscar Lao, Andreas Reif and Bru Cormand

Genes 2022, 13(1), 93; https://0-doi-org.brum.beds.ac.uk/10.3390/genes13010093 - 30 Dec 2021

Cited by 4 | Viewed by 4507

Abstract

Attention-deficit hyperactivity disorder (ADHD) is a complex neurodevelopmental disorder characterized by hyperactivity, impulsivity, and/or inattention, which are symptoms also observed in many rare genetic disorders. We searched for genes involved in Mendelian disorders presenting with ADHD symptoms in the Online Mendelian Inheritance in Man (OMIM) database, to curate a list of new candidate risk genes for ADHD. We explored the enrichment of functions and pathways in this gene list, and tested whether rare or common variants in these genes are associated with ADHD or with its comorbidities. We identified 139 genes, causal for 137 rare disorders, mainly related to neurodevelopmental and brain function. Most of these Mendelian disorders also present with other psychiatric traits that are often comorbid with ADHD. Using whole exome sequencing (WES) data from 668 ADHD cases, we found rare variants associated with the dimension of the severity of inattention symptoms in three genes: KIF11, WAC, and CRBN. Then, we focused on common variants and identified six genes associated with ADHD (in 19,099 cases and 34,194 controls): MANBA, UQCC2, HIVEP2, FOPX1, KANSL1, and AUH. Furthermore, HIVEP2, FOXP1, and KANSL1 were nominally associated with autism spectrum disorder (ASD) (18,382 cases and 27,969 controls), as well as HIVEP2 with anxiety (7016 cases and 14,475 controls), and FOXP1 with aggression (18,988 individuals), which is in line with the symptomatology of the rare disorders they are responsible for. In conclusion, inspecting Mendelian disorders and the genes responsible for them constitutes a valuable approach for identifying new risk genes and the mechanisms of complex disorders. Full article

(This article belongs to the Special Issue Advances in Genetics of Psychiatric Disorders)

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8 pages, 1291 KiB

Open AccessArticle

LRRTM4 Terminal Exon Duplicated in Family with Tourette Syndrome, Autism and ADHD

by Raymond A. Clarke and Valsamma Eapen

Genes 2022, 13(1), 66; https://0-doi-org.brum.beds.ac.uk/10.3390/genes13010066 - 27 Dec 2021

Cited by 3 | Viewed by 3979

Abstract

Tourette syndrome (TS) is a neurodevelopmental disorder characterised by motor and vocal tics and strong association with autistic deficits, obsessive–compulsive disorder (OCD) and attention-deficit/hyperactivity disorder (ADHD). The genetic overlap between TS and autism spectrum disorder (ASD) includes those genes that encode the neurexin trans-synaptic connexus (NTSC) inclusive of the presynaptic neurexins (NRXNs) and postsynaptic neuroligins (NLGNs), cerebellin precursors (CBLNs in complex with the glutamate ionotropic receptor deltas (GRIDs)) and the leucine-rich repeat transmembrane proteins (LRRTMs). In this study, we report the first evidence of a TS and ASD association with yet another NTSC gene family member, namely LRRTM4. Duplication of the terminal exon of LRRTM4 was found in two females with TS from the same family (mother and daughter) in association with autistic traits and ASD. Full article

(This article belongs to the Special Issue Advances in Genetics of Psychiatric Disorders)

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17 pages, 1110 KiB

Open AccessArticle

The Influence of CYP2D6 and CYP2C19 Genetic Variation on Diabetes Mellitus Risk in People Taking Antidepressants and Antipsychotics

by Isabelle Austin-Zimmerman, Marta Wronska, Baihan Wang, Haritz Irizar, Johan H. Thygesen, Anjali Bhat, Spiros Denaxas, Ghazaleh Fatemifar, Chris Finan, Jasmine Harju-Seppänen, Olga Giannakopoulou, Karoline Kuchenbaecker, Eirini Zartaloudi, Andrew McQuillin and Elvira Bramon

Genes 2021, 12(11), 1758; https://0-doi-org.brum.beds.ac.uk/10.3390/genes12111758 - 03 Nov 2021

Cited by 6 | Viewed by 3004

Abstract

CYP2D6 and CYP2C19 enzymes are essential in the metabolism of antidepressants and antipsychotics. Genetic variation in these genes may increase risk of adverse drug reactions. Antidepressants and antipsychotics have previously been associated with risk of diabetes. We examined whether individual genetic differences in CYP2D6 and CYP2C19 contribute to these effects. We identified 31,579 individuals taking antidepressants and 2699 taking antipsychotics within UK Biobank. Participants were classified as poor, intermediate, or normal metabolizers of CYP2D6, and as poor, intermediate, normal, rapid, or ultra-rapid metabolizers of CYP2C19. Risk of diabetes mellitus represented by HbA1c level was examined in relation to the metabolic phenotypes. CYP2D6 poor metabolizers taking paroxetine had higher Hb1Ac than normal metabolizers (mean difference: 2.29 mmol/mol; p < 0.001). Among participants with diabetes who were taking venlafaxine, CYP2D6 poor metabolizers had higher HbA1c levels compared to normal metabolizers (mean differences: 10.15 mmol/mol; p < 0.001. Among participants with diabetes who were taking fluoxetine, CYP2D6 intermediate metabolizers and decreased HbA1c, compared to normal metabolizers (mean difference −7.74 mmol/mol; p = 0.017). We did not observe any relationship between CYP2D6 or CYP2C19 metabolic status and HbA1c levels in participants taking antipsychotic medication. Our results indicate that the impact of genetic variation in CYP2D6 differs depending on diabetes status. Although our findings support existing clinical guidelines, further research is essential to inform pharmacogenetic testing for people taking antidepressants and antipsychotics. Full article

(This article belongs to the Special Issue Advances in Genetics of Psychiatric Disorders)

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22 pages, 1475 KiB

Open AccessArticle

Common and Unique Genetic Background between Attention-Deficit/Hyperactivity Disorder and Excessive Body Weight

by Monika Dmitrzak-Weglarz, Elzbieta Paszynska, Karolina Bilska, Paula Szczesniewska, Ewa Bryl, Joanna Duda, Agata Dutkiewicz, Marta Tyszkiewicz-Nwafor, Piotr Czerski, Tomasz Hanc and Agnieszka Slopien

Genes 2021, 12(9), 1407; https://0-doi-org.brum.beds.ac.uk/10.3390/genes12091407 - 13 Sep 2021

Cited by 7 | Viewed by 3051

Abstract

Comorbidity studies show that children with ADHD have a higher risk of being overweight and obese than healthy children. This study aimed to assess the genetic alternations that differ between and are shared by ADHD and excessive body weight (EBW). The sample consisted of 743 Polish children aged between 6 and 17 years. We analyzed a unique set of genes and polymorphisms selected for ADHD and/or obesity based on gene prioritization tools. Polymorphisms in the KCNIP1, SLC1A3, MTHFR, ADRA2A, and SLC6A2 genes proved to be associated with the risk of ADHD in the studied population. The COMT gene polymorphism was one that specifically increased the risk of EBW in the ADHD group. Using the whole-exome sequencing technique, we have shown that the ADHD group contains rare and protein-truncating variants in the FBXL17, DBH, MTHFR, PCDH7, RSPH3, SPTBN1, and TNRC6C genes. In turn, variants in the ADRA2A, DYNC1H1, MAP1A, SEMA6D, and ZNF536 genes were specific for ADHD with EBW. In this way, we confirmed, at the molecular level, the existence of genes specifically predisposing to EBW in ADHD patients, which are associated with the biological pathways involved in the regulation of the reward system, intestinal microbiome, and muscle metabolism. Full article

(This article belongs to the Special Issue Advances in Genetics of Psychiatric Disorders)

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15 pages, 860 KiB

Open AccessArticle

Genetic Variations Associated with Long-Term Treatment Response in Bipolar Depression

by Gerard Anmella, Silvia Vilches, Jordi Espadaler-Mazo, Andrea Murru, Isabella Pacchiarotti, Miquel Tuson, Marina Garriga, Eva Solé, Mercè Brat, Giovanna Fico and Eduard Vieta

Genes 2021, 12(8), 1259; https://0-doi-org.brum.beds.ac.uk/10.3390/genes12081259 - 18 Aug 2021

Cited by 1 | Viewed by 2565

Abstract

Several pharmacogenetic-based decision support tools for psychoactive medication selection are available. However, the scientific evidence of the gene-drug pairs analyzed is mainly based on pharmacogenetic studies in patients with major depression or schizophrenia, and their clinical utility is mostly assessed in major depression. This study aimed at evaluating the impact of individual genes, with pharmacogenetic relevance in other psychiatric conditions, in the response to treatment in bipolar depression. Seventy-six patients diagnosed with bipolar disorder and an index major depressive episode were included in an observational retrospective study. Sociodemographic and clinical data were collected, and all patients were genotyped using a commercial multigene pharmacogenomic-based tool (Neuropharmagen^®, AB-Biotics S.A., Barcelona, Spain). Multiple linear regression was used to identify pharmacogenetic and clinical predictors of efficacy and tolerability of medications. The pharmacogenetic variables response to serotonin-norepinephrine reuptake inhibitors (SNRIs) (ABCB1) and reduced metabolism of quetiapine (CYP3A4) predicted patient response to these medications, respectively. ABCB1 was also linked to the tolerability of SNRIs. An mTOR-related multigenic predictor was also associated with a lower number of adverse effects when including switch and autolytical ideation. Our results suggest that the predictors identified could be useful to guide the pharmacological treatment in bipolar disorder. Additional clinical studies are necessary to confirm these findings. Full article

(This article belongs to the Special Issue Advances in Genetics of Psychiatric Disorders)

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Review

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28 pages, 1133 KiB

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Association and Genetic Expression between Genes Involved in HPA Axis and Suicide Behavior: A Systematic Review

by Yazmín Hernández-Díaz, Alma Delia Genis-Mendoza, Thelma Beatriz González-Castro, Carlos Alfonso Tovilla-Zárate, Isela Esther Juárez-Rojop, María Lilia López-Narváez and Humberto Nicolini

Genes 2021, 12(10), 1608; https://0-doi-org.brum.beds.ac.uk/10.3390/genes12101608 - 13 Oct 2021

Cited by 9 | Viewed by 3309

Abstract

Background: Suicide behavior (SB) has been highly associated with the response to stress and the hypothalamic–pituitary–adrenal (HPA) axis. The aim of this study was to summarize the results obtained in genetic studies that analyzed the HPA axis—stress pathway and SB through a systematic review. Methods: We performed an online search in PubMed, EBSCO, Web of Science, Scopus, and PsycoInfo databases up to May 2021. We followed the PRISMA guidelines for systematic reviews. We included case-control and expression studies that provided data on mRNA expression and single-nucleotide polymorphisms of genes associated with SB. Results: A total of 21,926 individuals participated across 41 studies (not repeats); 34 studies provided data on single-nucleotide polymorphisms in 21,284 participants and 11 studies reported data on mRNA expression in 1034 participants. Ten genes were identified: FKBP5, CRH, CRHBP, CRHR1, CRHR2, NR3C1, NR3C2, SKA2, MC2R, and POMC. Conclusions: Our findings suggest that key stress pathway genes are significantly associated with SB and show potential as biomarkers for SB. Full article

(This article belongs to the Special Issue Advances in Genetics of Psychiatric Disorders)

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