Genetic relationship between five psychiatric disorders estimated from genome-wide SNPs
Open accessAbstract
Most psychiatric disorders are moderately to highly heritable. The degree to which genetic variation is unique to individual disorders or shared across disorders is unclear. To examine shared genetic etiology, we use genome-wide genotype data from the Psychiatric Genomics Consortium (PGC) for cases and controls in schizophrenia, bipolar disorder, major depressive disorder, autism spectrum disorders (ASD) and attention-deficit/hyperactivity disorder (ADHD). We apply univariate and bivariate methods for the estimation of genetic variation within and covariation between disorders. SNPs explained 17-29% of the variance in liability. The genetic correlation calculated using common SNPs was high between schizophrenia and bipolar disorder (0.68 ± 0.04 s.e.), moderate between schizophrenia and major depressive disorder (0.43 ± 0.06 s.e.), bipolar disorder and major depressive disorder (0.47 ± 0.06 s.e.), and ADHD and major depressive disorder (0.32 ± 0.07 s.e.), low between schizophrenia and ASD (0.16 ± 0.06 s.e.) and non-significant for other pairs of disorders as well as between psychiatric disorders and the negative control of Crohn's disease. This empirical evidence of shared genetic etiology for psychiatric disorders can inform nosology and encourages the investigation of common pathophysiologies for related disorders.
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Twin and family studies consistently demonstrate that ASD has a particularly large genetic contribution, with estimated heritability ranging from ~40 to 90%.
“Twin and family studies consistently demonstrate that ASD has a particularly large genetic contribution, with estimated heritability ranging from ~40 to 90% 31,32 .”
From Autism spectrum disorder (2020) · cites this paper as [31]
The Abstract says family and twin studies consistently find genetic contributions to psychiatric disorders, and the Discussion says the paper’s ASD SNP-based heritability estimate of 0.17 is considerably lower than family-study estimates. These passages support a substantial genetic contribution to ASD, but our copy does not give the claimed family-study heritability range of approximately 40–90%. (LLM, conf=0.86)
Experimental — accuracy not yet measuredSNP-based heritability of ADHD ranged between 10% and 28% according to SNP analysis studies.
“However, other studies using single-nucleotide polymorphism (SNP) analysis have estimated that SNP-based heritability ranged between 10% and 28% [57].”
From Molecular Characterisation of the Mechanism of Action of Stimulant Drugs Lisdexamfetamine and Methylphenidate on ADHD Neurobiology: A Review (2022) · cites this paper as [57]
The Discussion reports an ADHD SNP-based heritability estimate of 0.28 (28%). The Results describe variation between ADHD subsets, but the passages found do not give a 10% estimate or establish a 10%–28% range. (LLM, conf=0.87)
Experimental — accuracy not yet measuredThere is a surprising degree of overlap in genetic risk for overtly disparate neuropsychiatric phenotypes that remains to be further elucidated.
“although there is also a surprising degree of overlap in genetic risk for overtly disparate neuropsychiatric phenotypes that remains to be further elucidated 31 .”
From Autism spectrum disorder (2020) · cites this paper as [31]
Neurobiologically, ASD and schizophrenia share putative risk genes and may involve analogous abnormalities in the neuromodulatory regulation of postsynaptic gain.
“Furthermore, neurobiologically, ASD and schizophrenia share putative risk genes (96) and may involve analogous abnormalities in the neuromodulatory regulation of postsynaptic gain, as described further below (3, 92).”
From Can Bayesian Theories of Autism Spectrum Disorder Help Improve Clinical Practice? (2016) · cites this paper as [96]
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).
“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 [45]
Common genetic factors contributing to depression and autism have been reported.
“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 [45]
Studies have found remarkable pleiotropy among genetic risk variants for neurodevelopmental disorders.
“As more genetic risk variants for these disorders have been discovered, studies have found remarkable pleiotropy1,1,83,84.”
From Systems biology and gene networks in neurodevelopmental and neurodegenerative disorders (2015) · cites this paper as [84]
Many severe mutations do not converge on one specific phenotype but instead seem to cause a range of clinical disorders.
“Thus, many severe mutations do not converge on one specific phenotype but instead seem to cause a range of clinical disorders74,76,80,81,84,87,91.”
From Systems biology and gene networks in neurodevelopmental and neurodegenerative disorders (2015) · cites this paper as [84]
GWAS signal enrichment analysis found that common variants associated with schizophrenia and bipolar disorder were enriched in the neuronal differentiation module.
“Moreover, genome-wide association study (GWAS) signal enrichment analysis30 found that common variants associated with schizophrenia and bipolar disorder were enriched in the neuronal differentiation module, suggesting that disorders sharing a genetic architecture84 may also share functional transcriptional alterations: a hypothesis that warrants rigorous testing.”
From Systems biology and gene networks in neurodevelopmental and neurodegenerative disorders (2015) · cites this paper as [84]
Schizophrenia shares significant overlap with bipolar disorder, including PV-IN pathology.
“Schizophrenia also shares significant overlap with BPD [55,56], including PV-IN pathology.”
From Parvalbumin interneuron vulnerability and brain disorders (2021) · cites this paper as [55]
The clustering pattern matched the clinical similarity among these disorders and their genetic similarity, based on published genetic studies.
“This pattern matched the clinical similarity among these disorders and their genetic similarity, based on published genetic studies40.”
From Inflammation-related biomarkers in major psychiatric disorders: a cross-disorder assessment of reproducibility and specificity in 43 meta-analyses (2019) · cites this paper as [40]
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Autism, Gastrointestinal Symptoms and Modulation of Gut Microbiota by Nutritional Interventions
Ristori, M. V., Quagliariello, A., Reddel, S., Ianiro, G., Vicari, S., Gasbarrini, A., & Putignani, L. (2019) · Nutrients · doi:10.3390/nu11112812 · Cited by 214 · see citing works
Effect of polygenic risk scores on depression in childhood trauma
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From maps to multi-dimensional network mechanisms of mental disorders
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Association of autistic traits with depression from childhood to age 18 years
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- Authors
- Cross-Disorder Group of the Psychiatric Genomics Consortium
- Venue
- Nature Genetics
- Published
- 2013-08-11
- Volume
- 45
- Issue
- 9
- Pages
- 984-994
- ISSN
- 1061-4036 (ISSN-L)
- 1546-1718
- PMC
- PMC3800159
- OpenAlex
- W2045227722
- Cited by
- 2,263
- References
- 88
- Citations by year
- 2026: 57 · 2025: 76 · 2024: 99 · 2023: 101 · 2022: 137 · 2021: 182 · 2020: 224 · 2019: 223 · 2018: 210 · 2017: 253 · 2016: 246 · 2015: 229 · 2014: 191 · 2013: 32 · 2012: 3
- FWCI
- 154.38
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Genetics (publishedVersion)
- PubMed (publishedVersion)
- Pure Amsterdam UMC (publishedVersion)
- Research Explorer (The University of Manchester) (publishedVersion)
- Amsterdam UMC (VU Amsterdam) - Institutional Repository (publishedVersion)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (publishedVersion)
- VU Research Portal (publishedVersion, other-oa)
- Monash University Research Portal (Monash University) (acceptedVersion, other-oa)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Strathprints: The University of Strathclyde institutional repository (University of Strathclyde) (acceptedVersion)
- Arrow@dit (Dublin Institute of Technology) (submittedVersion)
- HAL (submittedVersion, cc-by)
- Ghent University Academic Bibliography (Ghent University) (submittedVersion, other-oa)
- DuEPublico (University of Duisburg-Essen) (submittedVersion)
- TSpace (University of Toronto) (submittedVersion, cc-by)
- Rutgers University Community Repository (Rutgers University) (submittedVersion)
- EPubDev Repository (submittedVersion)
- National University of Singapore (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (submittedVersion)
- Leiden Repository (Leiden University) (submittedVersion)
- Research Publications (Maastricht University) (submittedVersion, other-oa)
- Archivio istituzionale della ricerca (Alma Mater Studiorum Università di Bologna) (submittedVersion)
- Adelaide Research & Scholarship (AR&S) (University of Adelaide) (submittedVersion)
- Discovery Research Portal (University of Dundee) (submittedVersion)
- ePrints Soton (University of Southampton) (submittedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Max Planck Digital Library (submittedVersion, other-oa)
- JuSER (Forschungszentrum Jülich) (submittedVersion)
- Research Portal (King's College London) (submittedVersion)
- Lirias (KU Leuven) (submittedVersion)
- Lithuanian University of Health Sciences (submittedVersion)
- ORBi (University of Liège) (submittedVersion, other-oa)
- VBN Forskningsportal (Aalborg Universitet) (submittedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion, other-oa)
- Portuguese National Funding Agency for Science, Research and Technology (RCAAP Project by FCT) (submittedVersion)
- Radboud Repository (Radboud University) (submittedVersion)
- Bristol Research (University of Bristol) (submittedVersion)
- LSHTM Research Online (London School of Hygiene and Tropical Medicine) (submittedVersion)
- RUNE (Research UNE) (submittedVersion)
- Trinity's Access to Research Output (TARA) (Trinity College Dublin) (submittedVersion)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (submittedVersion)
- Research Publications (Maastricht University) (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion, other-oa)
- Newcastle University ePrints (Newcastle Univesity)
- Funders
- Wellcome Trust (090532)
- Vrije Universiteit Amsterdam
- Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
- Nederlandse Organisatie voor Wetenschappelijk Onderzoek (NWO 480‐05‐003, 480- 05-003)
- Crohn's and Colitis UK (M11-1)
- Directorate for Biological Sciences
- Goddard Space Flight Center
- Medical Research Council
- Australian Research Council (FT0991360, DE130100614)
- National Health and Medical Research Council (1047956, 613608, 1011506)
- National Institute on Alcohol Abuse and Alcoholism (K05AA017688)
- National Institute of Mental Health (R01MH041953, R01MH094293, R01MH100141, U01MH085520, R01MH100027, R01MH094400, K99MH101367, MH085520, R01MH085548, R01MH083094, K24MH094614)
- National Human Genome Research Institute (T32HG000040)
- National Cancer Institute (R01CA082659)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (P50HD055782)
- 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, shared genetic etiology, genetic correlation, schizophrenia, bipolar disorder, major depressive disorder, autism spectrum disorder, attention deficit hyperactivity disorder, heritability, single nucleotide polymorphisms, Psychiatric Genomics Consortium, disease classification
- MeSH terms
- Adult, Attention Deficit Disorder with Hyperactivity, Mental Disorders, Bipolar Disorder, Child, Child Development Disorders, Pervasive, Crohn Disease, Depressive Disorder, Major, Major Depressive Disorder, Humans, Schizophrenia, Genome, Human, Genetic Heterogeneity, Genetic Predisposition to Disease, Polymorphism, Single Nucleotide, Inheritance Patterns, Genome-Wide Association Study
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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