The DOI matches its Crossref record; 50 of the 52 references it cites were found in a registry or an index.
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.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The cited source doesn’t support the claim as written.
In the citing paper
“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]
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“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]
The cited source says what the claim attributes to it.
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]
The check wasn’t confident either way, so it gives no verdict — never disputed.
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]
Experimental — accuracy not yet measuredIn the citing paper
“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]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
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
Cited by
Sorted by citations
Items 401–500 of 1,027
A decade in psychiatric GWAS research
Horwitz, T. B., Lam, K., Chen, Y., Xia, Y., & Liu, C. (2018) · Molecular Psychiatry · doi:10.1038/s41380-018-0055-z · Cited by 108
Transcriptome analysis and functional characterization of cerebral organoids in bipolar disorder
Kathuria, A., Lopez-Lengowski, K., Vater, M., McPhie, D. L., Cohen, B. M., & Karmacharya, R. (2020) · Genome Medicine · doi:10.1186/s13073-020-00733-6 · Cited by 105
Wang, C., Martins-Bach, A. B., Alfaro‐Almagro, F., Douaud, G., Klein, J. C., Llera, A., Fiscone, C., Bowtell, R. W., Elliott, L. T., Smith, S. M., et al. (2022) · Nature Neuroscience · doi:10.1038/s41593-022-01074-w · Cited by 105
Chen, M.-H., Hsu, J.-W., Huang, K.-L., Su, T.-P., Li, C.-T., Lin, W.-C., Tsai, S.-J., Cheng, C.-M., Chang, W.-H., Pan, T.-L., et al. (2019) · Psychological Medicine · doi:10.1017/s003329171800332x · Cited by 106
Neurodevelopmental origins of bipolar disorder: iPSC models
O’Shea, K. S., & McInnis, M. G. (2015) · Molecular and Cellular Neuroscience · doi:10.1016/j.mcn.2015.11.006 · Cited by 111
Understanding Psychosis and Schizophrenia
Cooke, A. (2014) · Cited by 163
Liu, C. H., Keshavan, M. S., Tronick, E., & Seidman, L. J. (2015) · Schizophrenia Bulletin · doi:10.1093/schbul/sbv047 · Cited by 104
Duan, J., Shi, J., Fiorentino, A., Leites, C., Chen, X., Moy, W., Chen, J., Alexandrov, B. S., Usheva, A., S, D. H. B., et al. (2014) · The American Journal of Human Genetics · doi:10.1016/j.ajhg.2014.11.001 · Cited by 107
Associations between Polygenic Risk for Psychiatric Disorders and Substance Involvement
Carey, C. E., Arpana Agrawal, A., Bucholz, K. K., Hartz, S. M., Lynskey, M. T., Nelson, E. C., Bierut, L. J., & Bogdan, R. (2016) · Frontiers in Genetics · doi:10.3389/fgene.2016.00149 · Cited by 107
Pinto, J. V., Moulin, T. C., & Amaral, O. B. (2017) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2017.10.001 · Cited by 103
Biomarkers in Posttraumatic Stress Disorder: Overview and Implications for Future Research
Schmidt, U., Kaltwasser, S. F., & Wotjak, C. T. (2013) · Disease Markers · doi:10.1155/2013/835876 · Cited by 103
Crabtree, G. W., & Gogos, J. A. (2014) · Frontiers in Synaptic Neuroscience · doi:10.3389/fnsyn.2014.00028 · Cited by 106
Epigenetic mechanisms in schizophrenia
Shorter, K. R., & Miller, B. H. (2015) · Progress in Biophysics and Molecular Biology · doi:10.1016/j.pbiomolbio.2015.04.008 · Cited by 107
SorCS2 is required for BDNF-dependent plasticity in the hippocampus
Glerup, S., Bølcho, U., Mølgaard, S., Boggild, S., Vægter, C. B., Smith, A. H., Nieto-González, J. L., Ovesen, P. L., Pedersen, L. F., Fjorback, A. N., et al. (2016) · Molecular Psychiatry · doi:10.1038/mp.2016.108 · Cited by 99
Shared and Distinct Functional Architectures of Brain Networks Across Psychiatric Disorders
Xia, M., Womer, F. Y., Chang, M., Zhu, Y., Zhou, Q., Edmiston, E. K., Jiang, X., Wei, S., Duan, J., Xu, K., et al. (2018) · Schizophrenia Bulletin · doi:10.1093/schbul/sby046 · Cited by 103
Chang, M., Womer, F. Y., Edmiston, E. K., Bai, C., Zhou, Q., Jiang, X., Wei, S., Wei, Y., Ye, Y., Huang, H., et al. (2017) · Schizophrenia Bulletin · doi:10.1093/schbul/sbx028 · Cited by 102
Yang, Z., Wu, H., Lee, P. H., Tsetsos, F., Davis, L. K., Yu, D., Lee, S., Dalsgaard, S., Haavik, J., Barta, C., et al. (2021) · Biological Psychiatry · doi:10.1016/j.biopsych.2020.12.028 · Cited by 105
Atypical Lateralization in Neurodevelopmental and Psychiatric Disorders: What Is the Role of Stress?
Berretz, G., Wolf, O. T., Güntürkün, O., & Ocklenburg, S. (2020) · Cortex · doi:10.1016/j.cortex.2019.12.019 · Cited by 100
Bulik, C. M., Blake, L. E., & Austin, J. (2019) · Psychiatric Clinics of North America · doi:10.1016/j.psc.2018.10.007 · Cited by 129
Data use under the NIH GWAS Data Sharing Policy and future directions
Committees, T. N. I. O. H. G. D. S. G. (2014) · Nature Genetics · doi:10.1038/ng.3062 · Cited by 100
L-type calcium channels as drug targets in CNS disorders
Ortner, N. J., & Striessnig, J. (2015) · Channels · doi:10.1080/19336950.2015.1048936 · Cited by 107
Klein, M., Onnink, A. M. H., van Eijk, K. R., Wolfers, T., Harich, B., Shi, Y., Dammers, J. T., Vásquez, A. A., Hoogman, M., & Franke, B. (2017) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2017.01.013 · Cited by 116
Toward a Better Understanding of Neuronal Migration Deficits in Autism Spectrum Disorders
Pan, Y.-H., Wu, N., & Yuan, X. (2019) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2019.00205 · Cited by 100
Nutrient Sensing, Signaling and Ageing: The Role of IGF-1 and mTOR in Ageing and Age-Related Disease
Johnson, S. C. (2018) · Sub-cellular biochemistry/Subcellular biochemistry · doi:10.1007/978-981-13-2835-0_3 · Cited by 104
Linking risk factors and outcomes in autism spectrum disorder: is there evidence for resilience?
Elsabbagh, M. (2020) · BMJ · doi:10.1136/bmj.l6880 · Cited by 110
Cytokine Imbalance in Schizophrenia. From Research to Clinic: Potential Implications for Treatment
Reale, M., Costantini, E., & Greig, N. H. (2021) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2021.536257 · Cited by 111
Xue, K., Guo, L., Zhu, W., Liang, S., Xu, Q., Ma, L., Liu, M., Zhang, Y., & Liu, F. (2022) · Neuropsychopharmacology · doi:10.1038/s41386-022-01474-3 · Cited by 98
Harkness, A. R., Reynolds, S. M., & Lilienfeld, S. O. (2013) · Journal of Personality Assessment · doi:10.1080/00223891.2013.823438 · Cited by 105
Parental Mental Disorder and Offspring Criminal Behavior
Moffitt, T. E. (1987) · Psychiatry · doi:10.1080/00332747.1987.11024366 · Cited by 98
Stergiakouli, E., Davey Smith, G., Martin, J., Skuse, D. H., Viechtbauer, W., Ring, S. M., Ronald, A., Evans, D. E., Fisher, S. E., Thapar, A., et al. (2017) · Molecular Autism · doi:10.1186/s13229-017-0131-2 · Cited by 97
A Primer on the Genetics of Comorbid Eating Disorders and Substance Use Disorders
Munn‐Chernoff, M. A., & Baker, J. H. (2015) · European Eating Disorders Review · doi:10.1002/erv.2424 · Cited by 99
Amare, A. T., Vaez, A., Hsu, Y., Direk, N., Kamali, Z., Howard, D. M., McIntosh, A. M., Tiemeier, H. W., Bültmann, U., Snieder, H., et al. (2019) · Molecular Psychiatry · doi:10.1038/s41380-018-0336-6 · Cited by 97
Euesden, J., Danese, A., Lewis, C. M., & Maughan, B. (2017) · PLoS ONE · doi:10.1371/journal.pone.0173015 · Cited by 105
Methods and challenges for assessing heterogeneity
Feczko, E., & Fair, D. A. (2020) · Biological Psychiatry · doi:10.1016/j.biopsych.2020.02.015 · Cited by 96
The genomics of schizophrenia: update and implications
Giusti‐Rodríguez, P., & Sullivan, P. F. (2013) · Journal of Clinical Investigation · doi:10.1172/jci66031 · Cited by 99
Dunn, E. C., Solovieff, N., Lowe, S. R., Gallagher, P., Chaponis, J., Rosand, J. M., Koenen, K. C., Waters, M. C., Rhodes, J. E., & Smoller, J. W. (2013) · Journal of Affective Disorders · doi:10.1016/j.jad.2013.09.018 · Cited by 102
Liang, D., Elwell, A. L., Aygün, N., Krupa, O., Wolter, J. M., Kyere, F. A., Lafferty, M. J., Cheek, K. E., Courtney, K. P., Yusupova, M., et al. (2021) · Nature Neuroscience · doi:10.1038/s41593-021-00858-w · Cited by 91
Molecular substrates of schizophrenia: homeostatic signaling to connectivity
Landek‐Salgado, M. A., Faust, T. E., & Sawa, A. (2015) · Molecular Psychiatry · doi:10.1038/mp.2015.141 · Cited by 95
Genetic differential susceptibility to the effects of parenting
Belsky, J., & van IJzendoorn, M. H. (2017) · Current Opinion in Psychology · doi:10.1016/j.copsyc.2017.02.021 · Cited by 95
Biomarkers for bipolar disorder: current status and challenges ahead
Teixeira, A. L., Colpo, G. D., Fries, G. R., Bauer, I. E., & Selvaraj, S. (2018) · Expert Review of Neurotherapeutics · doi:10.1080/14737175.2019.1550361 · Cited by 95
Gao, X., Meng, L.-X., Ma, K.-L., Liang, J., Wang, H., Gao, Q., & Wang, T. (2019) · European Psychiatry · doi:10.1016/j.eurpsy.2019.05.004 · Cited by 94
Moser, D. A., Doucet, G. E., Lee, W. H., Rasgon, A., Krinsky, H., Leibu, E., Ing, A., Schumann, G., Rasgon, N., & Frangou, S. (2018) · JAMA Psychiatry · doi:10.1001/jamapsychiatry.2017.4741 · Cited by 94
Amare, A. T., Schubert, K. O., Hou, L., Clark, S. R., Papiol, S., Cearns, M., Heilbronner, U., Degenhardt, F., Ayele, F. T., Hsu, Y., et al. (2020) · Molecular Psychiatry · doi:10.1038/s41380-020-0689-5 · Cited by 94
Yuan, S., Yao, H., & Larsson, S. C. (2020) · Scientific Reports · doi:10.1038/s41598-020-70458-4 · Cited by 95
O’Reilly, K., Donohoe, G. J., Coyle, C., O’Sullivan, D., Rowe, A. R., Losty, M., McDonagh, T., McGuinness, L., Ennis, Y., Watts, E., et al. (2015) · BMC Psychiatry · doi:10.1186/s12888-015-0548-0 · Cited by 94
Tian, Y., Voineagu, I., Paşca, S. P., Won, H., Chandran, V., Horvath, S., Dolmetsch, R. E., & Geschwind, D. H. (2014) · Genome Medicine · doi:10.1186/s13073-014-0075-5 · Cited by 93
Bralten, J., Franke, B., Waldman, I., Rommelse, N., Hartman, C., Asherson, P., Banaschewski, T., Ebstein, R. P., Gill, M., Miranda, A., et al. (2013) · Journal of the American Academy of Child & Adolescent Psychiatry · doi:10.1016/j.jaac.2013.08.020 · Cited by 93
Rai, D., Heuvelman, H., Dalman, C., Culpin, I., Lundberg, M., Carpenter, P., & Magnusson, C. (2018) · JAMA Network Open · doi:10.1001/jamanetworkopen.2018.1465 · Cited by 93
Control of neuronal voltage-gated calcium ion channels from RNA to protein
Lipscombe, D., Allen, S. E., & Toro, C. P. (2013) · Trends in Neurosciences · doi:10.1016/j.tins.2013.06.008 · Cited by 94
Assessing the utility of intermediate phenotypes for genetic mapping of psychiatric disease
Flint, J., Timpson, N. J., & Munafo, M. R. (2014) · Trends in Neurosciences · doi:10.1016/j.tins.2014.08.007 · Cited by 98
Heck, A., Fastenrath, M., Ackermann, S., Auschra, B., Bickel, H., Coynel, D., Gschwind, L., Jessen, F., Kaduszkiewicz, H., Maier, W., et al. (2014) · Neuron · doi:10.1016/j.neuron.2014.01.010 · Cited by 97
Wigham, S., Rodgers, J., Berney, T. P., Couteur, A. S. L., Ingham, B., & Parr, J. R. (2018) · Autism · doi:10.1177/1362361317748245 · Cited by 98
Coexpression networks identify brain region–specific enhancer RNAs in the human brain
Yao, P., Lin, P., Gokoolparsadh, A., Assareh, A. A., Thang, M. W. C., & Voineagu, I. (2015) · Nature Neuroscience · doi:10.1038/nn.4063 · Cited by 94
The Genetics of Autism Spectrum Disorders
Huguet, G., Benabou, M., & Bourgeron, T. (2016) · Research and perspectives in endocrine interactions · doi:10.1007/978-3-319-27069-2_11 · Cited by 105
Questions about DISC1 as a genetic risk factor for schizophrenia
Sullivan, P. F. (2013) · Molecular Psychiatry · doi:10.1038/mp.2012.182 · Cited by 93
Chang, M., Womer, F. Y., Gong, X., Chen, X., Tang, L., Feng, R., Dong, S., Duan, J., Chen, Y., Zhang, R., et al. (2021) · Molecular Psychiatry · doi:10.1038/s41380-020-00892-3 · Cited by 92
The Role of Chronic Stress in Anxious Depression
Ross, R. A., Foster, S. L., & Ionescu, D. F. (2017) · Chronic Stress · doi:10.1177/2470547016689472 · Cited by 92
Hess, J., Tylee, D. S., Barve, R., de Jong, S., Ophoff, R. A., Kumarasinghe, N., Tooney, P. A., Schall, U., Gardiner, E. J., Beveridge, N. J., et al. (2016) · Schizophrenia Research · doi:10.1016/j.schres.2016.07.006 · Cited by 90
Beyond Mendelian randomization: how to interpret evidence of shared genetic predictors
Burgess, S., Butterworth, A. S., & Thompson, J. R. (2015) · Journal of Clinical Epidemiology · doi:10.1016/j.jclinepi.2015.08.001 · Cited by 93
Genetic evidence for role of integration of fast and slow neurotransmission in schizophrenia
Devor, A., Andreassen, O. A., Wang, Y., Mäki‐Marttunen, T., Smeland, O. B., Fan, C.-C., Schork, A. J., Holland, D., Thompson, W. K., Witoelar, A., et al. (2017) · Molecular Psychiatry · doi:10.1038/mp.2017.33 · Cited by 91
Schizophrenia as a Disorder of Molecular Pathways
Horváth, S., & Mirnics, K. (2014) · Biological Psychiatry · doi:10.1016/j.biopsych.2014.01.001 · Cited by 90
Pharmacogenetics of antidepressant response: A polygenic approach
García‐González, J., Tansey, K. E., Hauser, J., Henigsberg, N., Maier, W., Mors, O. N., Placentino, A., Rietschel, M., Souery, D., Žagar, T., et al. (2017) · Progress in Neuro-Psychopharmacology and Biological Psychiatry · doi:10.1016/j.pnpbp.2017.01.011 · Cited by 91
Association of depressive symptoms and suicidal ideation among university students in China
Wang, Y., Shi, Z.-T., & Luo, Q.-Y. (2017) · Medicine · doi:10.1097/md.0000000000006476 · Cited by 91
Pouget, J. G., Han, B., Wu, Y., Mignot, E. J.-M., Ollila, H. M., Barker, J., Spain, S. L., Dand, N., Trembath, R. C., Martin, J. J., et al. (2019) · Human Molecular Genetics · doi:10.1093/hmg/ddz145 · Cited by 95
Yamashita, M., Yoshihara, Y., Hashimoto, R., Yahata, N., Ichikawa, N., Sakai, Y., Yamada, T., Matsukawa, N., Okada, G., Tanaka, S., et al. (2018) · eLife · doi:10.7554/elife.38844 · Cited by 92
Bansal, V., Mitjans, M., Burik, C. A. P., Linnér, R. K., Okbay, A., Rietveld, C. A., Begemann, M., Bonn, S., Ripke, S., de Vlaming, R., et al. (2018) · Nature Communications · doi:10.1038/s41467-018-05510-z · Cited by 90
Kabir, Z. D., Che, A., Fischer, D. K., Rice, R. C., Rizzo, B. K., Byrne, M., Glass, M. J., García, N. V. D. M., & Rajadhyaksha, A. M. (2017) · Molecular Psychiatry · doi:10.1038/mp.2017.124 · Cited by 91
Cheng, S., Han, B., Ding, M., Wen, Y. F., Ma, M., Zhang, L., Qi, X., Cheng, B., Li, P., Kafle, O. P., et al. (2019) · Briefings in Bioinformatics · doi:10.1093/bib/bbz034 · Cited by 88
Half a century of research on Attention-Deficit/Hyperactivity Disorder: A scientometric study
Cortese, S., Sabé, M., Chen, C., Perroud, N. A., & Solmi, M. (2022) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2022.104769 · Cited by 99
Clauss, J. A., Avery, S. N., & Blackford, J. U. (2015) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2015.03.001 · Cited by 93
Revitalizing Psychiatric Therapeutics
Hyman, S. E. (2013) · Neuropsychopharmacology · doi:10.1038/npp.2013.181 · Cited by 92
Kamijo, S., Ishii, Y., Horigane, S.-I., Suzuki, K., Ohkura, M., Nakai, J., Fujii, H., Takemoto-Kimura, S., & Bito, H. (2018) · The Journal of Neuroscience · doi:10.1523/jneurosci.2357-17.2018 · Cited by 89
Kendler, K. S., Ohlsson, H., Sundquist, J., & Sundquist, K. (2021) · JAMA Psychiatry · doi:10.1001/jamapsychiatry.2021.0336 · Cited by 90
Papes, F., Camargo, A. P., de Souza, J. S., Carvalho, V. M. D. A., Szeto, R. A., LaMontagne, E., Júnior, J. R. T., Avansini, S. H., Sánchez-Sánchez, S. M., Nakahara, T. S., et al. (2022) · Nature Communications · doi:10.1038/s41467-022-29942-w · Cited by 95
Wang, T., Zhang, X., Li, A., Zhu, M., Liu, S., Qin, W., Li, J., Yu, C., Jiang, T., & Liu, B. (2017) · NeuroImage: Clinical · doi:10.1016/j.nicl.2017.02.011 · Cited by 88
Jiang, Z., Cowell, R. M., & Nakazawa, K. (2013) · Frontiers in Behavioral Neuroscience · doi:10.3389/fnbeh.2013.00116 · Cited by 91
Progress in the Genetics of Polygenic Brain Disorders: Significant New Challenges for Neurobiology
McCarroll, S. A., & Hyman, S. E. (2013) · Neuron · doi:10.1016/j.neuron.2013.10.046 · Cited by 90
Identification of shared risk loci and pathways for bipolar disorder and schizophrenia
Forstner, A. J., Hecker, J., Hofmann, A., Maaser, A., Reinbold, C. S., Mühleisen, T. W., Leber, M., Strohmaier, J., Degenhardt, F., Treutlein, J., et al. (2017) · PLoS ONE · doi:10.1371/journal.pone.0171595 · Cited by 90
A longitudinal approach to biological psychiatric research: The PsyCourse study
Budde, M., Anderson‐Schmidt, H., Gade, K., Reich‐Erkelenz, D., Adorjan, K., Kalman, J. L., Senner, F., Papiol, S., Andlauer, T. F. M., Comes, A. L., et al. (2018) · American Journal of Medical Genetics Part B Neuropsychiatric Genetics · doi:10.1002/ajmg.b.32639 · Cited by 87
Multi-omics data integration methods and their applications in psychiatric disorders
Sathyanarayanan, A., Mueller, T. T., Moni, M. A., Schueler, K., Baune, B. T., Lió, P., Mehta, D., Baune, B. T., Dierssen, M., Ebert, B., et al. (2023) · European Neuropsychopharmacology · doi:10.1016/j.euroneuro.2023.01.001 · Cited by 93
Guloksuz, S., van Nierop, M., Lieb, R., van Winkel, R., Wittchen, H.-U., & van Os, J. (2015) · Psychological Medicine · doi:10.1017/s0033291715000380 · Cited by 88
Pagani, L., Clair, P. A. S., Teshiba, T. M., Service, S. K., Fears, S. C., Araya, C., Araya, X., Bejarano, J., Ramirez, M., Castrillón, G., et al. (2015) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1513525113 · Cited by 88
Association Between Deliberate Self-harm and Violent Criminality
Sahlin, H., Kuja‐Halkola, R., Bjureberg, J., Lichtenstein, P., Molero, Y., Rosenqvist, M. A., Hedman‐Lagerlöf, E., Runeson, B., Jokinen, J., Ljótsson, B., et al. (2017) · JAMA Psychiatry · doi:10.1001/jamapsychiatry.2017.0338 · Cited by 92
Schizophrenia genetics: emerging themes for a complex disorder
Kavanagh, D. H., Tansey, K. E., O’Donovan, M. C., & Owen, M. J. (2014) · Molecular Psychiatry · doi:10.1038/mp.2014.148 · Cited by 93
Genome-scale neurogenetics: methodology and meaning
McCarroll, S. A., Feng, G., & Hyman, S. E. (2014) · Nature Neuroscience · doi:10.1038/nn.3716 · Cited by 89
Polygenic risk scores in imaging genetics: Usefulness and applications
Dima, D., & Breen, G. D. (2015) · Journal of Psychopharmacology · doi:10.1177/0269881115584470 · Cited by 88
Lotan, A., Fencková, M., Bralten, J., O’Leary, A., Dixson, L., Williams, R. W., & van der Voet, M. (2014) · Frontiers in Neuroscience · doi:10.3389/fnins.2014.00331 · Cited by 91
Delahaye‐Duriez, A., Srivastava, P. K., Shkura, K., Langley, S. R., Laaniste, L., Moreno‐Moral, A., Danis, B., Mazzuferi, M., Foerch, P., Gazina, E. V., et al. (2016) · Genome biology · doi:10.1186/s13059-016-1097-7 · Cited by 90
Kochunov, P., Hong, L. E., Dennis, E. L., Morey, R. A., Tate, D. F., Wilde, E. A., Logue, M. W., Kelly, S., Donohoe, G. J., Favre, P., et al. (2020) · Human Brain Mapping · doi:10.1002/hbm.24998 · Cited by 89
Twenty-Five Years of Progress: The View from NIMH and NINDS
Insel, T. R., & Landis, S. C. (2013) · Neuron · doi:10.1016/j.neuron.2013.09.041 · Cited by 91
The genetics of bone mass and susceptibility to bone diseases
Karasik, D., Rivadeneira, F., & Johnson, M. L. (2016) · Nature Reviews Rheumatology · doi:10.1038/nrrheum.2016.48 · Cited by 88
Ross, C. A., & Margolis, R. L. (2019) · Complex Psychiatry · doi:10.1159/000501797 · Cited by 93
Metabolic Aspects of Adenosine Functions in the Brain
Garcia‐Gil, M., Camici, M., Allegrini, S., Pesi, R., & Tozzi, M. G. (2021) · Frontiers in Pharmacology · doi:10.3389/fphar.2021.672182 · Cited by 90
Uher, R., Cumby, J., MacKenzie, L. E., Morash-Conway, J., Glover, J. M., Aylott, A., Propper, L., Abidi, S., Bagnell, A. L., Pavlová, B., et al. (2014) · BMC Psychiatry · doi:10.1186/s12888-014-0344-2 · Cited by 89
O’Connell, K. S., McGregor, N. W., Löchner, C., Emsley, R. A., & Warnich, L. (2018) · Molecular and Cellular Neuroscience · doi:10.1016/j.mcn.2018.02.010 · Cited by 92
Evolutionary modifications in human brain connectivity associated with schizophrenia
van den Heuvel, M. P., Scholtens, L. H., de Lange, S. C., Pijnenburg, R., Cahn, W., van Haren, N. E. M., Sommer, I. E., Bozzali, M., Koch, K., Boks, M. P., et al. (2019) · Brain · doi:10.1093/brain/awz330 · Cited by 84
The relative contribution of common and rare genetic variants to ADHD
Martin, J., O'Donovan, M. C., Thapar, A., Langley, K., & Williams, N. (2015) · Translational Psychiatry · doi:10.1038/tp.2015.5 · Cited by 85
Liberzon, I., King, A. P. J., Ressler, K. J., Almli, L. M., Zhang, P., Ma, S. T., Cohen, G. H., Tamburrino, M., Calabrese, J. R., & Galea, S. (2014) · JAMA Psychiatry · doi:10.1001/jamapsychiatry.2014.999 · Cited by 88
Genetics of glucocorticoid regulation and posttraumatic stress disorder -what do we know?
Castro-Vale, I., van Rossum, E. F. C., Machado, J. C., Mota-Cardoso, R., & Carvalho, D. (2016) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2016.02.005 · Cited by 85
Guan, J., Cai, J. J., Ji, G., & Sham, P. C. (2019) · Translational Psychiatry · doi:10.1038/s41398-019-0488-4 · Cited by 86
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
- Locations
- The Lancet (publishedVersion)
- PubMed (publishedVersion)
- Pure Amsterdam UMC (publishedVersion)
- Amsterdam UMC (VU Amsterdam) - Institutional Repository (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- QUT ePrints (Queensland University of Technology) (submittedVersion)
- DuEPublico (University of Duisburg-Essen) (submittedVersion)
- TSpace (University of Toronto) (submittedVersion, cc-by-nc-nd)
- UNSWorks (UNSW Sydney) (submittedVersion, cc-by-nc-nd)
- Research Publications (Maastricht University) (submittedVersion, cc-by-nc)
- ePrints Soton (University of Southampton) (submittedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Research Portal (King's College London) (submittedVersion)
- VBN Forskningsportal (Aalborg Universitet) (submittedVersion)
- Radboud Repository (Radboud University) (submittedVersion)
- VU Research Portal (submittedVersion)
- UNSWorks (University of New South Wales, Sydney, Australia) (submittedVersion, cc-by-nc-nd)
- Hirsla (Landspítali University Hospital) (submittedVersion)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion)
- Research Publications (Maastricht University) (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- 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 ›
Are you an author, or do you see a problem with this page? Request a review
