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Identification of risk loci with shared effects on five major psychiatric disorders: a genome-wide analysis
Open accessAbstract
Background Findings from family and twin studies suggest that genetic contributions to psychiatric disorders do not in all cases map to present diagnostic categories. We aimed to identify specific variants underlying genetic effects shared between the five disorders in the Psychiatric Genomics Consortium: autism spectrum disorder, attention deficit-hyperactivity disorder, bipolar disorder, major depressive disorder, and schizophrenia.Methods We analysed genome-wide single-nucleotide polymorphism (SNP) data for the five disorders in 33,332 cases and 27,888 controls of European ancestory. To characterise allelic effects on each disorder, we applied a multinomial logistic regression procedure with model selection to identify the best-fitting model of relations between genotype and phenotype. We examined cross-disorder effects of genome-wide significant loci previously identified for bipolar disorder and schizophrenia, and used polygenic risk-score analysis to examine such effects from a broader set of common variants. We undertook pathway analyses to establish the biological associations underlying genetic overlap for the five disorders. We used enrichment analysis of expression quantitative trait loci (eQTL) data to assess whether SNPs with cross-disorder association were enriched for regulatory SNPs in post-mortem brain-tissue samples.Findings SNPs at four loci surpassed the cutoff for genome-wide significance (p<5×10(-8)) in the primary analysis: regions on chromosomes 3p21 and 10q24, and SNPs within two L-type voltage-gated calcium channel subunits, CACNA1C and CACNB2. Model selection analysis supported effects of these loci for several disorders. Loci previously associated with bipolar disorder or schizophrenia had variable diagnostic specificity. Polygenic risk scores showed cross-disorder associations, notably between adult-onset disorders. Pathway analysis supported a role for calcium channel signalling genes for all five disorders. Finally, SNPs with evidence of cross-disorder association were enriched for brain eQTL markers.Interpretation Our findings show that specific SNPs are associated with a range of psychiatric disorders of childhood onset or adult onset. In particular, variation in calcium-channel activity genes seems to have pleiotropic effects on psychopathology. These results provide evidence relevant to the goal of moving beyond descriptive syndromes in psychiatry, and towards a nosology informed by disease cause.Funding National Institute of Mental Health.
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“Interestingly, common genetic factors contributing to depression and autism have been reported (45, 46).”
From Gene × Environment Interactions in Autism Spectrum Disorders: Role of Epigenetic Mechanisms (2014) · cites this paper as [46]
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“On the basis of data from genomewide association studies (GWAS), approximately 40% of the heritability of ADHD can be attributed to numerous common genetic variants 37 .”
From Attention-deficit/hyperactivity disorder (2015) · cites this paper as [37]
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“They include unhealthy lifestyle, poorer (self)care adherence, medication side effects, shared pathophysiology including e.g. upregulation of immune-endocrine stress systems and genetic pleiotropy (see 39, 247 for a review that gives more details).”
From Major depressive disorder (2016) · cites this paper as [39]
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“Furthermore, combined GWAS of ADHD, autism spectrum disorders, depression, bipolar disorder and schizophrenia identified four genome-wide significant loci shared by these disorders 37 .”
From Attention-deficit/hyperactivity disorder (2015) · cites this paper as [37]
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In the citing paper
“We suggest that although selfmedication plays a part in the co-occurrence of mental health disorders and substance-related disorders, a shared liability between the disorders likewise plays a role.”
From Childhood Psychiatric Disorders as Risk Factor for Subsequent Substance Abuse: A Meta-Analysis. (2017) · cites this paper as [64]
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“Given the significant genetic overlap between various psychiatric conditions and ASD, heritability likely contributes to these relationships (53–55).”
From Maternal Psychiatric Conditions, Treatment With Selective Serotonin Reuptake Inhibitors, and Neurodevelopmental Disorders (2021) · cites this paper as [54]
In the citing paper
“Recent findings suggest the possibility that not only single, but also aggregate molecular genetic risk factors, linked in particular to alterations in calcium-channel signaling, are shared between autism and four other psychiatric disorders (schizophrenia, attention-deficit hyperactivity disorder, bipolar disorder, and major depressive disorder) (45, 46).”
From Gene × Environment Interactions in Autism Spectrum Disorders: Role of Epigenetic Mechanisms (2014) · cites this paper as [46]
In the citing paper
“Studies with full genomic analyses of tens or even hundreds of thousands of participants sometimes identify cumulatively meaningful genetic risk factors, but they involve hundreds if not thousands of alleles, the specific functions of which are often not understood (Crespi, 2020; Cross-Disorder Group of the Psychiatric Genomics Consortium, 2013).”
From A process-based approach to psychological diagnosis and treatment:The conceptual and treatment utility of an extended evolutionary meta model (2020) · cites this paper as Cross-Disorder Group of the Psychiatric Genomics Consortium, 2013
In the citing paper
“High levels of psychiatric comorbidity and heterogeneity, fluid symptom trajectories, cross-diagnostic overlap in genetic and neurobiological factors, and the limited efficacy of many psychiatric treatments restrict our understanding of the neurobiology of mental illness based on categorical diagnoses [3–6].”
From Toward a neurocircuit-based taxonomy to guide treatment of obsessive-compulsive disorder (2021) · cites this paper as [4]
In the citing paper
“We note that the most significant pathway identified from the PGC cross-disorder analysis3 (GO:0005262, calcium channel activity) also showed nominally significant enrichment in our analysis, confirming a role for calcium channel activity in these disorders.”
From Psychiatric genome-wide association study analyses implicate neuronal, immune and histone pathways (2015) · cites this paper as [3]
In the citing paper
“has also shown clear evidence of shared genetic risk at individual loci3”
From Psychiatric genome-wide association study analyses implicate neuronal, immune and histone pathways (2015) · cites this paper as [3]
In the citing paper
“the most significant pathway (GO:0005262, calcium channel activity) from the previous PGC Cross Disorder group SNP-based meta-analysis GWAS3 across the five disorders was found to show nominally significant association in our pathway level meta-analysis across all five disorders (P = 3.13 × 10−3) and also in SCZ, MDD and BIP (P = 8.07 × 10−3).”
From Psychiatric genome-wide association study analyses implicate neuronal, immune and histone pathways (2015) · cites this paper as [3]
In the citing paper
“Stringent and standardized quality control procedures were applied as previously described3.”
From Psychiatric genome-wide association study analyses implicate neuronal, immune and histone pathways (2015) · cites this paper as [3]
In the citing paper
“However, evidence is increasing that inflammation and specifically cytokine signaling play a role in the pathophysiology of psychiatric disorders.”
From Cytokine Research in Depression: Principles, Challenges, and Open Questions (2019) · cites this paper as [118]
In the citing paper
“There is considerable evidence that genetic risk factors for psychiatric disorders are closely related to cytokines or other functions of the immune system.”
From Cytokine Research in Depression: Principles, Challenges, and Open Questions (2019) · cites this paper as [118]
In the citing paper
“Genome-wide association studies (GWAS) have identified immune pathway genes that significantly contribute to the risk of psychiatric disorders (118).”
From Cytokine Research in Depression: Principles, Challenges, and Open Questions (2019) · cites this paper as [118]
In the citing paper
“Alterations in other genes implicated in E/T coupling have been observed before in ASD individuals and include Ca2+ signaling components such as the voltage-dependent channels Cav1.2 (CACNA1C), Cav1.3 (CACNA1D) and the α-δ auxiliary subunit of L-type voltage-gated Ca2+ channels (CACNA2D3) [102, 103].”
In the citing paper
“Several reports have now confirmed an association between the LTCC CACNA1C gene and neurodevelopmental disorders25,58.”
From Neuronal defects in a human cellular model of 22q11.2 deletion syndrome (2020) · cites this paper as [25]
In the citing paper
“Biological links such as single nucleotide polymorphisms (4,5), brain structure (6,7), or functional connectivity (8,9) to specific disorders are limited.”
From Methods and challenges for assessing heterogeneity (2020) · cites this paper as [5]
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Citations
Cites
Model selection and multimodel inference: a practical information-theoretic approach.
Guthery, F. S., Burnham, K. P., & Anderson, D. R. (2003) · The Journal of Wildlife Management · doi:10.2307/3802723 · Cited by 41,495
Common polygenic variation contributes to risk of schizophrenia and bipolar disorder
The International Schizophrenia Consortium (2009) · Nature · doi:10.1038/nature08185 · Cited by 4,821
Lichtenstein, P., Yip, B. H., Björk, C., Pawitan, Y., Cannon, T. D., Sullivan, P. F., & Hultman, C. M. (2009) · The Lancet · doi:10.1016/s0140-6736(09)60072-6 · Cited by 2,125
Genome-wide association study identifies five new schizophrenia loci
The Schizophrenia Psychiatric Genome-Wide Association Study (GWAS) Consortium (2011) · Nature Genetics · doi:10.1038/ng.940 · Cited by 1,919
Psychiatric GWAS Consortium Bipolar Disorder Working Group, Sklar, P., Ripke, S., Scott, L. J., Andreassen, O. A., Cichon, S., Craddock, N., Edenberg, H. J., Nurnberger, J. I., Rietschel, M., et al. (2011) · Nature Genetics · doi:10.1038/ng.943 · Cited by 1,344
Trait-associated SNPs are more likely to be eQTLs: annotation to enhance discovery from GWAS
Nicolae, D. L., Gamazon, E., Zhang, W., Duan, S., Dolan, M. E., & Cox, N. J. (2010) · PLoS Genetics · doi:10.1371/journal.pgen.1000888 · Cited by 1,292
Wellcome Trust Case Control Consortium, Ferreira, M. A. R., O'Donovan, M. C., Meng, Y. A., Jones, I. R., Ruderfer, D. M., Jones, L., Fan, J., Kirov, G., Perlis, R. H., et al. (2008) · Nature Genetics · doi:10.1038/ng.209 · Cited by 1,237
Population genomics of human gene expression
Stranger, B. E., Nica, A. C., Forrest, M. S., Dimas, A. S., Bird, C., Beazley, C., Ingle, C., Dunning, M., Flicek, P., Koller, D., et al. (2007) · Nature Genetics · doi:10.1038/ng2142 · Cited by 1,153
A mega-analysis of genome-wide association studies for major depressive disorder
Major Depressive Disorder Working Group of the Psychiatric GWAS Consortium, Ripke, S., Wray, N. R., Lewis, C. M., Hamilton, S. P., Weissman, M. M., Breen, G., Byrne, E. M., Blackwood, D. H. R., Boomsma, D. I., et al. (2013) · Molecular Psychiatry · doi:10.1038/mp.2012.21 · Cited by 1,120
Identification of loci associated with schizophrenia by genome-wide association and follow-up
Molecular Genetics of Schizophrenia Collaboration, O'Donovan, M. C., Craddock, N., Norton, N., Williams, H., Peirce, T., Moskvina, V., Nikolov, I., Hamshere, M., Carroll, L., et al. (2008) · Nature Genetics · doi:10.1038/ng.201 · Cited by 1,070
Mapping the Genetic Architecture of Gene Expression in Human Liver
Schadt, E. E., Molony, C. M., Chudin, E., Hao, K., Yang, X., Lum, P. Y., Kasarskis, A., Zhang, B., Wang, S. S.-M., Suver, C., et al. (2008) · PLoS Biology · doi:10.1371/journal.pbio.0060107 · Cited by 918
CNVs: Harbingers of a Rare Variant Revolution in Psychiatric Genetics
Malhotra, D., & Sebat, J. (2012) · Cell · doi:10.1016/j.cell.2012.02.039 · Cited by 854
The genetics of autism spectrum disorders and related neuropsychiatric disorders in childhood
Lichtenstein, P., Carlström, E., Råstam, M., Gillberg, C., & Anckarsäter, H. (2010) · American Journal of Psychiatry · doi:10.1176/appi.ajp.2010.10020223 · Cited by 738
Family, twin, and adoption studies of bipolar disorder
Smoller, J. W., & Finn, C. T. (2003) · American Journal of Medical Genetics Part C Seminars in Medical Genetics · doi:10.1002/ajmg.c.20013 · Cited by 714
Temporal dynamics and genetic control of transcription in the human prefrontal cortex
Colantuoni, C., Lipska, B. K., Ye, T., Hyde, T. M., Tao, R., Leek, J. T., Colantuoni, E. A., Elkahloun, A. G., Herman, M. M., Weinberger, D. R., et al. (2011) · Nature · doi:10.1038/nature10524 · Cited by 685
Pervasive Sharing of Genetic Effects in Autoimmune Disease
Cotsapas, C., Voight, B. F., Rossin, E., Lage, K., Neale, B. M., Wallace, C., Abecasis, G. R., Barrett, J. C., Behrens, T., Cho, J., et al. (2011) · PLoS Genetics · doi:10.1371/journal.pgen.1002254 · Cited by 606
Shared heritability of attention-deficit/hyperactivity disorder and autism spectrum disorder
Rommelse, N. N. J., Franke, B., Geurts, H. M., Hartman, C. A., & Buitelaar, J. K. (2010) · European Child & Adolescent Psychiatry · doi:10.1007/s00787-010-0092-x · Cited by 564
Practical aspects of imputation-driven meta-analysis of genome-wide association studies
de Bakker, P. I. W., Ferreira, M. A. R., Jia, X., Neale, B. M., Raychaudhuri, S., & Voight, B. F. (2008) · Human Molecular Genetics · doi:10.1093/hmg/ddn288 · Cited by 531
Wellcome Trust Case Control Consortium, Green, E. K., Grozeva, D., Jones, I., Jones, L., Kirov, G., Caesar, S., Gordon-Smith, K., Fraser, C., Forty, L., et al. (2010) · Molecular Psychiatry · doi:10.1038/mp.2009.49 · Cited by 526
A survey of genetic human cortical gene expression
Myers, A. J., Gibbs, J. R., Webster, J. A., Rohrer, K., Zhao, A., Marlowe, L., Kaleem, M., Leung, D., Bryden, L., Nath, P., et al. (2007) · Nature Genetics · doi:10.1038/ng.2007.16 · Cited by 479
Ronald, A., Simonoff, E., Kuntsi, J., Asherson, P., & Plomin, R. (2008) · Journal of Child Psychology and Psychiatry · doi:10.1111/j.1469-7610.2007.01857.x · Cited by 466
Meta-Analysis of Genome-Wide Association Studies of Attention-Deficit/Hyperactivity Disorder
Neale, B. M., Medland, S. E., Ripke, S., Asherson, P., Franke, B., Lesch, K.-P., Faraone, S. V., Nguyen, T. T., Schäfer, H., Holmans, P., et al. (2010) · Journal of the American Academy of Child & Adolescent Psychiatry · doi:10.1016/j.jaac.2010.06.008 · Cited by 450
Levinson, D. F., Duan, J., Oh, S., Wang, K., Sanders, A. R., Shi, J., Zhang, N., Mowry, B. J., Olincy, A., Amin, F., et al. (2011) · American Journal of Psychiatry · doi:10.1176/appi.ajp.2010.10060876 · Cited by 434
Rapoport, J. L., Chavez, A. M., GREENSTEIN, D. K., Addington, A. M., & Gogtay, N. (2008) · Journal of the American Academy of Child & Adolescent Psychiatry · doi:10.1097/chi.0b013e31818b1c63 · Cited by 409
The β Subunit of Voltage-Gated Ca 2+ Channels
Buraei, Z., & Yang, J. (2010) · Physiological Reviews · doi:10.1152/physrev.00057.2009 · Cited by 399
Continuity and Discontinuity of Affective Disorders and Schizophrenia
Maier, W. (1993) · Archives of General Psychiatry · doi:10.1001/archpsyc.1993.01820230041004 · Cited by 384
Zhernakova, A., Stahl, E. A., Trynka, G., Raychaudhuri, S., Festen, E. A. M., Franke, L., Westra, H.-J., Fehrmann, R. S. N., Kurreeman, F. A. S., Thomson, B. P., et al. (2011) · PLoS Genetics · doi:10.1371/journal.pgen.1002004 · Cited by 362
Genetic Variation in CACNA1C Affects Brain Circuitries Related to Mental Illness
Bigos, K. L., Mattay, V. S., Callicott, J. H., Straub, R. E., Vakkalanka, R., Kolachana, B. S., Hyde, T. M., Lipska, B. K., Kleinman, J. E., & Weinberger, D. R. (2010) · Archives of General Psychiatry · doi:10.1001/archgenpsychiatry.2010.96 · Cited by 323
Genome-wide association and meta-analysis of bipolar disorder in individuals of European ancestry
Scott, L. J., Muglia, P., Kong, X., Guan, W., Flickinger, M., Upmanyu, R., Tozzi, F., Li, J. Z., Burmeister, M., Absher, D., et al. (2009) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0813386106 · Cited by 322
Genetic Control of Human Brain Transcript Expression in Alzheimer Disease
Webster, J. A., Gibbs, J. R., Clarke, J., Ray, M., Zhang, W., Holmans, P., Rohrer, K., Zhao, A., Marlowe, L., Kaleem, M., et al. (2009) · The American Journal of Human Genetics · doi:10.1016/j.ajhg.2009.03.011 · Cited by 304
Williams, N. M., Franke, B., Mick, E., Anney, R. J. L., Freitag, C. M., Gill, M., Thapar, A., O'Donovan, M. C., Owen, M. J., Holmans, P., et al. (2012) · American Journal of Psychiatry · doi:10.1176/appi.ajp.2011.11060822 · Cited by 290
Cichon, S., Mühleisen, T. W., Degenhardt, F. A., Mattheisen, M., Miró, X., Strohmaier, J., Steffens, M., Meesters, C., Herms, S., Weingarten, M., et al. (2011) · The American Journal of Human Genetics · doi:10.1016/j.ajhg.2011.01.017 · Cited by 286
Is schizophrenia on the autism spectrum?
King, B. H., & Lord, C. (2010) · Brain Research · doi:10.1016/j.brainres.2010.11.031 · Cited by 260
Athanasiu, L., Mattingsdal, M., Kähler, A. K., Brown, A. A., Gústafsson, Ó., Agartz, I., Giegling, I., Muglia, P., Cichon, S., Rietschel, M., et al. (2010) · Journal of Psychiatric Research · doi:10.1016/j.jpsychires.2010.02.002 · Cited by 218
Cross-disorder genomewide analysis of schizophrenia, bipolar disorder, and depression
Huang, J., Perlis, R. H., Lee, P. H., Rush, A. J., Fava, M., Sachs, G. S., Lieberman, J., Hamilton, S. P., Sullivan, P., Sklar, P., et al. (2010) · American Journal of Psychiatry · doi:10.1176/appi.ajp.2010.09091335 · Cited by 213
Willemsen, M. H., Vallès, A., Kirkels, L. A. M. H., Mastebroek, M., Olde Loohuis, N., Kos, A., Wissink-Lindhout, W. M., de Brouwer, A. P. M., Nillesen, W. M., Pfundt, R., et al. (2011) · Journal of Medical Genetics · doi:10.1136/jmedgenet-2011-100294 · Cited by 202
Meta-analysis of genome-wide association data of bipolar disorder and major depressive disorder
Liu, Y., Blackwood, D., Caesar, S., de Geus, E. J. C., FARMER, A. E., Ferreira, M. A. R., Ferrier, I. N., Fraser, C., Gordon‐Smith, K., Green, E., et al. (2010) · Molecular Psychiatry · doi:10.1038/mp.2009.107 · Cited by 190
CACNA1C (rs1006737) is associated with schizophrenia
Nyegaard, M., Demontis, D., Foldager, L., Hedemand, A., Flint, T. J., Sørensen, K. M., Andersen, P. S., Nordentoft, M., Werge, T., Pedersen, C. B., et al. (2010) · Molecular Psychiatry · doi:10.1038/mp.2009.69 · Cited by 182
McMahon, F. J., Akula, N., Schulze, T. G., Detera‐Wadleigh, S. D., Steele, C. J. M., Wendland, J. R., Breuer, R., Strohmaier, J., Rietschel, M., Muglia, P., et al. (2010) · Nature Genetics · doi:10.1038/ng.523 · Cited by 180
Ding, J., Gudjonsson, J. E., Liang, L., Stuart, P. E., Li, Y., Chen, W., Weichenthal, M., Ellinghaus, E., Franke, A., Cookson, W., et al. (2010) · The American Journal of Human Genetics · doi:10.1016/j.ajhg.2010.10.024 · Cited by 180
Brain Function in Carriers of a Genome-wide Supported Bipolar Disorder Variant
Erk, S., Meyer‐Lindenberg, A., Schnell, K., von Boberfeld, C. O., Esslinger, C., Kirsch, P., Grimm, O., Arnold, C., Haddad, L., Witt, S. H., et al. (2010) · Archives of General Psychiatry · doi:10.1001/archgenpsychiatry.2010.94 · Cited by 176
Genome-wide association study of bipolar I disorder in the Han Chinese population
Lee, M. T. M., Chen, C. H., Lee, C. S., Chen, C. C., Chong, M. Y., Ouyang, W. C., Chiu, N. Y., Chuo, L. J., Chen, C. Y., Tan, H. K. L., et al. (2011) · Molecular Psychiatry · doi:10.1038/mp.2010.43 · Cited by 157
CaV1.2 channelopathies: from arrhythmias to autism, bipolar disorder, and immunodeficiency
Liao, P. H., & Soong, T. W. (2009) · Pflügers Archiv - European Journal of Physiology · doi:10.1007/s00424-009-0753-0 · Cited by 99
Effects of aCACNA1Cgenotype on attention networks in healthy individuals
Thimm, M., Kircher, T. T. J., Kellermann, T., Markov, V., Krach, S., Jansen, A., Zerres, K., Eggermann, T., Stöcker, T., Shah, N. J., et al. (2010) · Psychological Medicine · doi:10.1017/s0033291710002217 · Cited by 96
Mühleisen, T. W., Mattheisen, M., Strohmaier, J., Degenhardt, F., Priebe, L., Schultz, C. C., Breuer, R., Meier, S., Hoffmann, P., Rivandeneira, F., et al. (2012) · Schizophrenia Research · doi:10.1016/j.schres.2012.03.007 · Cited by 80
Wray, N. R., Lee, S., & Kendler, K. S. (2012) · European Journal of Human Genetics · doi:10.1038/ejhg.2011.257 · Cited by 79
Zeng, Z., Wang, T., Li, T., Li, Y., Chen, P., Zhao, Q., Liu, J., Li, J., Feng, G., He, L., et al. (2010) · Molecular Psychiatry · doi:10.1038/mp.2010.86 · Cited by 47
Breen, G. D., Lewis, C. M., Vassos, E., Pergadia, M. L., Blackwood, D., Boomsma, D. I., Penninx, B. W. J. H., Sullivan, P. F., Pedroso, I., Collier, D. A., et al. (2010) · Nature Genetics · doi:10.1038/ng0111-3 · Cited by 27
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Boomsma, D. I. (2006) · Twin Research and Human Genetics · doi:10.1375/183242706776382473 · Cited by 16
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Metadata
- Venue
- The Lancet
- Publisher
- Elsevier BV
- Published
- 2013-04
- Volume
- 381
- Issue
- 9875
- Pages
- 1371-1379
- ISSN
- 0099-5355 (ISSN-L)
- 0140-6736
- PMC
- PMC3714010
- OpenAlex
- W2139852368
- Cited by
- 3,010
- References
- 52
- Citations by year
- 2026: 70 · 2025: 104 · 2024: 141 · 2023: 117 · 2022: 166 · 2021: 223 · 2020: 249 · 2019: 235 · 2018: 282 · 2017: 317 · 2016: 288 · 2015: 322 · 2014: 303 · 2013: 176
- FWCI
- 240.86
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
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- The Lancet (publishedVersion)
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- Zurich Open Repository and Archive (University of Zurich) (submittedVersion)
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- Funders
- National Institutes of Health
- National Institute on Alcohol Abuse and Alcoholism (K05AA017688)
- National Institute of Mental Health (R01MH077139, U01MH085520, R01MH100027, R01MH094400, U01MH094421, K99MH101367, MH085520, R01MH083094, K24MH094614, R01MH106595)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Health Sciences › Medicine › Psychiatry and Mental health › Bipolar Disorder and Treatment
- Keywords
- mental illness, genetic susceptibility loci, autism spectrum disorder, attention deficit hyperactivity disorder, bipolar disorder, major depressive disorder, schizophrenia, CACNA1C, CACNB2, L-type calcium channels, polygenic risk score, expression quantitative trait loci, pleiotropy, disease classification, childhood-onset disorders
- MeSH terms
- Adult, Attention Deficit Disorder with Hyperactivity, Bipolar Disorder, Child, Child Development Disorders, Pervasive, Depressive Disorder, Major, Major Depressive Disorder, Humans, Schizophrenia, Logistic Models, Age of Onset, Polymorphism, Single Nucleotide, Calcium Channels, L-Type, Genome-Wide Association Study, Genetic Loci
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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