The DOI matches its Crossref record; 86 of the 90 references it cites were found in a registry or an index; none of the 57 sources its claims cite is checked for support yet.
Genomic Relationships, Novel Loci, and Pleiotropic Mechanisms across Eight Psychiatric Disorders
Open accessAbstract
Genetic influences on psychiatric disorders transcend diagnostic boundaries, suggesting substantial pleiotropy of contributing loci. However, the nature and mechanisms of these pleiotropic effects remain unclear. We performed analyses of 232,964 cases and 494,162 controls from genome-wide studies of anorexia nervosa, attention-deficit/hyperactivity disorder, autism spectrum disorder, bipolar disorder, major depression, obsessive-compulsive disorder, schizophrenia, and Tourette syndrome. Genetic correlation analyses revealed a meaningful structure within the eight disorders, identifying three groups of inter-related disorders. Meta-analysis across these eight disorders detected 109 loci associated with at least two psychiatric disorders, including 23 loci with pleiotropic effects on four or more disorders and 11 loci with antagonistic effects on multiple disorders. The pleiotropic loci are located within genes that show heightened expression in the brain throughout the lifespan, beginning prenatally in the second trimester, and play prominent roles in neurodevelopmental processes. These findings have important implications for psychiatric nosology, drug development, and risk prediction.
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“while 35 loci (25.7%) represented novel genome-wide significant associations.”
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In the paper
“Meta-analysis across these eight disorders detected 109 loci associated with at least two psychiatric disorders”
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In the paper
“The pleiotropic loci are located within genes that show heightened expression in the brain throughout the lifespan, beginning prenatally in the second trimester”
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“The first factor consisted primarily of disorders characterized by compulsive/perfectionistic behaviors, specifically AN, OCD, and, more weakly, TS.”
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In the paper
“and the third factor by three early-onset neurodevelopmental disorders (ASD, ADHD, TS) as well as MD.”
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In the paper
“and 11 loci with antagonistic effects onmultiple disorders”
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“We identified 136 LD-independent regions with genome-wide significant association ( P meta % 5 3 10 8 ).”
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In the paper
“and ADHD (rg = 0.44 ± 0.03)”
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“followed by OCD and AN (rg = 0.50 ± 0.12).”
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“Similar to our EFA results, hierarchical clustering analyses also identified three sub-groups among the eight disorders”
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In the paper
“Genetic correlation analyses revealed a meaningful structure within the eight disorders, identifying three groups of inter-related disorders.”
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“Within these 136 loci, multi-SNP-based conditional analysis (Yang et al., 2012) identified 10 additional SNPs with independent associations, resulting in a total of 146 independent lead SNPs”
What the sources say
- Not checked yetcites Yang et al., 2012 source
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“Enrichment analyses using the genes preferentially expressed in specific cortical regions suggested that pleiotropic loci were over-represented among genes expressed in the frontal cortex, while non-pleiotropic loci were enriched in the occipital cortex (FDR q <0.05; Figure 5C).”
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“two loci between SCZ and ASD (rs9329221, rs2921036)”
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“Eleven of the 23 lead SNPs map to the intron of a protein-coding gene, and seven additional lead SNPs had at least one protein-coding gene within 100 kb.”
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“Gene expression data indicate that DCC expression peaks during early prenatal development (Figure S3).”
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“More than 41% of the genes associated with our genome-wide significant loci, both pleiotropic and non-pleiotropic, were intolerant of loss of function mutations (pLI score R 0.9); this is highly unlikely to occur by chance (Fisher's exact p = 4.90 3 10 8 ).”
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In the paper
“The 109 pleiotropic risk loci were enriched for genes involved in neurogenesis (gene-set enrichment p = 9.67 3 10 6 ), regulation of nervous system development (p = 3.41 3 10 5 ), and neuron differentiation (p = 3.30 3 10 5 )”
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“Overall, they showed significant enrichment of genes expressed in the brain ( beta = 0.123, SE = 0.0109, enrichment p = 1.22 3 10 29 ) and pituitary ( beta = 0.0916, SE = 0.0136, p = 8.74 3 10 12 ), but not in the other Genotype-Tissue Expression (GTEx) tissues.”
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In the paper
“Expression levels were associated with the degree of pleiotropy, with the pleiotropy > 2 group showing higher gene expression than either the pleiotropy = 2 group (t test p < 2.10 3 10 4 ) or non-pleiotropic risk loci (t test p < 2.2 3 10 16 ).”
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In the paper
“The other disorders, ADHD, TS, OCD, and AN featured associations in 16%, 14%, 11%, and 7% of the pleiotropic loci, respectively.”
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In the paper
“Neither did we find differences between disorder-specific lead SNPs and pleiotropic SNPs with respect to their minor allele frequencies, average heterozygosity, or predicted allele ages (Kiezun et al., 2013).”
What the sources say
- Not checked yetcites Kiezun et al., 2013 source
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“Pleiotropic and non-pleiotropic SNPs also did not differ in terms of the distance to nearest genes, distance to splicing sites, chromosome compositions, and predicted functional consequences of non-coding regulatory elements.”
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“Cell-type-specific analysis indicated that genes implicated in pleiotropic loci were mainly expressed in neurons (FDR q <0.05) but not in glial cell types.”
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In the paper
“and KDM7A (encoding Lysine Demethylase 7A)”
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In the paper
“Pleiotropic risk loci also showed enrichment of genes involved in specific neurotransmitter-related pathwaysglutamate receptor signaling (p = 2.45 3 10 6 ) and voltagegated calcium channel complex (p = 5.72 3 10 4 )”
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“Of the single-disorderspecific loci, 81% and 16% were associated with SCZ and MD, respectively.”
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“Of the 109 pleiotropic loci, 76 were identified in the GWAS of individual disorders, while the remaining 33 are novel.”
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In the paper
“Of the 109 pleiotropic loci, 83% and 72% involved SCZ and BIP, respectively.”
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“In contrast to DCC , however, developmental gene-expression of RBFOX1 showed gradually increasing gene expression throughout the prenatal period (Figure S3).”
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In the paper
“average expression of genes related to pleiotropic loci peaked in the second trimester and remained overexpressed throughout the lifespan.”
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In the paper
“Finally, we found that genes associated with multiple psychiatric disorders are disproportionately associated with biological pathways related to neurodevelopment and exhibit distinctive gene expression patterns, with enhanced expression beginning in the second prenatal trimester and persistently elevated expression relative to less pleiotropic genes.”
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In the paper
“we identified 146 LD-independent lead SNPs associated with at least one disorder, including 35 novel loci.”
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In the paper
“Consistent with prior research (Brainstorm Consortium et al., 2018; CrossDisorder Group of the Psychiatric Genomics Consortium, 2013), we found substantial pairwise genetic correlations across child- and adult-onset disorders and extended these findings by demonstrating clusters of genetically-related disorders.”
What the sources say
- Not checked yetcites Brainstorm Consortium et al., 2018
- Not checked yetcites CrossDisorder Group of the Psychiatric Genomics Consortium, 2013
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In the paper
“Of these, 109 loci were found to affect two or more disorders, although characterization of this pleiotropy is partly dependent on per-disorder sample size.”
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In the paper
“We also identified 109 genomic loci with pleiotropic effects, of which 33 had not previously been associated with any of the individual disorders.”
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In the paper
“These pleiotropic genes, on average, begin to come online by the second trimester of fetal development and exhibit differentially high expression thereafter.”
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In the paper
“In general, as power increased, so did the number of identified SNPs.”
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In the paper
“A model that included additional negative cross-loadings provided similar fit to the data and highly similar correlations across the genetic factors.”
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In the paper
“Note that, in both the WLS and the ML solution, the standard errors are smaller for the loadings involving the better-powered GWAS phenotypes, as we would expect.”
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In the paper
“Despite variation in magnitude, significant genetic correlations were apparent for most pairs of disorders, suggesting a complex, higher-order genetic structure underlying psychopathology”
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In the paper
“Psychiatric disorders are highly polygenic, with a large proportion of heritability contributed by common variation.”
What the sources say
- Not checked yetcites Sullivan et al., 2018 source
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In the paper
“Many risk loci have emerged from genome-wide association studies (GWAS) of, amongothers, schizophrenia (SCZ), bipolar disorder (BIP), major depression (MD), and attention-deficit/hyperactivity disorder (ADHD) from the Psychiatric Genomics Consortium (PGC) and other efforts”
What the sources say
- Not checked yetcites Sullivan et al., 2018 source
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In the paper
“in a sample comprising 33,332 cases and 27,888 controls”
What the sources say
- Not checked yetcites CrossDisorder Group of the Psychiatric Genomics Consortium, 2013
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In the paper
“The factor structure described above is based on average effects across the genome, but does not address more finegrained cross-disorder effects at the level of genomic regions or individual loci.”
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In the paper
“Genetic influences on psychiatric disorders transcend diagnostic boundaries, suggesting substantial pleiotropy of contributing loci.”
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In the paper
“All study participants were of self-identified European ancestry, which was supported by principal component analysis of genome-wide data.”
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In the paper
“As a member of the NOX family genes that encode subunits of NADPH oxidase, NOX4 is a major source of superoxide production in human brain and a promoter of neural stem cell growth (Kuroda et al., 2014; Topchiy et al., 2013).”
What the sources say
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In the paper
“BRAF , which contributes to the MAP kinase signal transduction pathway and plays a role in postsynaptic responses of hippocampal neurons (Grantyn and Grantyn, 1973)”
What the sources say
- Not checked yetcites Grantyn and Grantyn, 1973 source
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In the paper
“The signal in our meta-analysis colocalizes with brain eQTLs for DCC (eQTL association FDR q = 2.27 3 10 5 ), supporting DCC as a plausible candidate gene”
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In the paper
“KDM7A (encoding Lysine Demethylase 7A), which plays a central role in the nervous system and midbrain development (Horton et al., 2010; Qi et al., 2010; Tsukada et al., 2010).”
What the sources say
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In the paper
“The product of DCC plays a key role in guiding axonal growth during neurodevelopment and serves as a master regulator of midline crossing and white matter projections (Bendriem and Ross, 2017).”
What the sources say
- Not checked yetcites Bendriem and Ross, 2017 source
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In the paper
“RBFOX1 (also called A2BP1 ) encodes a splicing regulator mainly expressed in neurons and known to target several genes important to neuronal development, including NMDA receptor 1 and voltage-gated calcium channels (Gandal et al., 2018; Gehman et al., 2011; Hamada et al., 2015).”
What the sources say
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In the paper
“Previous studies of model organisms using gene knock-out experiments suggested that pleiotropic risk loci may undergo stronger selection than non-pleiotropic loci (Hill and Zhang, 2012).”
What the sources say
- Not checked yetcites Hill and Zhang, 2012 source
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In the paper
“and has been previously associated with both MD and neuroticism (Turley et al., 2018; Wray et al., 2018).”
What the sources say
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In the paper
“These results are based on average expression profiles, and not all individual gene expression patterns follow this pattern.”
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In the paper
“Overall, these results indicate a substantial pairwise genetic correlation between multiple disorders along with a higher-level genetic structure that point to broader domains underlying genetic risk to psychopathology.”
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In the paper
“the method we applied to detect cross-phenotype association, which combines an all-subsets fixed-effects GWAS meta-analysis with a Bayesian method for evaluating the best-fit configuration of genotype-phenotype associations, is one of several approaches (Solovieff et al., 2013).”
What the sources say
- Not checked yetcites Solovieff et al., 2013 source
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In the paper
“Prior studies showed that DCC is a master regulator of axon guidance (through its interactions with netrin-1 and draxin (Liu et al., 2018).”
What the sources say
- Not checked yetcites Liu et al., 2018 source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, some of the ''non-pleiotropic'' loci may have additional effects on psychiatric phenotypes that were not included in our meta-analysis and/or on non-psychiatric phenotypes.”
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What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Standardized genomic inflation factor ( l 1000) for the meta-analysis result was close to one. LDSC intercept was substantially less than l GC (0.79 versus 1.55), suggesting that the increase in mean c 2 statistics in the cross-disorder meta-analysis is mainly due to polygenicity and not due to stratification or other confounding biases.”
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In the paper
“As shown in Data S1 .4, the results were consistent with those from the primary analysis reported in the main text that is based on a Weighted Least-squares (WLS) estimator, which does take into account the differing precisions of the genetic covariance estimates. Specifically, the nontrivial standardized factor loadings of MD on two of the three factors is evident in both the WLS and ML solutions”
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In the paper
“It should be noted that the average expression values of each gene set correspond to representative expression patterns of the disease risk genes, so individual genes may behave differently.”
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In the paper
“while sample size will affect the precision of a genetic correlation estimate (ie standard error) it should not affect the magnitude of the estimate itself (Bulik-Sullivan et al., 2015).”
What the sources say
- Not checked yetcites Bulik-Sullivan et al., 2015 source
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None of the sources cited for this claim have been checked yet.
In the paper
“however, these estimates are generally consistent with previously reported ones when sample sizes are much smaller (except for ASD) (Brainstorm Consortium et al., 2018) (Cross-Disorder Group of the Psychiatric Genomics et al., 2013)”
What the sources say
- Not checked yetcites Brainstorm Consortium et al., 2018
- Not checked yetcites Cross-Disorder Group of the Psychiatric Genomics et al., 2013
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
The paper relies on this without support.
The nature and mechanisms of pleiotropic effects across psychiatric disorders are not yet clear.
“However, the nature and mechanisms of these pleiotropic effects remain unclear.”
The authors state this as an assumption.
Effects are either present or absent in studies.
“This estimation, known as the mvalue, relies on two assumptions, 1) effects are either present or absent in studies, and 2) if they are present, they are similarly sized across studies.”
The authors state this as an assumption.
If effects are present, they are similarly sized across studies.
“This estimation, known as the mvalue, relies on two assumptions, 1) effects are either present or absent in studies, and 2) if they are present, they are similarly sized across studies.”
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?
In the citing paper
“This result highlights mid-gestation as a critical window during neurodevelopment that may confer risk to multiple psychiatric disorders, consistent with recent results from cross-disorder GWAS14,15.”
From A computational tool (H-MAGMA) for improved prediction of brain-disorder risk genes by incorporating brain chromatin interaction profiles (2020) · cites this paper as [14]
In the citing paper
“Notably, pleiotropic genes showed higher enrichment for genes mapped to pleiotropic cross-disorder GWS loci than those mapped to non-pleiotropic (disease-specific) GWS loci14 (Fig. 5a).”
From A computational tool (H-MAGMA) for improved prediction of brain-disorder risk genes by incorporating brain chromatin interaction profiles (2020) · cites this paper as [14]
In the citing paper
“Cross-disorder GWAS of eight psychiatric disorders recently identified more than a hundred GWS loci increasing risk for multiple disorders, further providing evidence of widespread pleiotropy among psychiatric disorders14.”
From A computational tool (H-MAGMA) for improved prediction of brain-disorder risk genes by incorporating brain chromatin interaction profiles (2020) · cites this paper as [14]
In the citing paper
“Importantly, this characteristic was also observed for pleiotropic genes identified by meta-analysis of eight psychiatric disorders14.”
From A computational tool (H-MAGMA) for improved prediction of brain-disorder risk genes by incorporating brain chromatin interaction profiles (2020) · cites this paper as [14]
In the citing paper
“given the strong genetic overlap between BD and SCZ53,62”
From Neuronal and glial 3D chromatin architecture informs the cellular etiology of brain disorders (2021) · cites this paper as [62]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Schizophrenia control counts differ
MinorTable 1 lists 43,456 schizophrenia controls, while the methods list 43,546 for the European-ancestry cohorts. The two counts differ by 90 people.
“| SCZ | 33,640 | 43,456 | 77,096 |”
“For the current study, the 46 case-control cohorts of European ancestry were retained, totaling 33,640 cases and 43,546 controls.”
Anorexia nervosa control counts differ
MinorTable 1 lists 10,983 anorexia nervosa controls, but the methods list 10,982 and say all participants from that study were included in the current analyses.
“| AN | 3,495 | 10,983 | 14,478 |”
“3,495 cases from two consortia and 10,982 matched controls from the Psychiatric Genomics Consortium, all of European descent, were meta-analyzed to identify one locus associated with anorexia nervosa. Cases met criteria as defined by DSM-IV for lifetime diagnosis of anorexia nervosa (restricting or binge-purging subtype), bulimia nervosa, or anorexia nervosa - not otherwise specified, anorexia nervosa subtype. All individuals included in the primary study were included in the current analyses.”
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BackgroundMAGMA: Generalized Gene-Set Analysis of GWAS Data
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“As expected, the associated traits included SCZ, BIP, and ASD.”
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BackgroundSelf-citationGenetic relationship between five psychiatric disorders estimated from genome-wide SNPs
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BackgroundInfluentialSelf-citationSpatio-temporal transcriptome of the human brain
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“(B) Brain developmental expression trajectory displayed for the three groups of genes based on (Kang et al., 2011) The 146 genome-wide significant loci from the cross-disorder meta analysis were clustered into three groups based on predicted disorder-specific associations: (1) no-pleiotopy; (2) pleiotropy = 2; and (3)…”
BackgroundAnalysis of shared heritability in common disorders of the brain
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“Various comparative genomics resources, including PhyloP (Pollard et al., 2010), PhastCons (Siepel et al., 2005), and GERP++ (Davydov et al., 2010), showed our top loci to have similar properties regardless of the extent of pleiotropy.”
BackgroundFast and accurate genotype imputation in genome-wide association studies through pre-phasing
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MethodSelf-citationDepression and obesity: evidence of shared biological mechanisms
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Self-citationPsychiatric Genomics: An Update and an Agenda
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“Cases met criteria for lifetime diagnosis of bipolar disorder as defined by DSM-IV, ICD-9, or ICD-10, which was established using interview-based structured assessment, clinician-administered checklists, or review of medical records.”
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“The substantial influence of genetic variation on risk for a broad range of psychiatric disorders has been established by both twin and, more recently, large-scale genomic studies (Smoller et al., 2019).”
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“The brain Hi-C data indicated interaction of the associated region with the promoters of two nearby genes:BRAF, which contributes to theMAP kinase signal transduction pathway and plays a role in postsynaptic responses of hippocampal neurons (Grantyn and Grantyn, 1973), and KDM7A (encoding Lysine Demethylase 7A), which…”
BackgroundRegional missense constraint improves variant deleteriousness prediction
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“In supplementary analyses, we did not find evidence of significant overrepresentation of genes related to pleiotropic SNPs identified here among previously defined genomic disorder regions or genes associated with neurodevelopmental disorders from rare variant studies (including ASD, intellectual disability, and devel…”
BackgroundThe splicing regulator Rbfox1 (A2BP1) controls neuronal excitation in the mammalian brain
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“These results underscore the complexity of genetic relationships among related disorders and suggest that overall genetic correlations may obscure a more complex set of genetic relationships at the level of specific loci and pathways, as seen in immune-mediated diseases (Baurecht et al., 2015; Lettre and Rioux, 2008;…”
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“Cell tween a range of neuropsychiatric disorders and obesity (Hartwig et al., 2016; Lopresti and Drummond, 2013; Milaneschi et al., 2019).”
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“These results are consistent with those of a smaller recent analysis in the population-based Danish iPSYCH cohort (comprising 46,008 cases and 19,526 controls across six neuropsychiatric disorders) (Schork et al., 2019).”
ResultSelf-citationSchmitt, J., Schwarz, K., Baurecht, H., Hotze, M., Fölster-Holst, R., Rodríguez, E., Lee, Y. A. E., Franke, A., Degenhardt, F., Lieb, W., et al. (2016) · Journal of Allergy and Clinical Immunology · doi:10.1016/j.jaci.2015.06.029 · Cited by 215 · cited 2×
“These results underscore the complexity of genetic relationships among related disorders and suggest that overall genetic correlations may obscure a more complex set of genetic relationships at the level of specific loci and pathways, as seen in immune-mediated diseases (Baurecht et al., 2015; Lettre and Rioux, 2008;…”
BackgroundSelf-citationBaurecht, H., Hotze, M., Brand, S., Büning, C., Cormican, P., Corvin, A., Ellinghaus, D., Ellinghaus, E., Esparza-Gordillo, J., Fölster-Holst, R., et al. (2015) · The American Journal of Human Genetics · doi:10.1016/j.ajhg.2014.12.004 · Cited by 193
Self-citationInterpreting Meta-Analyses of Genome-Wide Association Studies
Han, B., & Eskin, E. (2012) · PLoS Genetics · doi:10.1371/journal.pgen.1002555 · Cited by 177
Rice, F., Riglin, L., Thapar, A. K., Heron, J., Anney, R., O’Donovan, M. C., & Thapar, A. (2019) · JAMA Psychiatry · doi:10.1001/jamapsychiatry.2018.3338 · Cited by 167 · cited 1×
“The loading of MD on two factors may reflect biological heterogeneity within MD, consistent with recent evidence showing that early-onset depression is associated with genetic risk for ADHD and with neurodevelopmental phenotypes (Rice et al., 2019).”
BackgroundSelf-citationUllah, A. Z. M. D., Oscanoa, J., Wang, J., Nagano, A., Lemoine, N. R., & Chelala, C. (2018) · Nucleic Acids Research · doi:10.1093/nar/gky399 · Cited by 166
Making Dopamine Connections in Adolescence
Hoops, D., & Flores, C. (2017) · Trends in Neurosciences · doi:10.1016/j.tins.2017.09.004 · Cited by 162 · cited 2×
“…with childhood and adolescent onset would be consistent with its role in both early organization of neuronal circuits and the maturation of mesolimbic dopaminergic connections to the prefrontal cortex during adolescence (Hoops and Flores, 2017; Reynolds et al., 2018; Vosberg et al., 2018).”
BackgroundKDM7 is a dual demethylase for histone H3 Lys 9 and Lys 27 and functions in brain development
Tsukada, Y.-I., Ishitani, T., & Nakayama, K. I. (2010) · Genes & Development · doi:10.1101/gad.1864410 · Cited by 158 · cited 2×
“The brain Hi-C data indicated interaction of the associated region with the promoters of two nearby genes:BRAF, which contributes to theMAP kinase signal transduction pathway and plays a role in postsynaptic responses of hippocampal neurons (Grantyn and Grantyn, 1973), and KDM7A (encoding Lysine Demethylase 7A), which…”
BackgroundMeta-Analysis of Genome-wide Association Studies with Overlapping Subjects
Lin, D.-Y., & Sullivan, P. F. (2009) · The American Journal of Human Genetics · doi:10.1016/j.ajhg.2009.11.001 · Cited by 156 · cited 1×
“The numbers of shared subjects across eight disorder studies were identified using the PGC checksum algorithm, and Z meta was standardized so that covariance between the statistics can be accounted for as previously described (Bhattacharjee et al., 2012; Lin and Sullivan, 2009).”
MethodSelf-citationReynolds, L. M., Pokinko, M., Torres-Berrío, A., Cuesta, S., Lambert, L. C., Del Cid Pellitero, E., Wodzinski, M., Manitt, C., Krimpenfort, P., Kolb, B., et al. (2018) · Biological Psychiatry · doi:10.1016/j.biopsych.2017.06.009 · Cited by 129 · cited 2×
“…with childhood and adolescent onset would be consistent with its role in both early organization of neuronal circuits and the maturation of mesolimbic dopaminergic connections to the prefrontal cortex during adolescence (Hoops and Flores, 2017; Reynolds et al., 2018; Vosberg et al., 2018).”
BackgroundMutations in DCC cause isolated agenesis of the corpus callosum with incomplete penetrance
Marsh, A. P. L., Heron, D., Edwards, T. J., Quartier, A., Galea, C., Nava, C., Rastetter, A., Moutard, M.-L., Anderson, V., Bitoun, P., et al. (2017) · Nature Genetics · doi:10.1038/ng.3794 · Cited by 101 · cited 2×
“Loss-of-function mutations in DCC cause severe neuro-developmental syndromes involving loss of midline commissural tracts and diffuse disorganization of white matter tracts (Bend-riem and Ross, 2017; Jamuar et al., 2017; Marsh et al., 2017).”
BackgroundSelf-citationHamada, N., Ito, H., Nishijo, T., Iwamoto, I., Morishita, R., Tabata, H., Momiyama, T., & Nagata, K.-I. (2016) · Scientific Reports · doi:10.1038/srep30805 · Cited by 86 · cited 1×
“Knockdown and silencing of RBFOX1 during mouse corticogenesis impairs neuronal migration and synapse formation (Hamada et al., 2015; Hamada et al., 2016), implying its pivotal role in early cortical maturation.”
BackgroundTranslating insights from neuropsychiatric genetics and genomics for precision psychiatry
Rees, E., & Owen, M. J. (2020) · Genome Medicine · doi:10.1186/s13073-020-00734-5 · Cited by 86
Self-citationBiallelic mutations in human DCC cause developmental split-brain syndrome
Jamuar, S. S., Schmitz-Abe, K., D'Gama, A. M., Drottar, M., Chan, W.-M., Peeva, M., Servattalab, S., Lam, A.-T. N., Delgado, M. R., Clegg, N. J., et al. (2017) · Nature Genetics · doi:10.1038/ng.3804 · Cited by 81 · cited 1×
“Loss-of-function mutations in DCC cause severe neurodevelopmental syndromes involving loss of midline commissural tracts and diffuse disorganization of white matter tracts (Bendriem and Ross, 2017; Jamuar et al., 2017; Marsh et al., 2017).”
BackgroundBody mass index and psychiatric disorders: a Mendelian randomization study
Hartwig, F. P., Bowden, J., de Mola, C. L., Tovo‐Rodrigues, L., Smith, G. D., & Horta, B. L. (2016) · Scientific Reports · doi:10.1038/srep32730 · Cited by 77 · cited 2×
“Cell tween a range of neuropsychiatric disorders and obesity (Hartwig et al., 2016; Lopresti and Drummond, 2013; Milaneschi et al., 2019).”
BackgroundInfluentialNox4 Is a Major Source of Superoxide Production in Human Brain Pericytes
Kuroda, J., Ago, T., Nishimura, A., Nakamura, K., Matsuo, R., Wakisaka, Y., Kamouchi, M., & Kitazono, T. (2014) · Journal of Vascular Research · doi:10.1159/000369930 · Cited by 73 · cited 1×
“As a member of the NOX family genes that encode subunits of NADPH oxidase, NOX4 is a major source of superoxide production in human brain and a promoter of neural stem cell growth (Kuroda et al., 2014; Topchiy et al., 2013).”
BackgroundKiezun, A., Pulit, S. L., Francioli, L. C., van Dijk, F., Swertz, M., Boomsma, D. I., van Duijn, C. M., Slagboom, P. E., van Ommen, G. J. B., Wijmenga, C., et al. (2013) · PLoS Genetics · doi:10.1371/journal.pgen.1003301 · Cited by 72
Heterogeneity and Polygenicity in Psychiatric Disorders: A Genome-Wide Perspective
Wendt, F. R., Pathak, G. A., Tylee, D. S., Goswami, A., & Polimanti, R. A. (2020) · Chronic Stress · doi:10.1177/2470547020924844 · Cited by 65
RBFOX1, encoding a splicing regulator, is a candidate gene for aggressive behavior
Fernàndez‐Castillo, N., Gan, G., van Donkelaar, M. M. J., Vaht, M., Weber, H., Retz, W., Meyer‐Lindenberg, A., Franke, B., Harro, J., Reif, A., et al. (2017) · European Neuropsychopharmacology · doi:10.1016/j.euroneuro.2017.11.012 · Cited by 65 · cited 2×
“Animal models and association studies have implicated RBFOX1 in aggressive behaviors, a trait observed in several of the disorders in our analysis (Fernàndez-Castillo et al., 2017).”
BackgroundSelf-citationStructural Basis for Draxin-Modulated Axon Guidance and Fasciculation by Netrin-1 through DCC
Liu, Y., Bhowmick, T., Liu, Y., Gao, X., Mertens, H. D. T., Svergun, D. I., Xiao, J., Zhang, Y., Wang, J.-H., & Meijers, R. (2018) · Neuron · doi:10.1016/j.neuron.2018.02.010 · Cited by 60 · cited 1×
“Prior studies showed that DCC is a master regulator of axon guidance (through its interactions with netrin-1 and draxin (Liu et al., 2018).”
Hamada, N., Ito, H., Iwamoto, I., Morishita, R., Tabata, H., & Nagata, K.-I. (2015) · Molecular Autism · doi:10.1186/s13229-015-0049-5 · Cited by 59 · cited 3×
“Knockdown and silencing of RBFOX1 during mouse corticogenesis impairs neuronal migration and synapse formation (Hamada et al., 2015; Hamada et al., 2016), implying its pivotal role in early cortical maturation.”
BackgroundShared polygenic risk for ADHD, executive dysfunction and other psychiatric disorders
Chang, S., Yang, L., Wang, Y., & Faraone, S. V. (2020) · Translational Psychiatry · doi:10.1038/s41398-020-00872-9 · Cited by 53
Self-citationNox4-Generated Superoxide Drives Angiotensin II-Induced Neural Stem Cell Proliferation
Topchiy, E., Panzhinskiy, E., Griffin, W. S. T., Barger, S. W., Das, M., & Zawada, W. M. (2013) · Developmental Neuroscience · doi:10.1159/000350502 · Cited by 49 · cited 1×
“As a member of the NOX family genes that encode subunits of NADPH oxidase, NOX4 is a major source of superoxide production in human brain and a promoter of neural stem cell growth (Kuroda et al., 2014; Topchiy et al., 2013).”
BackgroundZhu, Z., Anttila, V., Smoller, J. W., & Lee, P. H. (2018) · PLOS ONE · doi:10.1371/journal.pone.0193256 · Cited by 47 · cited 1×
“However, we have previously shown that this method outperforms a range of alternatives for detecting pleiotropy under various settings (Zhu et al., 2018).”
MethodSelf-citationHill, W. G., & Zhang, X.-S. (2012) · Nature Reviews Genetics · doi:10.1038/nrg2949-c1 · Cited by 46 · cited 2×
“…loci in neuronal cells was also associated with the degree of pleiotropy, as highlighted in Figure 5D. Previous studies of model organisms using gene knock-out experiments suggested that pleiotropic risk loci may undergo stronger selection than non-pleiotropic loci (Hill and Zhang, 2012).”
Result(2020) · doi:10.1038/s41398-020-0817-7 · Cited by 42
Self-citationMah, W., & Won, H. (2020) · Schizophrenia Research · doi:10.1016/j.schres.2019.03.007 · Cited by 38
Self-citationGrantyn, R., & Grantyn, A. A. (1973) · Brain Research · doi:10.1016/0006-8993(73)90766-x · Cited by 33 · cited 1×
“…genes: BRAF , which contributes to the MAP kinase signal transduction pathway and plays a role in postsynaptic responses of hippocampal neurons (Grantyn and Grantyn, 1973), and KDM7A (encoding Lysine Demethylase 7A), which plays a central role in the nervous system and midbrain development…”
BackgroundMesocorticolimbic Connectivity and Volumetric Alterations in DCC Mutation Carriers
Vosberg, D. E., Zhang, Y., Menegaux, A., Chalupa, A., Manitt, C., Zehntner, S., Eng, C., DeDuck, K., Allard, D., Durand, F., et al. (2018) · The Journal of Neuroscience · doi:10.1523/jneurosci.3251-17.2018 · Cited by 25 · cited 2×
“…with childhood and adolescent onset would be consistent with its role in both early organization of neuronal circuits and the maturation of mesolimbic dopaminergic connections to the prefrontal cortex during adolescence (Hoops and Flores, 2017; Reynolds et al., 2018; Vosberg et al., 2018).”
BackgroundSelf-citationOn the diagnostic and neurobiological origins of bipolar disorder
Charney, A. W., Mullins, N., Park, Y. J., & Xu, J. (2020) · Translational Psychiatry · doi:10.1038/s41398-020-0796-8 · Cited by 21
Self-citationWiring the Human Brain: A User’s Handbook
Bendriem, R. M., & Ross, M. E. (2017) · Neuron · doi:10.1016/j.neuron.2017.07.008 · Cited by 15 · cited 3×
“Loss-of-function mutations in DCC cause severe neurodevelopmental syndromes involving loss of midline commissural tracts and diffuse disorganization of white matter tracts (Bendriem and Ross, 2017; Jamuar et al., 2017; Marsh et al., 2017).”
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Faraone, S. V., Banaschewski, T., Coghill, D., Zheng, Y., Biederman, J., Bellgrove, M. A., Newcorn, J. H., Gignac, M., Al Saud, N. M., Manor, I., et al. (2021) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2021.01.022 · Cited by 1,545
Self-citationMullins, N., Forstner, A. J., O’Connell, K. S., Coombes, B., Coleman, J. R. I., Qiao, Z., Als, T. D., Bigdeli, T. B., Børte, S., Bryois, J., et al. (2021) · Nature Genetics · doi:10.1038/s41588-021-00857-4 · Cited by 1,517
Self-citationAutism Spectrum Disorder: A Review
Hirota, T., & King, B. H. (2023) · JAMA · doi:10.1001/jama.2022.23661 · Cited by 957
Thapar, A., Eyre, O., Patel, V., & Brent, D. (2022) · The Lancet · doi:10.1016/s0140-6736(22)01012-1 · Cited by 869
“Depression genetic risk variants are highly pleiotropic and also are associated with schizophrenia, bipolar disorder, ADHD and ASD among other disorders 55 .”
Demontis, D., Walters, G. B., Athanasiadis, G., Walters, R., Therrien, K., Nielsen, T. T., Farajzadeh, L., Voloudakis, G., Bendl, J., Zeng, B., et al. (2022) · Nature Genetics · doi:10.1016/j.euroneuro.2022.07.018 · Cited by 863
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Metadata
- Authors
- Lee, P. H., Anttila, V., Won, H., Feng, Y.-C. A., Rosenthal, J., Zhu, Z., Tucker-Drob, E. M., Nivard, M. G., Grotzinger, A. D., Posthuma, D., Wang, M. M.-J., Yu, D., Stahl, E. A., Walters, R. K., Anney, R. J. L., Duncan, L. E., Ge, T., Adolfsson, R., Banaschewski, T., Belangero, S., Cook, E. H., Coppola, G., Derks, E. M., Hoekstra, P. J., Kaprio, J., Keski-Rahkonen, A., Kirov, G., Kranzler, H. R., Luykx, J. J., Rohde, L. A., Zai, C. C., Agerbo, E., Arranz, M. J., Asherson, P., Bækvad-Hansen, M., Baldursson, G., Bellgrove, M., Belliveau, R. A., Buitelaar, J., Burton, C. L., Bybjerg-Grauholm, J., Casas, M., Cerrato, F., Chambert, K., Churchhouse, C., Cormand, B., Crosbie, J., Dalsgaard, S., Demontis, D., Doyle, A. E., Dumont, A., Elia, J., Grove, J., Gudmundsson, O. O., Haavik, J., Hakonarson, H., Hansen, C. S., Hartman, C. A., Hawi, Z., Hervás, A., Hougaard, D. M., Howrigan, D. P., Huang, H., Kuntsi, J., Langley, K., Lesch, K.-P., Leung, P. W. L., Loo, S. K., Martin, J., Martin, A. R., McGough, J. J., Medland, S. E., Moran, J. L., Mors, O., Mortensen, P. B., Oades, R. D., Palmer, D. S., Pedersen, C. B., Pedersen, M. G., Peters, T., Poterba, T., Poulsen, J. B., Ramos-Quiroga, J. A., Reif, A., Ribasés, M., Rothenberger, A., Rovira, P., Sánchez-Mora, C., Satterstrom, F. K., Schachar, R., Artigas, M. S., Steinberg, S., Stefansson, H., Turley, P., Walters, G. B., Werge, T., Zayats, T., Arking, D. E., Bettella, F., Buxbaum, J. D., Christensen, J. H., Collins, R. L., Coon, H., De Rubeis, S., Delorme, R., Grice, D. E., Hansen, T. F., Holmans, P. A., Hope, S., Hultman, C. M., Klei, L., Ladd-Acosta, C., Magnusson, P., Nærland, T., Nyegaard, M., Pinto, D., Qvist, P., Rehnström, K., Reichenberg, A., Reichert, J., Roeder, K., Rouleau, G. A., Saemundsen, E., Sanders, S. J., Sandin, S., St Pourcain, B., Stefansson, K., Sutcliffe, J. S., Talkowski, M. E., Weiss, L. A., Willsey, A. J., Agartz, I., Akil, H., Albani, D., Alda, M., Als, T. D., Anjorin, A., Backlund, L., Bass, N., Bauer, M., Baune, B. T., Bellivier, F., Bergen, S. E., Berrettini, W. H., Biernacka, J. M., Blackwood, D. H. R., Bøen, E., Budde, M., Bunney, W., Burmeister, M., Byerley, W., Byrne, E. M., Cichon, S., Clarke, T.-K., Coleman, J. R. I., Craddock, N., Curtis, D., Czerski, P. M., Dale, A. M., Dalkner, N., Dannlowski, U., Degenhardt, F., Di Florio, A., Elvsåshagen, T., Etain, B., Fischer, S. B., Forstner, A. J., Forty, L., Frank, J., Frye, M., Fullerton, J. M., Gade, K., Gaspar, H. A., Gershon, E. S., Gill, M., Goes, F. S., Gordon, S. D., Gordon-Smith, K., Green, M. J., Greenwood, T. A., Grigoroiu-Serbanescu, M., Guzman-Parra, J., Hauser, J., Hautzinger, M., Heilbronner, U., Herms, S., Hoffmann, P., Holland, D., Jamain, S., Jones, I., Jones, L. A., Kandaswamy, R., Kelsoe, J. R., Kennedy, J. L., Joachim, O. K., Kittel-Schneider, S., Kogevinas, M., Koller, A. C., Lavebratt, C., Lewis, C. M., Li, Q. S., Lissowska, J., Loohuis, L. M. O., Lucae, S., Maaser, A., Malt, U. F., Martin, N. G., Martinsson, L., McElroy, S. L., McMahon, F. J., McQuillin, A., Melle, I., Metspalu, A., Millischer, V., Mitchell, P. B., Montgomery, G. W., Morken, G., Morris, D. W., Müller-Myhsok, B., Mullins, N., Myers, R. M., Nievergelt, C. M., Nordentoft, M., Adolfsson, A. N., Nöthen, M. M., Ophoff, R. A., Owen, M. J., Paciga, S. A., Pato, C. N., Pato, M. T., Perlis, R. H., Perry, A., Potash, J. B., Reinbold, C. S., Rietschel, M., Rivera, M., Roberson, M., Schalling, M., Schofield, P. R., Schulze, T. G., Scott, L. J., Serretti, A., Sigurdsson, E., Smeland, O. B., Stordal, E., Streit, F., Strohmaier, J., Thorgeirsson, T. E., Treutlein, J., Turecki, G., Vaaler, A. E., Vieta, E., Vincent, J. B., Wang, Y., Witt, S. H., Zandi, P., Adan, R. A. H., Alfredsson, L., Ando, T., Aschauer, H., Baker, J. H., Bencko, V., Bergen, A. W., Birgegård, A., Perica, V. B., Brandt, H., Burghardt, R., Carlberg, L., Cassina, M., Clementi, M., Courtet, P., Crawford, S., Crow, S., Crowley, J. J., Danner, U. N., Davis, O. S. P., Degortes, D., DeSocio, J. E., Dick, D. M., Dina, C., Docampo, E., Egberts, K., Ehrlich, S., Espeseth, T., Fernández-Aranda, F., Fichter, M. M., Foretova, L., Forzan, M., Gambaro, G., Giegling, I., Gonidakis, F., Gorwood, P., Mayora, M. G., Guo, Y., Halmi, K. A., Hatzikotoulas, K., Hebebrand, J., Helder, S. G., Herpertz-Dahlmann, B., Herzog, W., Hinney, A., Imgart, H., Jiménez-Murcia, S., Johnson, C., Jordan, J., Julià, A., Kaminská, D., Karhunen, L., Karwautz, A., Kas, M. J. H., Kaye, W. H., Kennedy, M. A., Kim, Y.-R., Klareskog, L., Klump, K. L., Knudsen, G. P. S., Landén, M., Le Hellard, S., Levitan, R. D., Li, D., Lichtenstein, P., Maj, M., Marsal, S., McDevitt, S., Mitchell, J., Monteleone, P., Monteleone, A. M., Munn-Chernoff, M. A., Nacmias, B., Navratilova, M., O’Toole, J. K., Padyukov, L., Pantel, J., Papezova, H., Rabionet, R., Raevuori, A., Ramoz, N., Reichborn-Kjennerud, T., Ricca, V., Roberts, M., Rujescu, D., Rybakowski, F., Scherag, A., Schmidt, U., Seitz, J., Slachtova, L., Slof-Op‘t Landt, M. C. T., Slopien, A., Sorbi, S., Southam, L., Strober, M., Tortorella, A., Tozzi, F., Treasure, J., Tziouvas, K., van Elburg, A. A., Wade, T. D., Wagner, G., Walton, E., Watson, H. J., Wichmann, H.-E., Woodside, D. B., Zeggini, E., Zerwas, S., Zipfel, S., Adams, M. J., Andlauer, T. F. M., Berger, K., Binder, E. B., Boomsma, D. I., Castelao, E., Colodro-Conde, L., Direk, N., Docherty, A. R., Domenici, E., Domschke, K., Dunn, E. C., Foo, J. C., de. Geus, E. J. C., Grabe, H. J., Hamilton, S. P., Horn, C., Hottenga, J.-J., Howard, D., Ising, M., Kloiber, S., Levinson, D. F., Lewis, G., Magnusson, P. K. E., Mbarek, H., Middeldorp, C. M., Mostafavi, S., Nyholt, D. R., Penninx, B. W., Peterson, R. E., Pistis, G., Porteous, D. J., Preisig, M., Quiroz, J. A., Schaefer, C., Schulte, E. C., Shi, J., Smith, D. J., Thomson, P. A., Tiemeier, H., Uher, R., van der Auwera, S., Weissman, M. M., Alexander, M., Begemann, M., Bramon, E., Buccola, N. G., Cairns, M. J., Campion, D., Carr, V. J., Cloninger, C. R., Cohen, D., Collier, D. A., Corvin, A., DeLisi, L. E., Donohoe, G., Dudbridge, F., Duan, J., Freedman, R., Gejman, P. V., Golimbet, V., Godard, S., Ehrenreich, H., Hartmann, A. M., Henskens, F. A., Ikeda, M., Iwata, N., Jablensky, A. V., Joa, I., Jönsson, E. G., Kelly, B. J., Knight, J., Konte, B., Laurent-Levinson, C., Lee, J., Lencz, T., Lerer, B., Loughland, C. M., Malhotra, A. K., Mallet, J., McDonald, C., Mitjans, M., Mowry, B. J., Murphy, K. C., Murray, R. M., O’Neill, F. A., Oh, S.-Y., Palotie, A., Pantelis, C., Pulver, A. E., Petryshen, T. L., Quested, D. J., Riley, B., Sanders, A. R., Schall, U., Schwab, S. G., Scott, R. J., Sham, P. C., Silverman, J. M., Sim, K., Steixner, A. A., Tooney, P. A., van Os, J., Vawter, M. P., Walsh, D., Weiser, M., Wildenauer, D. B., Williams, N. M., Wormley, B. K., Zhang, F., Androutsos, C., Arnold, P. D., Barr, C. L., Barta, C., Bey, K., Bienvenu, O. J., Black, D. W., Brown, L. W., Budman, C., Cath, D., Cheon, K.-A., Ciullo, V., Coffey, B. J., Cusi, D., Davis, L. K., Denys, D., Depienne, C., Dietrich, A., Eapen, V., Falkai, P., Fernandez, T. V., Garcia-Delgar, B., Geller, D. A., Gilbert, D. L., Grados, M. A., Greenberg, E., Grünblatt, E., Hagstrøm, J., Hanna, G. L., Hartmann, A., Hedderly, T., Heiman, G. A., Heyman, I., Hong, H. J., Huang, A., Huyser, C., Ibanez-Gomez, L., Khramtsova, E. A., Kim, Y. K., Kim, Y.-S., King, R. A., Koh, Y.-J., Konstantinidis, A., Kook, S., Kuperman, S., Leventhal, B. L., Lochner, C., Ludolph, A. G., Madruga-Garrido, M., Malaty, I., Maras, A., McCracken, J. T., Meijer, I. A., Mir, P., Morer, A., Müller-Vahl, K. R., Münchau, A., Murphy, T. L., Naarden, A., Nagy, P., Nestadt, G., Nestadt, P. S., Nicolini, H., Nurmi, E. L., Okun, M. S., Paschou, P., Piras, F., Piras, F., Pittenger, C., Plessen, K. J., Richter, M. A., Rizzo, R., Robertson, M., Roessner, V., Ruhrmann, S., Samuels, J. F., Sandor, P., Schlögelhofer, M., Shin, E.-Y., Singer, H., Song, D.-H., Song, J., Spalletta, G., Stein, D. J., Stewart, S. E., Storch, E. A., Stranger, B., Stuhrmann, M., Tarnok, Z., Tischfield, J. A., Tübing, J., Visscher, F., Vulink, N., Wagner, M., Walitza, S., Wanderer, S., Woods, M., Worbe, Y., Zai, G., Zinner, S. H., Sullivan, P. F., Franke, B., Daly, M. J., Bulik, C. M., Lewis, C. M., McIntosh, A. M., O’Donovan, M. C., Zheutlin, A., Andreassen, O. A., Børglum, A. D., Breen, G., Edenberg, H. J., Fanous, A. H., Faraone, S. V., Gelernter, J., Mathews, C. A., Mattheisen, M., Mitchell, K. S., Neale, M. C., Nurnberger, J. I., Ripke, S., Santangelo, S. L., Scharf, J. M., Stein, M. B., Thornton, L. M., Walters, J. T. R., Wray, N. R., Geschwind, D. H., Neale, B. M., Kendler, K. S., & Smoller, J. W.
- Affiliations
- University of Kansas Medical Center (US)
- Massachusetts General Hospital (US)
- University of North Carolina at Chapel Hill (US)
- Broad Institute (US)
- Harvard University (US)
- The University of Texas at Austin (US)
- Icahn School of Medicine at Mount Sinai (US)
- Cardiff University (GB)
- Wuhan University of Technology (CN)
- Umeå University (SE)
- Heidelberg University (DE)
- Universidade Federal de São Paulo (BR)
- University of Illinois Chicago (US)
- University of Helsinki (FI)
- Mental Illness Research, Education and Clinical Centers (US)
- Amsterdam Public Health (NL)
- Stanford University (US)
- University of Pennsylvania (US)
- Radboud University Medical Center (NL)
- Karolinska Institutet (SE)
- Amsterdam Neuroscience (NL)
- Charité – Universitätsmedizin Berlin (DE)
- Aarhus University (DK)
- Institut des Sciences Moléculaires (FR)
- Corresponding author
- Jordan, Jennifer
- Smoller, Jordan W.
- ORCID
- Lee, Phil H.
- Anttila, Verneri
- Won, Hyejung
- Feng, Yen-Chen A.
- Rosenthal, Jacob
- Zhu, Zhaozhong
- Nivard, Michel G.
- Grotzinger, Andrew D.
- Yu, Dongmei
- Stahl, Eli A.
- Walters, Raymond K.
- Anney, Richard J.L.
- Duncan, Laramie E.
- Ge, Tian
- Adolfsson, Rolf
- Banaschewski, Tobias
- Belangero, Sintia
- Cook, Edwin H.
- Coppola, Giovanni
- Derks, Eske M.
- Hoekstra, Pieter J.
- Kaprio, Jaakko
- Kirov, George
- Kranzler, Henry R.
- Luykx, Jurjen J.
- Zai, Clement C.
- Agerbo, Esben
- Arranz, M.J.
- Asherson, Philip
- Bellgrove, Mark
- Buitelaar, Jan
- Burton, Christie L.
- Cerrato, Felecia
- Cormand, Bru
- Crosbie, Jennifer
- Dalsgaard, Søren
- Demontis, Ditte
- Doyle, Alysa E.
- Elia, Josephine
- Grove, Jakob
- Haavik, Jan
- Hakonarson, Hakon
- Hansen, Christine S.
- Hartman, Catharina A.
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- Hougaard, David M.
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- Huang, Hailiang
- Kuntsi, Jonna
- Langley, Kate
- Lesch, Klaus-Peter
- Leung, Patrick W.L.
- Loo, Sandra K.
- Martin, Joanna
- Martin, Alicia R.
- McGough, James J.
- Medland, Sarah E.
- Moran, Jennifer L.
- Mors, Ole
- Mortensen, Preben B.
- Palmer, Duncan S.
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- Peters, Triinu
- Poterba, Timothy
- Reif, Andreas
- Ribasés, Marta
- Rothenberger, Aribert
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- Satterstrom, F. Kyle
- Schachar, Russell
- Steinberg, Stacy
- Turley, Patrick
- Walters, G. Bragi
- Werge, Thomas
- Zayats, Tetyana
- Arking, Dan E.
- Bettella, Francesco
- Buxbaum, Joseph D.
- Christensen, Jane H.
- Collins, Ryan L.
- Coon, Hilary
- Delorme, Richard
- Grice, Dorothy E.
- Hansen, Thomas F.
- Holmans, Peter A.
- Hope, Sigrun
- Hultman, Christina M.
- Klei, Lambertus
- Nærland, Terje
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- Qvist, Per
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- Roeder, Kathryn
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- Sandin, Sven
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- Talkowski, Michael E.
- Weiss, Lauren A.
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- Agartz, Ingrid
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- Backlund, Lena
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- Bergen, Sarah E.
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- Blackwood, Douglas H.R.
- Bøen, Erlend
- Budde, Monika
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- Burmeister, Margit
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- Cichon, Sven
- Clarke, Toni-Kim
- Coleman, Jonathan R.I.
- Curtis, David
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- Dale, Anders M.
- Dalkner, Nina
- Dannlowski, Udo
- Degenhardt, Franziska
- Elvsåshagen, Torbjørn
- Fischer, Sascha B.
- Forty, Liz
- Frank, Josef
- Frye, Mark
- Fullerton, Janice M.
- Gade, Katrin
- Gaspar, Héléna A.
- Gershon, Elliot S.
- Gill, Michael
- Goes, Fernando S.
- Gordon, Scott D.
- Green, Melissa J.
- Greenwood, Tiffany A.
- Hauser, Joanna
- Hautzinger, Martin
- Heilbronner, Urs
- Herms, Stefan
- Hoffmann, Per
- Holland, Dominic
- Jamain, Stéphane
- Jones, Ian
- Jones, Lisa A.
- Kandaswamy, Radhika
- Kelsoe, John R.
- Kennedy, James L.
- Kogevinas, Manolis
- Koller, Anna C.
- Lavebratt, Catharina
- Li, Qingqin S.
- Lissowska, Jolanta
- Loohuis, Loes M.O.
- Lucae, Susanne
- Maaser, Anna
- Malt, Ulrik F.
- Martin, Nicholas G.
- Martinsson, Lina
- McElroy, Susan L.
- McMahon, Francis J.
- McQuillin, Andrew
- Melle, Ingrid
- Metspalu, Andres
- Millischer, Vincent
- Mitchell, Philip B.
- Montgomery, Grant W.
- Morken, Gunnar
- Morris, Derek W.
- Mullins, Niamh
- Myers, Richard M.
- Nievergelt, Caroline M.
- Nordentoft, Merete
- Adolfsson, Annelie Nordin
- Nöthen, Markus M.
- Ophoff, Roel A.
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- Paciga, Sara A.
- Pato, Carlos N.
- Pato, Michele T.
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- Rietschel, Marcella
- Rivera, Margarita
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- Serretti, Alessandro
- Smeland, Olav B.
- Stordal, Eystein
- Streit, Fabian
- Strohmaier, Jana
- Thorgeirsson, Thorgeir E.
- Treutlein, Jens
- Turecki, Gustavo
- Vieta, Eduard
- Vincent, John B.
- Wang, Yunpeng
- Witt, Stephanie H.
- Zandi, Peter
- Adan, Roger A.H.
- Alfredsson, Lars
- Ando, Tetsuya
- Aschauer, Harald
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- Bergen, Andrew W.
- Birgegård, Andreas
- Perica, Vesna Boraska
- Burghardt, Roland
- Cassina, Matteo
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- Danner, Unna N.
- Davis, Oliver S.P.
- Dick, Danielle M.
- Egberts, Karin
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- Gonidakis, Fragiskos
- Gorwood, Philip
- Guo, Yiran
- Halmi, Katherine A.
- Hatzikotoulas, Konstantinos
- Hebebrand, Johannes
- Herzog, Wolfgang
- Hinney, Anke
- Imgart, Hartmut
- Jordan, Jennifer
- Julià, Antonio
- Kaminská, Deborah
- Karhunen, Leila
- Karwautz, Andreas
- Kas, Martien J.H.
- Kaye, Walter H.
- Kennedy, Martin A.
- Kim, Youl-Ri
- Klareskog, Lars
- Klump, Kelly L.
- Knudsen, Gun Peggy S.
- Landén, Mikael
- Li, Dong
- Lichtenstein, Paul
- Maj, Mario
- Marsal, Sara
- McDevitt, Sara
- Mitchell, James
- Monteleone, Palmiero
- Monteleone, Alessio Maria
- Nacmias, Benedetta
- Padyukov, Leonid
- Pantel, Jacques
- Rabionet, Raquel
- Raevuori, Anu
- Ricca, Valdo
- Roberts, Marion
- Rujescu, Dan
- Rybakowski, Filip
- Scherag, André
- Schmidt, Ulrike
- Seitz, Jochen
- Slachtova, Lenka
- Sorbi, Sandro
- Tortorella, Alfonso
- Tozzi, Federica
- Treasure, Janet
- Tziouvas, Konstantinos
- Wade, Tracey D.
- Wagner, Gudrun
- Walton, Esther
- Watson, Hunna J.
- Wichmann, H-Erich
- Woodside, D. Blake
- Zeggini, Eleftheria
- Zerwas, Stephanie
- Andlauer, Till F.M.
- Binder, Elisabeth B.
- Boomsma, Dorret I.
- Castelao, Enrique
- Docherty, Anna R.
- Domenici, Enrico
- Domschke, Katharina
- Dunn, Erin C.
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- Grabe, Hans J.
- Hamilton, Steven P.
- Hottenga, Jouke-Jan
- Howard, David
- Kloiber, Stefan
- Levinson, Douglas F.
- Lewis, Glyn
- Magnusson, Patrik K.E.
- Mbarek, Hamdi
- Middeldorp, Christel M.
- Mostafavi, Sara
- Nyholt, Dale R.
- Penninx, Brenda WJH.
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- Cloninger, C. Robert
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- Cheon, Keun-Ah
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- Cusi, Daniele
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- Depienne, Christel
- Dietrich, Andrea
- Eapen, Valsamma
- Falkai, Peter
- Fernandez, Thomas V.
- Geller, Daniel A.
- Grados, Marco A.
- Greenberg, Erica
- Grünblatt, Edna
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- Heyman, Isobel
- Hong, Hyun Ju
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- Ibanez-Gomez, Laura
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- Kim, Young Key
- Kim, Young-Shin
- King, Robert A.
- Koh, Yun-Joo
- Kook, Sodahm
- Leventhal, Bennett L.
- Ludolph, Andrea G.
- Malaty, Irene
- Maras, Athanasios
- McCracken, James T.
- Meijer, Inge A.
- Mir, Pablo
- Münchau, Alexander
- Murphy, Tara L.
- Nestadt, Gerald
- Nestadt, Paul S.
- Nicolini, Humberto
- Okun, Michael S.
- Paschou, Peristera
- Piras, Fabrizio
- Piras, Federica
- Pittenger, Christopher
- Plessen, Kerstin J.
- Richter, Margaret A.
- Rizzo, Renata
- Roessner, Veit
- Ruhrmann, Stephan
- Samuels, Jack F.
- Sandor, Paul
- Schlögelhofer, Monika
- Singer, Harvey
- Song, Dong-Ho
- Song, Jungeun
- Stein, Dan J.
- Stewart, S Evelyn
- Storch, Eric A.
- Stranger, Barbara
- Tischfield, Jay A.
- Visscher, Frank
- Vulink, Nienke
- Wagner, Michael
- Walitza, Susanne
- Worbe, Yulia
- Zai, Gwyneth
- Zinner, Samuel H.
- Sullivan, Patrick F.
- Franke, Barbara
- Daly, Mark J.
- Bulik, Cynthia M.
- McIntosh, Andrew M.
- O’Donovan, Michael C.
- Zheutlin, Amanda
- Andreassen, Ole A.
- Børglum, Anders D.
- Breen, Gerome
- Edenberg, Howard J.
- Fanous, Ayman H.
- Faraone, Stephen V.
- Gelernter, Joel
- Mathews, Carol A.
- Mattheisen, Manuel
- Mitchell, Karen S.
- Neale, Michael C.
- Ripke, Stephan
- Santangelo, Susan L.
- Scharf, Jeremiah M.
- Thornton, Laura M.
- Walters, James T.R.
- Wray, Naomi R.
- Geschwind, Daniel H.
- Neale, Benjamin M.
- Kendler, Kenneth S.
- Smoller, Jordan W.
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2019-12
- Volume
- 179
- Issue
- 7
- Pages
- 1469-1482.e11
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC7077032
- OpenAlex
- W2995971356
- Cited by
- 1,381
- References
- 90
- Citations by year
- 2026: 134 · 2025: 188 · 2024: 183 · 2023: 188 · 2022: 266 · 2021: 280 · 2020: 130 · 2019: 11
- FWCI
- 103.81
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Cell (publishedVersion, other-oa)
- Research at the University of Copenhagen (University of Copenhagen) (publishedVersion, other-oa)
- PubMed (publishedVersion)
- Pure Amsterdam UMC (publishedVersion)
- Amsterdam UMC (VU Amsterdam) - Institutional Repository (publishedVersion)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (publishedVersion, other-oa)
- ENLIGHTEN (Jurnal Bimbingan dan Konseling Islam) (acceptedVersion, cc-by-sa)
- Lancaster EPrints (Lancaster University) (acceptedVersion)
- ORCA Online Research @Cardiff (Cardiff University) (acceptedVersion)
- Worcester Research and Publications (University of Worcester) (acceptedVersion)
- PubMed Central (acceptedVersion)
- LSHTM Research Online (London School of Hygiene and Tropical Medicine) (acceptedVersion)
- Työväentutkimus Vuosikirja (submittedVersion, other-oa)
- Pure (University of Bath) (submittedVersion, cc-by-nc-nd)
- Radboud Repository (Radboud University) (submittedVersion, other-oa)
- SUNY Digital Repository Support (State University of New York System) (submittedVersion, cc-by-nc-nd)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- HAL (submittedVersion)
- Archivio istituzionale della ricerca (Alma Mater Studiorum Università di Bologna) (submittedVersion)
- UCL Discovery (University College London) (submittedVersion)
- NORA - Norwegian Open Research Archives (submittedVersion, other-oa)
- ORCA Online Research @Cardiff (Cardiff University) (submittedVersion, cc-by-nc-nd)
- YUHSpace (Yonsei University Medical Library) (submittedVersion, cc-by-nc-nd)
- Archivio Istituzionale della Ricerca - Università degli Studi della Campania "Luigi Vanvitelli" (submittedVersion)
- IRIS (submittedVersion)
- JuSER (Forschungszentrum Jülich) (submittedVersion)
- Research Portal (King's College London) (submittedVersion, other-oa)
- Site cant be reached (submittedVersion, cc-by)
- ORBi (University of Liège) (submittedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion)
- Research Portal (Queen's University Belfast) (submittedVersion)
- PuSH - Publication Server of Helmholtz Zentrum München (submittedVersion)
- Queen Mary Research Online (Queen Mary University of London) (submittedVersion)
- VU Research Portal (submittedVersion, other-oa)
- SERVAL (Université de Lausanne) (submittedVersion)
- Padua Research Archive (University of Padova) (submittedVersion)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (submittedVersion)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (submittedVersion, other-oa)
- NOVA (University of Newcastle Australia) (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion, other-oa)
- Columbia Academic Commons (Columbia University)
- Funders
- National Institutes of Health
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Mapping and Diversity in Plants and Animals
- Keywords
- mental illness, pleiotropy, genetic correlation, shared genetic loci, anorexia nervosa, attention deficit hyperactivity disorder, autism spectrum disorder, bipolar disorder, major depressive disorder, obsessive-compulsive disorder, schizophrenia, Tourette syndrome, brain gene expression, brain development, psychiatric classification, risk prediction
- MeSH terms
- Mental Disorders, Humans, Genetic Predisposition to Disease, Quantitative Trait Loci, Genome-Wide Association Study, Neurogenesis, Genetic Pleiotropy
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.
A language model drew the claims from the paper on 2026-10-06, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-06 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
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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