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  1. Article ; Online: Mapping microRNA expression quantitative trait loci in the prenatal human brain implicates miR-1908-5p expression in bipolar disorder and other brain-related traits.

    Toste, Carolina C / O'Donovan, Michael C / Bray, Nicholas J

    Human molecular genetics

    2023  Volume 32, Issue 20, Page(s) 2941–2949

    Abstract: MicroRNA (miRNA) are small non-coding RNA involved in post-transcriptional gene regulation. Given their known involvement in early neurodevelopment processes, we here sought to identify common genetic variants associated with altered miRNA expression in ... ...

    Abstract MicroRNA (miRNA) are small non-coding RNA involved in post-transcriptional gene regulation. Given their known involvement in early neurodevelopment processes, we here sought to identify common genetic variants associated with altered miRNA expression in the prenatal human brain. We performed small RNA sequencing on brain tissue from 112 genome-wide genotyped fetuses from the second trimester of gestation, identifying high-confidence (false discovery rate < 0.05) expression quantitative trait loci for 30 mature miRNA. Integrating our findings with genome-wide association study data for brain-related disorders, we implicate increased prenatal expression of miR-1908-5p as a risk mechanism for bipolar disorder and find that predicted mRNA targets of miR-1908-5p that are expressed in the fetal brain are enriched for common variant genetic association with the condition. Extending these analyses to other brain-related traits, we find that common genetic variation associated with increased miR-1908-5p expression in fetal brain is additionally associated with depressive symptoms, irritability, increased right cerebellum exterior volume and increased sleep duration in the general population. Our findings provide support to the view that altered miRNA expression can influence susceptibility to neuropsychiatric illness and suggest an early neurodevelopmental risk mechanism for bipolar disorder.
    MeSH term(s) Humans ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Quantitative Trait Loci/genetics ; Bipolar Disorder/genetics ; Genome-Wide Association Study ; Brain/metabolism
    Chemical Substances MicroRNAs ; MIRN1908 microRNA, human
    Language English
    Publishing date 2023-07-18
    Publishing country England
    Document type Journal Article
    ZDB-ID 1108742-0
    ISSN 1460-2083 ; 0964-6906
    ISSN (online) 1460-2083
    ISSN 0964-6906
    DOI 10.1093/hmg/ddad118
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  2. Article ; Online: The relationship between case-control differential gene expression from brain tissue and genetic associations in schizophrenia.

    Clifton, Nicholas E / Schulmann, Anton / Holmans, Peter A / O'Donovan, Michael C / Vawter, Marquis P

    American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics

    2023  Volume 192, Issue 5-6, Page(s) 85–92

    Abstract: Large numbers of genetic loci have been identified that are known to contain common risk alleles for schizophrenia, but linking associated alleles to specific risk genes remains challenging. Given that most alleles that influence liability to ... ...

    Abstract Large numbers of genetic loci have been identified that are known to contain common risk alleles for schizophrenia, but linking associated alleles to specific risk genes remains challenging. Given that most alleles that influence liability to schizophrenia are thought to do so by altered gene expression, intuitively, case-control differential gene expression studies should highlight genes with a higher probability of being associated with schizophrenia and could help identify the most likely causal genes within associated loci. Here, we test this hypothesis by comparing transcriptome analysis of the dorsolateral prefrontal cortex from 563 schizophrenia cases and 802 controls with genome-wide association study (GWAS) data from the third wave study of the Psychiatric Genomics Consortium. Genes differentially expressed in schizophrenia were not enriched for common allelic association statistics compared with other brain-expressed genes, nor were they enriched for genes within associated loci previously reported to be prioritized by genetic fine-mapping. Genes prioritized by Summary-based Mendelian Randomization were underexpressed in cases compared to other genes in the same GWAS loci. However, the overall strength and direction of expression change predicted by SMR were not related to that observed in the differential expression data. Overall, this study does not support the hypothesis that genes identified as differentially expressed from RNA sequencing of bulk brain tissue are enriched for those that show evidence for genetic associations. Such data have limited utility for prioritizing genes in currently associated loci in schizophrenia.
    MeSH term(s) Humans ; Schizophrenia/genetics ; Genome-Wide Association Study ; Genetic Predisposition to Disease ; Brain ; Gene Expression/genetics ; Polymorphism, Single Nucleotide/genetics
    Language English
    Publishing date 2023-01-18
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2108616-3
    ISSN 1552-485X ; 1552-4841 ; 0148-7299
    ISSN (online) 1552-485X
    ISSN 1552-4841 ; 0148-7299
    DOI 10.1002/ajmg.b.32931
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  3. Article ; Online: Genomic findings in schizophrenia and their implications.

    Owen, Michael J / Legge, Sophie E / Rees, Elliott / Walters, James T R / O'Donovan, Michael C

    Molecular psychiatry

    2023  Volume 28, Issue 9, Page(s) 3638–3647

    Abstract: There has been substantial progress in understanding the genetics of schizophrenia over the past 15 years. This has revealed a highly polygenic condition with the majority of the currently explained heritability coming from common alleles of small effect ...

    Abstract There has been substantial progress in understanding the genetics of schizophrenia over the past 15 years. This has revealed a highly polygenic condition with the majority of the currently explained heritability coming from common alleles of small effect but with additional contributions from rare copy number and coding variants. Many specific genes and loci have been implicated that provide a firm basis upon which mechanistic research can proceed. These point to disturbances in neuronal, and particularly synaptic, functions that are not confined to a small number of brain regions and circuits. Genetic findings have also revealed the nature of schizophrenia's close relationship to other conditions, particularly bipolar disorder and childhood neurodevelopmental disorders, and provided an explanation for how common risk alleles persist in the population in the face of reduced fecundity. Current genomic approaches only potentially explain around 40% of heritability, but only a small proportion of this is attributable to robustly identified loci. The extreme polygenicity poses challenges for understanding biological mechanisms. The high degree of pleiotropy points to the need for more transdiagnostic research and the shortcomings of current diagnostic criteria as means of delineating biologically distinct strata. It also poses challenges for inferring causality in observational and experimental studies in both humans and model systems. Finally, the Eurocentric bias of genomic studies needs to be rectified to maximise benefits and ensure these are felt across diverse communities. Further advances are likely to come through the application of new and emerging technologies, such as whole-genome and long-read sequencing, to large and diverse samples. Substantive progress in biological understanding will require parallel advances in functional genomics and proteomics applied to the brain across developmental stages. For these efforts to succeed in identifying disease mechanisms and defining novel strata they will need to be combined with sufficiently granular phenotypic data.
    MeSH term(s) Humans ; Child ; Schizophrenia/genetics ; Bipolar Disorder/genetics ; Genome ; Genomics ; Emotions ; Genetic Predisposition to Disease/genetics ; Genome-Wide Association Study
    Language English
    Publishing date 2023-10-18
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 1330655-8
    ISSN 1476-5578 ; 1359-4184
    ISSN (online) 1476-5578
    ISSN 1359-4184
    DOI 10.1038/s41380-023-02293-8
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  4. Article ; Online: Enrichment of the Local Synaptic Translatome for Genetic Risk Associated With Schizophrenia and Autism Spectrum Disorder.

    Clifton, Nicholas E / Lin, Julie Qiaojin / Holt, Christine E / O'Donovan, Michael C / Mill, Jonathan

    Biological psychiatry

    2023  Volume 95, Issue 9, Page(s) 888–895

    Abstract: Background: Genes that encode synaptic proteins or messenger RNA targets of the RNA-binding protein FMRP (fragile X messenger ribonucleoprotein) have been linked to schizophrenia and autism spectrum disorder (ASD) through the enrichment of genetic ... ...

    Abstract Background: Genes that encode synaptic proteins or messenger RNA targets of the RNA-binding protein FMRP (fragile X messenger ribonucleoprotein) have been linked to schizophrenia and autism spectrum disorder (ASD) through the enrichment of genetic variants that confer risk for these disorders. FMRP binds many transcripts with synaptic functions and is thought to regulate their local translation, a process that enables rapid and compartmentalized protein synthesis required for development and plasticity.
    Methods: We used summary statistics from large-scale genome-wide association studies of schizophrenia (74,776 cases, 101,023 controls) and ASD (18,381 cases, 27,969 controls) to test the hypothesis that the subset of synaptic genes that encode localized transcripts is more strongly associated with each disorder than nonlocalized transcripts. We also postulated that this subset of synaptic genes is responsible for associations attributed to FMRP targets.
    Results: Schizophrenia associations were enriched in genes encoding localized synaptic transcripts compared to the remaining synaptic genes or to the remaining localized transcripts; this also applied to ASD associations, although only for transcripts observed after stimulation by fear conditioning. The genetic associations with either disorder captured by these gene sets were independent of those derived from FMRP targets. Schizophrenia association was related to FMRP interactions with messenger RNAs in somata, but not in dendrites, while ASD association was related to FMRP binding in either compartment.
    Conclusions: Our data suggest that synaptic transcripts capable of local translation are particularly relevant to the pathogenesis of schizophrenia and ASD, but they do not characterize the associations attributed to current sets of FMRP targets.
    MeSH term(s) Humans ; Autism Spectrum Disorder/genetics ; Autism Spectrum Disorder/metabolism ; Genome-Wide Association Study ; Schizophrenia/genetics ; Schizophrenia/metabolism ; Fragile X Mental Retardation Protein/genetics ; Fragile X Mental Retardation Protein/metabolism ; Neurons/metabolism
    Chemical Substances Fragile X Mental Retardation Protein (139135-51-6)
    Language English
    Publishing date 2023-12-14
    Publishing country United States
    Document type Journal Article
    ZDB-ID 209434-4
    ISSN 1873-2402 ; 0006-3223
    ISSN (online) 1873-2402
    ISSN 0006-3223
    DOI 10.1016/j.biopsych.2023.12.006
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  5. Article ; Online: Large-Scale Genomics: A Paradigm Shift in Psychiatry?

    Owen, Michael J / O'Donovan, Michael C

    Biological psychiatry

    2020  Volume 89, Issue 1, Page(s) 5–7

    MeSH term(s) Genomics ; Humans ; Mental Disorders/genetics ; Psychiatry
    Language English
    Publishing date 2020-01-31
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 209434-4
    ISSN 1873-2402 ; 0006-3223
    ISSN (online) 1873-2402
    ISSN 0006-3223
    DOI 10.1016/j.biopsych.2020.01.017
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  6. Article: What have we learned from the Psychiatric Genomics Consortium.

    O'Donovan, Michael C

    World psychiatry : official journal of the World Psychiatric Association (WPA)

    2015  Volume 14, Issue 3, Page(s) 291–293

    Language English
    Publishing date 2015-09-25
    Publishing country Italy
    Document type Journal Article
    ZDB-ID 2236130-3
    ISSN 2051-5545 ; 1723-8617
    ISSN (online) 2051-5545
    ISSN 1723-8617
    DOI 10.1002/wps.20270
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  7. Article: Genetic implication of prenatal GABAergic and cholinergic neuron development in susceptibility to schizophrenia.

    Cameron, Darren / Vinh, Ngoc-Nga / Prapaiwongs, Parinda / Perry, Elizabeth A / Walters, James T R / Li, Meng / O'Donovan, Michael C / Bray, Nicholas J

    medRxiv : the preprint server for health sciences

    2023  

    Abstract: Background: The ganglionic eminences are fetal-specific structures that give rise to gamma-aminobutyric acid (GABA)- and acetylcholine- releasing neurons of the forebrain. Given evidence for GABAergic and cholinergic disturbances in schizophrenia, as ... ...

    Abstract Background: The ganglionic eminences are fetal-specific structures that give rise to gamma-aminobutyric acid (GABA)- and acetylcholine- releasing neurons of the forebrain. Given evidence for GABAergic and cholinergic disturbances in schizophrenia, as well as an early neurodevelopmental component to the disorder, we tested the potential involvement of developing cells of the ganglionic eminences in mediating genetic risk for the condition.
    Study design: We combined data from a recent large-scale genome-wide association study of schizophrenia with single cell RNA sequencing data from the human ganglionic eminences to test enrichment of schizophrenia risk variation in genes with high expression specificity for particular developing cell populations within these structures. We additionally performed the single nuclei Assay for Transposase-Accessible Chromatin with Sequencing (snATAC-Seq) to map potential regulatory genomic regions operating in individual cell populations of the human ganglionic eminences, using these to additionally test for enrichment of schizophrenia common genetic variant liability and to functionally annotate non-coding variants associated with the disorder.
    Study results: Schizophrenia common variant liability was enriched in genes with high expression specificity for developing neuron populations that are predicted to form dopamine D1 and D2 receptor expressing GABAergic medium spiny neurons of the striatum, cortical somatostatin-positive GABAergic interneurons, calretinin-positive GABAergic neurons and cholinergic neurons. Consistent with these findings, schizophrenia genetic risk was also concentrated in predicted regulatory genomic sequence mapped in developing neuronal populations of the ganglionic eminences.
    Conclusions: Our study provides evidence for a role of prenatal GABAergic and cholinergic neuron development in later susceptibility to schizophrenia.
    Language English
    Publishing date 2023-12-14
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.12.14.23299948
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  8. Article ; Online: Stratifying early-onset emotional disorders: using genetics to assess persistence in young people of European and South Asian ancestry.

    Dennison, Charlotte A / Martin, Joanna / Shakeshaft, Amy / Riglin, Lucy / Rice, Frances / Lewis, Cathryn M / O'Donovan, Michael C / Thapar, Anita

    Journal of child psychology and psychiatry, and allied disciplines

    2023  Volume 65, Issue 1, Page(s) 42–51

    Abstract: Background: Depression and anxiety are the most common mental health problems in young people. Currently, clinicians are advised to wait before initiating treatment for young people with these disorders as many spontaneously remit. However, others ... ...

    Abstract Background: Depression and anxiety are the most common mental health problems in young people. Currently, clinicians are advised to wait before initiating treatment for young people with these disorders as many spontaneously remit. However, others develop recurrent disorder but this subgroup cannot be identified at the outset. We examined whether psychiatric polygenic scores (PGS) could help inform stratification efforts to predict those at higher risk of recurrence.
    Methods: Probable emotional disorder was examined in two UK population cohorts using the emotional symptoms subscale of the Strengths and Difficulties Questionnaire (SDQ). Those with emotional disorder at two or more time points between ages 5 and 25 years were classed as 'recurrent emotional disorder' (n = 1,643) and those with emotional disorder at one time point as having 'single episode emotional disorder' (n = 1,435, controls n = 8,715). We first examined the relationship between psychiatric PGS and emotional disorders in childhood and adolescence. Second, we tested whether psychiatric PGS added to predictor variables of known association with emotional disorder (neurodevelopmental comorbidity, special educational needs, family history of depression and socioeconomic status) when discriminating between single-episode and recurrent emotional disorder. Analyses were conducted separately in individuals of European and South Asian ancestry.
    Results: Probable emotional disorder was associated with higher PGS for major depressive disorder (MDD), anxiety, broad depression, ADHD and autism spectrum disorder (ASD) in those of European ancestry. Higher MDD and broad depression PGS were associated with emotional disorder in people of South Asian ancestry. Recurrent, compared to single-episode, emotional disorder was associated with ASD and parental psychiatric history. PGS were not associated with episode recurrence, and PGS did not improve discrimination of recurrence when combined with clinical predictors.
    Conclusions: Our findings do not support the use of PGS as a tool to assess the likelihood of recurrence in young people experiencing their first episode of emotional disorder.
    MeSH term(s) Adolescent ; Humans ; Depressive Disorder, Major/epidemiology ; Autism Spectrum Disorder/epidemiology ; Comorbidity ; Anxiety/genetics ; Anxiety Disorders/epidemiology ; Anxiety Disorders/genetics
    Language English
    Publishing date 2023-07-19
    Publishing country England
    Document type Journal Article
    ZDB-ID 218136-8
    ISSN 1469-7610 ; 0021-9630 ; 0373-8086
    ISSN (online) 1469-7610
    ISSN 0021-9630 ; 0373-8086
    DOI 10.1111/jcpp.13862
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  9. Article ; Online: Family-based analysis of the contribution of rare and common genetic variants to school performance in schizophrenia.

    Rammos, Alexandros / Kirov, George / Hubbard, Leon / Walters, James T R / Holmans, Peter / Owen, Michael J / O'Donovan, Michael C / Rees, Elliott

    Molecular psychiatry

    2023  Volume 28, Issue 5, Page(s) 2081–2087

    Abstract: Impaired cognition in schizophrenia is associated with worse functional outcomes. While genetic factors are known to contribute to variation in cognition in schizophrenia, few rare coding variants with strong effects have been identified, and the ... ...

    Abstract Impaired cognition in schizophrenia is associated with worse functional outcomes. While genetic factors are known to contribute to variation in cognition in schizophrenia, few rare coding variants with strong effects have been identified, and the relative effects from de novo, inherited and non-transmitted alleles are unknown. We used array and exome sequencing data from 656 proband-parent trios to examine the contribution of common and rare variants to school performance, and by implication cognitive function, in schizophrenia. Parental transmission of common alleles contributing to higher educational attainment (p value = 0.00015; OR = 2.63) and intelligence (p value = 0.00009; OR = 2.80), but not to schizophrenia, were associated with higher proband school performance. No significant effects were seen for non-transmitted parental common alleles. Probands with lower school performance were enriched for damaging de novo coding variants in genes associated with developmental disorders (DD) (p value = 0.00026; OR = 11.6). Damaging, ultra-rare coding variants in DD genes that were transmitted or non-transmitted from parents, had no effects on school performance. Among probands with lower school performance, those with damaging de novo coding variants in DD genes had a higher rate of comorbid mild intellectual disability (p value = 0.0002; OR = 15.6). Overall, we provide evidence for rare and common genetic contributions to school performance in schizophrenia. The strong effects for damaging de novo coding variants in DD genes provide further evidence that cognitive impairment in schizophrenia has a shared aetiology with developmental disorders. Furthermore, we report no evidence in this sample that non-transmitted parental common alleles for cognitive traits contributed to school performance in schizophrenia via indirect effects on the environment.
    MeSH term(s) Humans ; Schizophrenia/genetics ; Mutation ; Genetic Predisposition to Disease/genetics ; Intellectual Disability/genetics ; Family
    Language English
    Publishing date 2023-03-13
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1330655-8
    ISSN 1476-5578 ; 1359-4184
    ISSN (online) 1476-5578
    ISSN 1359-4184
    DOI 10.1038/s41380-023-02013-2
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  10. Article ; Online: Estimating the impact of transmitted and non-transmitted psychiatric and neurodevelopmental polygenic scores on youth emotional problems.

    Shakeshaft, Amy / Martin, Joanna / Dennison, Charlotte A / Riglin, Lucy / Lewis, Cathryn M / O'Donovan, Michael C / Thapar, Anita

    Molecular psychiatry

    2023  

    Abstract: Anxiety and depression (emotional disorders) are familial and heritable, especially when onset is early. However, other cross-generational studies suggest transmission of youth emotional problems is explained by mainly environmental risks. We set out to ... ...

    Abstract Anxiety and depression (emotional disorders) are familial and heritable, especially when onset is early. However, other cross-generational studies suggest transmission of youth emotional problems is explained by mainly environmental risks. We set out to test the contribution of parental non-transmitted genetic liability, as indexed by psychiatric/neurodevelopmental common polygenic liability, to youth emotional problems using a UK population-based cohort: the Millennium Cohort Study. European (N = 6328) and South Asian (N = 814) ancestries were included, as well as a subset with genomic data from both parents (European: N = 2809; South Asian: N = 254). We examined the association of transmitted (PGS
    Language English
    Publishing date 2023-11-21
    Publishing country England
    Document type Journal Article
    ZDB-ID 1330655-8
    ISSN 1476-5578 ; 1359-4184
    ISSN (online) 1476-5578
    ISSN 1359-4184
    DOI 10.1038/s41380-023-02319-1
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