Yr Athro Peter Holmans

2026

• Glatt, S. et al., 2026. Profiling the molecular state of the living brain in schizophrenia and Alzheimer's disease using BrainGENIE: The brain gene expression and network imputation engine [Conference Abstract]. European Neuropsychopharmacology 111 (S1), pp.112963. (10.1016/j.euroneuro.2026.112963)
• Hadfield, O. et al. 2026. W125. Using physical and mental health polygenic risk scores to identify subtypes of schizophrenia and related diagnoses. European Neuropsychopharmacology 111 (S1) 113243. (10.1016/j.euroneuro.2026.113243)
• Razavi, A. et al., 2026. Predicted brain-regional gene expression patterns in individuals living with Alzheimer’s Disease. Neurobiology of Aging 166 , pp.29-40. (10.1016/j.neurobiolaging.2026.04.006)
• Fenner, E. et al. 2026. Analysis of rare coding variants in schizophrenia-associated genes and generalised cognition in the UK Biobank. Molecular Psychiatry 31 , pp.5104-5113. (10.1038/s41380-026-03601-8)
• Qvist Thomassen, J. et al., 2026. APOE-stratified genome-wide association analyses provide insights into the genetic etiology of Alzheimers’s disease. Nature Genetics (10.1038/s41588-026-02713-9)
• Mclauchlan, D. et al. 2026. Exploring the association between antidepressants, progression and mortality in Huntington’s disease. Brain 149 (8) awag009. (10.1093/brain/awag009)
• Barnett, E. J. et al., 2026. A novel method to disentangle tightly linked risk and resilience genes for brain disorders: application to Alzheimer’s disease. Molecular Psychiatry (10.1038/s41380-026-03814-x)
• Vaez, M. et al., 2026. Recurrent copy number variants and psychiatric outcomes in the context of polygenic scores. JAMA Psychiatry 83 (8), pp.827-836. (10.1001/jamapsychiatry.2026.1064)
• Stow, D. et al., 2026. Genetic and sociodemographic factors associated with trajectories of physical and mental health multimorbidity in a South Asian cohort in the UK: A multistate modelling analysis. PLoS Medicine 23 (7) e1004844. (10.1371/journal.pmed.1004844)
• Katzourou, I. K. et al. 2026. Neurodevelopmental copy-number variants increase risk of internalizing and cardiometabolic multimorbidity: Findings from the UK Biobank. American Journal of Human Genetics 113 (6), pp.1319-1329. (10.1016/j.ajhg.2026.02.021)
• Cameron, D. et al. 2026. Developmental, neuroanatomical and cellular expression of genes causing dystonia. Annals of Clinical and Translational Neurology 13 (5), pp.1005-1019. (10.1002/acn3.70285)
• Kreft, K. L. et al. 2026. Genetic subtypes associated with multiple sclerosis severity and response to treatment. Journal of Neurology, Neurosurgery and Psychiatry 97 (5), pp.413-421. (10.1136/jnnp-2025-337337)
• Stow, D. et al., 2026. Combining polygenic risk scores to understand genetic liability to physical-mental health multimorbidity in UK Biobank. Human Molecular Genetics 35 (7) ddag012. (10.1093/hmg/ddag012)
• Hensman Moss, D. J. et al., 2026. Genetic testing for Huntington's disease: Past, present and future. How could genetic data be used to improve clinical practice?. Journal of Huntington's Disease 15 (1), pp.167-178. (10.1177/18796397251391953)
• Smart, S. E. et al. 2026. Genetics to Improve Outcomes in Schizophrenia (GENios): A within-case molecular genetic study protocol. PLoS ONE 21 (2) e0340584. (10.1371/journal.pone.0340584)
• Kendall, K. M. et al. 2026. The relationship between schizophrenia polygenic scores, blood-based proteins and psychosis diagnosis in the UK Biobank. Schizophrenia 12 24. (10.1038/s41537-025-00725-8)

2025

• Harrison, J. R. et al., 2025. Alzheimer’s polygenic risk scores associate with atherogenic lipids and reduced CRP in mid‐life women. Alzheimer's & Dementia: The Journal of the Alzheimer's Association 21 (S7) e108460. (10.1002/alz70861_108460)
• Richards, A. L. et al. 2025. Effects of shared and nonshared schizophrenia and bipolar disorder alleles on cognition and educational attainment in the UK Biobank. Biological Society: Global Open Science 5 (6) 100601. (10.1016/j.bpsgos.2025.100601)
• Smart, S. E. et al. 2025. The role of SLC39A8.p.( Ala391Thr ) in schizophrenia symptom severity and cognitive ability: cross‐sectional studies of schizophrenia and the general UK population. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics 198 (7), pp.135-146. (10.1002/ajmg.b.33037)
• Harrison, J. R. et al. 2025. White matter microstructure in mid- to late adulthood is influenced by pathway-stratified polygenic risk for Alzheimer’s disease. Frontiers in Neuroscience 19 1638503. (10.3389/fnins.2025.1638503)
• Chick, S. L. et al. 2025. Whole-exome sequencing analysis identifies risk genes for schizophrenia. Nature Communications 16 (1) 7102. (10.1038/s41467-025-62429-y)
• Nicolas, A. et al., 2025. Transferability of European-derived Alzheimer's disease polygenic risk scores across multiancestry populations. Nature Genetics 57 , pp.1598-1610. (10.1038/s41588-025-02227-w)
• Bracher-Smith, M. et al. 2025. Machine learning in Alzheimer’s disease genetics. Nature Communications 16 (1) 6726. (10.1038/s41467-025-61650-z)
• Genetic Modifiers of Huntington’s Disease (GeM-HD) Consortium, et al., 2025. Genetic modifiers of somatic expansion and clinical phenotypes in Huntington’s disease highlight shared and tissue-specific effects. Nature Genetics 57 , pp.1426-1436. (10.1038/s41588-025-02191-5)
• Hou, J. et al., 2025. Meta‐analysis of transcriptomic studies of blood and six brain regions identifies a consensus of 15 cross‐tissue mechanisms in Alzheimer's disease and suggests an origin of cross‐study heterogeneity. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics 198 (4) e33019. (10.1002/ajmg.b.33019)
• Katzourou, I. et al. 2025. Contributions of common and rare genetic variation to different measures of mood and anxiety disorder in UK Biobank. BJPsych Open 11 (3) e97. (10.1192/bjo.2025.43)
• O'Connell, K. S. et al., 2025. Genomics yields biological and phenotypic insights into bipolar disorder. Nature 639 , pp.968-975. (10.1038/s41586-024-08468-9)
• Cardno, A. G. et al., 2025. Associations of psychotic symptom dimensions with clinical and developmental variables in twin and general clinical samples. The British Journal of Psychiatry 226 (1), pp.16-23. (10.1192/bjp.2024.129)

2024

• Benger, L. et al. 2024. Adverse childhood experiences and multimorbidity of internalising and cardiometabolic conditions in an older-age population. Presented at: International Population Data Linkage Conference Chicago, USA 15-18 September 2025. Conference Proceedings for International Population Data Linkage Conference. Vol. 9.Vol. 5. Swansea University. , pp.133. (10.23889/ijpds.v9i5.2617)
• Tume, C. E. et al. 2024. Genetic implication of specific glutamatergic neurons of the prefrontal cortex in the pathophysiology of schizophrenia. Biological Psychiatry 4 (5) 100345. (10.1016/j.bpsgos.2024.100345)
• McLauchlan, D. et al. 2024. J020 Antidepressants are associated with slower clinical, imaging and fluid biomarkers of progression in Huntington's disease [Abstract]. Journal of Neurology, Neurosurgery and Psychiatry 95 A167. (10.1136/jnnp-2024-EHDN.341)
• McLauchlan, D. et al., 2024. J021 Antidepressant prescribing patterns in Huntington’s disease: regional and case-control differences. Journal of Neurology, Neurosurgery and Psychiatry 95 , pp.A167-A168. A167. (10.1136/jnnp-2024-EHDN.342)
• Legge, S. E. et al. 2024. Genetic and phenotypic features of Schizophrenia in the UK Biobank. JAMA Psychiatry 81 , pp.681-690. (10.1001/jamapsychiatry.2024.0200)
• Trastulla, L. et al., 2024. Distinct genetic liability profiles define clinically relevant patient strata across common diseases. Nature Communications 15 5534. (10.1038/s41467-024-49338-2)
• Uzochukwu, E. C. et al. 2024. Modelling disease progression of Multiple Sclerosis in a South Wales cohort. Neuroepidemiology 58 (3), pp.218-226. (10.1159/000536427)
• Hall, J. H. et al. 2024. Irritability in young people with copy number variants associated with neurodevelopmental disorders (ND-CNVs). Translational Psychiatry 14 (1) 259. (10.1038/s41398-024-02975-z)
• Kim, K. et al., 2024. Posttranscriptional regulation of FAN1 by miR-124-3p at rs3512 underlies onset-delaying genetic modification in Huntington's disease. Proceedings of the National Academy of Sciences 121 (16) e2322924121. (10.1073/pnas.2322924121)
• Hess, J. L. et al., 2024. A polygenic resilience score moderates the genetic risk for schizophrenia: Replication in 18,090 cases and 28,114 controls from the Psychiatric Genomics Consortium. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics 195 (2) e32957. (10.1002/ajmg.b.32957)
• Kreft, K. L. et al. 2024. Relevance of multiple sclerosis severity genotype in predicting disease course: A real-world cohort. Annals of Neurology 95 (3), pp.459-470. (10.1002/ana.26831)
• Hong, E. P. et al., 2024. Modification of Huntington's disease by short tandem repeats. Brain Communications 6 (2) fcae016. (10.1093/braincomms/fcae016)

2023

• Clifton, N. et al. 2023. The relationship between case-control differential gene expression from brain tissue and genetic associations in schizophrenia. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics 192 (5-6), pp.85-92. (10.1002/ajmg.b.32931)
• Harrison, J. R. et al. 2023. Pathway-specific polygenic scores for Alzheimer's disease are associated with changes in brain structure in younger and older adults. Brain Communications 5 (5) fcad229. (10.1093/braincomms/fcad229)
• Le Guen, Y. et al., 2023. Multiancestry analysis of the HLA locus in Alzheimer’s and Parkinson’s diseases uncovers a shared adaptive immune response mediated by HLA-DRB1*04 subtypes. Proceedings of the National Academy of Sciences 120 (36) e2302720120. (10.1073/pnas.2302720120)
• Millrine, D. et al., 2023. Th1 cells alter the inflammatory signature of IL-6 by channeling STAT transcription factors to Alu-like retroelements. The Journal of Immunology 211 (2), pp.274-286. (10.4049/jimmunol.2300114)
• Allardyce, J. et al. 2023. Specificity of polygenic signatures across symptom dimensions in bipolar disorder: an analysis of UK Bipolar Disorder Research Network data. The Lancet Psychiatry 10 (8), pp.623-631. (10.1016/S2215-0366(23)00186-4)
• Markoulidakis, A. et al. 2023. A tutorial comparing different covariate balancing methods with an application evaluating the causal effects of substance use treatment programs for adolescents. Health Services and Outcomes Research Methodology 23 , pp.115-148. (10.1007/s10742-022-00280-0)
• Rammos, A. et al. 2023. Family-based analysis of the contribution of rare and common genetic variants to school performance in schizophrenia. Molecular Psychiatry 28 , pp.2081-2087. (10.1038/s41380-023-02013-2)
• Dimitriadis, S. I. et al. 2023. Genetic risk for schizophrenia is associated with increased proportion of indirect connections in brain networks revealed by a semi-metric analysis: evidence from population sample stratified for polygenic risk. Cerebral Cortex 33 (6), pp.2997-3011. (10.1093/cercor/bhac256)

2022

• Crawford, K. et al. 2022. Golgi apparatus, endoplasmic reticulum and mitochondrial function implicated in Alzheimer's disease through polygenic risk and RNA sequencing. Molecular Psychiatry (10.1038/s41380-022-01926-8)
• Mirza-Davies, A. et al. 2022. The impact of genetic risk for Alzheimer’s disease on the structural brain networks of young adults. Frontiers in Neuroscience 16 987677. (10.3389/fnins.2022.987677)
• Clifton, N. et al. 2022. Developmental disruption to the cortical transcriptome and synaptosome in a model of SETD1A loss-of-function. Human Molecular Genetics 31 (18), pp.3095-3106. (10.1093/hmg/ddac105)
• Markoulidakis, A. et al. 2022. Covariate balancing & weighting web app (COBWEB): an online tool simplifying robust causal inference in observational studies. Journal of Neurology, Neurosurgery and Psychiatry 93 (S1) A44. (10.1136/jnnp-2022-ehdn.114)
• Lobanov, S. et al. 2022. Huntington’s disease age at motor onset is modified by the tandem hexamer repeat in TCERG1. npj Genomic Medicine 7 53. (10.1038/s41525-022-00317-w)
• Creeth, H. D. J. et al. 2022. Ultrarare coding variants and cognitive function in schizophrenia. JAMA Psychiatry 79 (10), pp.963-970. (10.1001/jamapsychiatry.2022.2289)
• Croft, J. et al., 2022. A computational analysis of abnormal belief-updating processes and their association with psychotic experiences and childhood trauma in a UK birth cohort. Biological Psychiatry: Cognitive Neuroscience and Neuroimaging 7 (7), pp.725-734. (10.1016/j.bpsc.2021.12.007)
• Hou, J. et al., 2022. Polygenic resilience scores capture protective genetic effects for Alzheimer’s disease. Translational Psychiatry 12 (1) 296. (10.1038/s41398-022-02055-0)
• Crawford, K. et al., 2022. Analysis of Alzheimer's disease Polygenic Risk Scores using RNA-sequencing provides further novel biological pathways. medRxiv (10.1101/2022.06.29.22276952)
• Hwang, Y. et al., 2022. Both cis and trans-acting genetic factors drive somatic instability in female carriers of the FMR1 premutation. Scientific Reports 12 10419. (10.1038/s41598-022-14183-0)
• Lee, J. et al., 2022. Genetic modifiers of Huntington disease differentially influence motor and cognitive domains. American Journal of Human Genetics 109 (5), pp.885-899. (10.1016/j.ajhg.2022.03.004)
• Bellenguez, C. et al., 2022. New insights into the genetic etiology of Alzheimer's disease and related dementias. Nature Genetics 54 (4), pp.412-436. (10.1038/s41588-022-01024-z)
• McAllister, B. et al. 2022. Exome sequencing of individuals with Huntington’s disease implicates FAN1 nuclease activity in slowing CAG expansion and disease onset. Nature Neuroscience 25 , pp.446-457. (10.1038/s41593-022-01033-5)
• Trubetskoy, V. et al., 2022. Mapping genomic loci prioritises genes and implicates synaptic biology in schizophrenia. Nature 604 , pp.502-508. (10.1038/s41586-022-04434-5)
• Jones, H. J. et al., 2022. Examining pathways between genetic liability for schizophrenia and patterns of tobacco and cannabis use in adolescence. Psychological Medicine 52 (1), pp.132-139. (10.1017/S0033291720001798)
• Pardinas, A. et al. 2022. Interaction testing and polygenic risk scoring to estimate the contribution of common genetic variants to treatment resistance in schizophrenia. JAMA Psychiatry 79 (3), pp.260-269. (10.1001/jamapsychiatry.2021.3799)

2021

• Markoulidakis, A. et al. 2021. CoBWeb: a user-friendly web application to estimate causal treatment effects from observational data using multiple algorithms. arXiv
• Dimitriadis, S. I. et al. 2021. Genetic risk for schizophrenia is associated with altered visually-induced gamma band activity: evidence from a population sample stratified polygenic risk. Translational Psychiatry 11 592. (10.1038/s41398-021-01678-z)
• Dennison, C. et al. 2021. Risk factors, clinical features, and polygenic risk scores in schizophrenia and schizoaffective disorder depressive-type. Schizophrenia Bulletin 47 (5), pp.1375-1384. (10.1093/schbul/sbab036)
• Clifton, N. E. et al. 2021. Developmental profile of psychiatric risk associated with voltage-gated cation channel activity. Biological Psychiatry 90 (6)(10.1016/j.biopsych.2021.03.009)
• Rees, E. et al. 2021. Schizophrenia, autism spectrum disorders and developmental disorders share specific disruptive coding mutations. Nature Communications 12 5353. (10.1038/s41467-021-25532-4)
• Markoulidakis, A. et al. 2021. Examining the effect of exercise on the progression and severity of Huntington's disease using different covariate balancing methods and simulated data derived from the PACE-HD study [Abstract]. Journal of Neurology, Neurosurgery & Psychiatry 92 (Sup1), pp.A31. (10.1136/jnnp-2021-EHDN.74)
• Cleynen, I. et al., 2021. Genetic contributors to risk of schizophrenia in the presence of a 22q11.2 deletion. Molecular Psychiatry , pp.4496-4510. (10.1038/s41380-020-0654-3)
• Legge, S. et al. 2021. Associations between schizophrenia polygenic liability, symptom dimensions, and cognitive ability in schizophrenia. JAMA Psychiatry 78 (10), pp.1143-1151. (10.1001/jamapsychiatry.2021.1961)
• Clifton, N. E. et al. 2021. Genetic association of FMRP targets with psychiatric disorders. Molecular Psychiatry 26 , pp.2977-2990. (10.1038/s41380-020-00912-2)
• Jones, R. E. et al. 2021. Modest changes in Spi1 dosage reveal the potential for altered microglial function as seen in Alzheimer's disease. Scientific Reports 11 (1) 14935. (10.1038/s41598-021-94324-z)
• Hubbard, L. et al. 2021. Rare copy number variations are associated with poorer cognition in schizophrenia. Biological Psychiatry 90 (1), pp.28-34. (10.1016/j.biopsych.2020.11.025)
• Mullins, N. et al., 2021. Genome-wide association study of more than 40,000 bipolar disorder cases provides new insights into the underlying biology. Nature Genetics 53 , pp.817-829. (10.1038/s41588-021-00857-4)
• Hong, E. P. et al., 2021. Association analysis of chromosome X to identify genetic modifiers of Huntington's disease. Journal of Huntington's Disease 10 (3), pp.367-375. (10.3233/JHD-210485)
• de Rojas, I. et al., 2021. Common variants in Alzheimer's disease and risk stratification by polygenic risk scores. Nature Communications 12 (1) 3417. (10.1038/s41467-021-22491-8)
• Andlauer, T. F. M. et al., 2021. Bipolar multiplex families have an increased burden of common risk variants for psychiatric disorders. Molecular Psychiatry 26 (4), pp.1286-1298. (10.1038/s41380-019-0558-2)
• Harwood, J. et al. 2021. Defining functional variants associated with Alzheimer's disease in the induced immune response. Brain Communications 3 (2) fcab083. (10.1093/braincomms/fcab083)
• Chen, Z. et al., 2021. Human-lineage-specific genomic elements are associated with neurodegenerative disease and APOE transcript usage. Nature Communications 12 (1) 2076. (10.1038/s41467-021-22262-5)
• Hess, J. L. et al., 2021. A polygenic resilience score moderates the genetic risk for schizophrenia. Molecular Psychiatry 26 (3), pp.800-815. (10.1038/s41380-019-0463-8)
• McAllister, B. et al. 2021. Timing and impact of psychiatric, cognitive, and motor abnormalities in Huntington disease. Neurology 96 (19), pp.e2395-e2406. (10.1212/WNL.0000000000011893)
• Hong, E. P. et al., 2021. Huntington's disease pathogenesis: two sequential components. Journal of Huntington's Disease 10 (1), pp.35-51. (10.3233/JHD-200427)
• Donaldson, J. et al. 2021. What is the pathogenic CAG expansion length in Huntington’s disease?. Journal of Huntington's Disease 10 (1), pp.175-202. (10.3233/JHD-200445)
• Katzourou, I. et al. 2021. Cognitive decline in Alzheimer’s disease is not associated with APOE. Journal of Alzheimer's Disease 84 (1), pp.141-149. (10.3233/jad-210685)
• Markoulidakis, A. et al. 2021. How balance and sample size impact bias in the estimation of causal treatment effects: a simulation study. arXiv 2107.09009.

2020

• Holmans, P. 2020. Using genetics to increase specificity of outcome prediction in psychiatric disorders: prospects for progression. American Journal of Psychiatry 177 (10), pp.884-887. (10.1176/appi.ajp.2020.20081181)
• Akingbuwa, W. A. et al., 2020. Genetic associations between childhood psychopathology and adult depression and associated traits in 42 998 individuals. JAMA Psychiatry 77 (7), pp.715-728. (10.1001/jamapsychiatry.2020.0527)
• Kim, K. et al., 2020. Genetic and functional analyses point to FAN1 as the source of multiple Huntington Disease modifier effects. American Journal of Human Genetics 107 (1), pp.96-110. (10.1016/j.ajhg.2020.05.012)
• Ellis, N. et al., 2020. Genetic risk underlying psychiatric and cognitive symptoms in Huntington’s Disease. Biological Psychiatry 87 (9), pp.857-865. (10.1016/j.biopsych.2019.12.010)
• Flower, M. et al., 2020. Reply: The repeat variant in MSH3 is not a genetic modifier for spinocerebellar ataxia type 3 and Friedreich’s ataxia. Brain 143 (4) e26. (10.1093/brain/awaa044)
• Szatkiewicz, J. P. et al., 2020. Characterization of single gene copy number variants in schizophrenia. Biological Psychiatry 87 (8), pp.736-744. (10.1016/j.biopsych.2019.09.023)
• Sullivan, S. A. et al., 2020. A population-based cohort study examining the incidence and impact of psychotic experiences from childhood to adulthood, and prediction of psychotic disorder. American Journal of Psychiatry 177 (4), pp.308-317. (10.1176/appi.ajp.2019.19060654)
• Richards, A. et al. 2020. The relationship between polygenic risk scores and cognition in schizophrenia. Schizophrenia Bulletin 46 (2), pp.-. (10.1093/schbul/sbz061)
• Rees, E. et al. 2020. De novo mutations identified by exome sequencing implicate rare missense variants in SLC6A1 in schizophrenia. Nature Neuroscience 23 (2), pp.179-184. (10.1038/s41593-019-0565-2)
• Hall, L. S. et al. 2020. A transcriptome-wide association study implicates specific pre- and post-synaptic abnormalities in schizophrenia. Human Molecular Genetics 29 (1), pp.159-167. (10.1093/hmg/ddz253)
• Markoulidakis, A. et al. 2020. A tutorial comparing different covariate balancing methods with an application evaluating the causal effect of exercise on the progression of Huntington’s disease. [Online].arXiv. Available at: https://arxiv.org/abs/2010.09563.
• McAllister, B. et al. 2020. The onset and prevalence of motor and psychiatric symptoms in Huntington’s disease. [Online].bioRxiv. (10.1101/2020.05.26.116798)

2019

• Lam, M. et al., 2019. Comparative genetic architectures of schizophrenia in East Asian and European populations. Nature Genetics 51 , pp.1670-1678. (10.1038/s41588-019-0512-x)
• Legge, S. E. et al. 2019. Association of genetic liability to psychotic experiences with neuropsychotic disorders and traits. JAMA Psychiatry 76 (12), pp.1256-1265. (10.1001/jamapsychiatry.2019.2508)
• Lee, P. H. et al., 2019. Genomic relationships, novel loci, and pleiotropic mechanisms across eight psychiatric disorders. Cell 179 (7), pp.1469-1482.e11. (10.1016/j.cell.2019.11.020)
• Ciosi, M. et al., 2019. A genetic association study of glutamine-encoding DNA sequence structures, somatic CAG expansion, and DNA repair gene variants, with Huntington disease clinical outcomes. EBioMedicine 48 , pp.568-580. (10.1016/j.ebiom.2019.09.020)
• Pain, O. et al. 2019. Novel insight into the etiology of autism spectrum disorder gained by integrating expression data with genome-wide association statistics. Biological Psychiatry 86 (4), pp.265-273. (10.1016/j.biopsych.2019.04.034)
• Lee, J. et al., 2019. CAG repeat not polyglutamine length determines timing of Huntington’s disease onset. Cell 178 (4), pp.887-099.e14. (10.1016/j.cell.2019.06.036)
• Baker, E. et al. 2019. Gene-based analysis in HRC imputed genome wide association data identifies three novel genes for Alzheimer’s disease. PLoS ONE 14 (7) e0218111. (10.1371/journal.pone.0218111)
• Flower, M. et al., 2019. MSH3 modifies somatic instability and disease severity in Huntington’s and myotonic dystrophy type 1. Brain 142 (7), pp.1876-1886. (10.1093/brain/awz115)
• Chawner, S. J. R. A. et al. 2019. Genotype–phenotype associations in children with copy number variants associated with high neuropsychiatric risk in the UK (IMAGINE-ID): a case-control cohort study. Lancet Psychiatry 6 (6), pp.493 - 505. (10.1016/S2215-0366(19)30123-3)
• Stahl, E. A. et al., 2019. Genome-wide association study identifies 30 loci associated with bipolar disorder. Nature Genetics 51 , pp.793-803. (10.1038/s41588-019-0397-8)
• Gorman, K. M. et al., 2019. Bi-allelic loss-of-function CACNA1B mutations in progressive epilepsy-dyskinesia. American Journal of Human Genetics 104 (5), pp.948-956. (10.1016/j.ajhg.2019.03.005)
• Rees, E. et al. 2019. Targeted sequencing of 10,198 samples confirms abnormalities in neuronal activity and implicates voltage-gated sodium channels in schizophrenia pathogenesis. Biological Psychiatry 85 (7), pp.554-562. (10.1016/j.biopsych.2018.08.022)
• Kunkle, B. W. et al., 2019. Genetic meta-analysis of diagnosed Alzheimer's disease identifies new risk loci and implicates Aβ, tau, immunity and lipid processing. Nature Genetics 51 (3), pp.414-430. (10.1038/s41588-019-0358-2)
• Lancaster, T. M. et al. 2019. Structural and functional neuroimaging of polygenic risk for schizophrenia: a recall-by-genotype-based approach. Schizophrenia Bulletin 45 (2), pp.405-414. (10.1093/schbul/sby037)
• Chawner, S. et al. 2019. Genotype-phenotype relationships in children with copy number variants associated with high neuropsychiatric risk: Findings from the Intellectual Disability & Mental Health: Assessing the Genomic Impact on Neurodevelopment (IMAGINE-ID) study.. bioRxiv (10.1101/535708)
• Goold, R. et al., 2019. FAN1 modifies Huntington's disease progression by stabilising the expanded HTT CAG repeat. Human Molecular Genetics 28 (4), pp.650-661. ddy375. (10.1093/hmg/ddy375)
• Clifton, N. E. et al. 2019. Dynamic expression of genes associated with schizophrenia and bipolar disorder across development. Translational Psychiatry 9 74. (10.1038/s41398-019-0405-x)
• Vivian-Griffiths, T. et al. 2019. Predictive modeling of schizophrenia from genomic data: Comparison of polygenic risk score with kernel support vector machines approach. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics 180 (1), pp.80-85. (10.1002/ajmg.b.32705)

2018

• Beltrami, C. et al., 2018. Association of elevated urinary miR-126, miR-155, and miR-29b with diabetic kidney disease. American Journal of Pathology 188 (9), pp.1982-1992. (10.1016/j.ajpath.2018.06.006)
• Jones, H. J. et al., 2018. Investigating the genetic architecture of general and specific psychopathology in adolescence. Translational Psychiatry 8 (1) 145. (10.1038/s41398-018-0204-9)
• Ahmad, S. et al., 2018. Disentangling the biological pathways involved in early features of Alzheimer's disease in the Rotterdam Study. Alzheimer's and Dementia 14 (7), pp.848-857. (10.1016/j.jalz.2018.01.005)
• McNulty, P. et al., 2018. Reduced cancer incidence in Huntington's disease: analysis in the Registry study. Journal of Huntington's Disease 7 (3), pp.209-222. (10.3233/JHD-170263)
• Baker, E. et al. 2018. POLARIS: polygenic LD-adjusted risk score approach for set-based analysis of GWAS data. Genetic Epidemiology 42 (4), pp.366-377. (10.1002/gepi.22117)
• Anttila, V. et al., 2018. Analysis of shared heritability in common disorders of the brain. Science 360 (6395) eaap8757. (10.1126/science.aap8757)
• Martin, J. et al. 2018. A genetic investigation of sex bias in the prevalence of attention-deficit/hyperactivity disorder. Biological Psychiatry 83 (12), pp.1044-1053. (10.1016/j.biopsych.2017.11.026)
• Ruderfer, D. M. et al., 2018. Genomic dissection of bipolar disorder and schizophrenia, including 28 subphenotypes. Cell 173 (7), pp.1705-1715.e16. (10.1016/j.cell.2018.05.046)
• Holmans, P. and Stone, T. 2018. Using genomic data to find disease-modifying loci in Huntington's Disease (HD). In: Precious, S. V. , Rosser, A. E. and Dunnett, S. eds. Huntington’s Disease. Vol. 1780, Methods in Molecular Biology Humana Press. , pp.443-461. (10.1007/978-1-4939-7825-0_20)
• Chao, M. J. et al., 2018. Population-specific genetic modification of Huntington's disease in Venezuela. PLoS Genetics 14 (5) e1007274. (10.1371/journal.pgen.1007274)
• Pardinas, A. F. et al. 2018. Common schizophrenia alleles are enriched in mutation-intolerant genes and in regions under strong background selection. Nature Genetics 50 , pp.381-389. (10.1038/s41588-018-0059-2)
• McColgan, P. et al., 2018. Brain regions showing white matter loss in Huntington's Disease are enriched for synaptic and metabolic genes. Biological Psychiatry 83 (5), pp.456-465. (10.1016/j.biopsych.2017.10.019)
• Allardyce, J. et al. 2018. Association between schizophrenia-related polygenic liability and the occurrence and level of mood-incongruent psychotic symptoms in bipolar disorder. JAMA Psychiatry 75 (1), pp.28-35. (10.1001/jamapsychiatry.2017.3485)

2017

• Leonenko, G. et al. 2017. Mutation intolerant genes and targets of FMRP are enriched for nonsynonymous alleles in schizophrenia. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics 174 (7), pp.724-731. (10.1002/ajmg.b.32560)
• Legge, S. E. et al. 2017. Genome-wide common and rare variant analysis provides novel insights into clozapine-associated neutropenia. Molecular Psychiatry 22 , pp.1502-1508. (10.1038/mp.2016.97)
• Holmans, P. A. , Massey, T. H. and Jones, L. 2017. Genetic modifiers of Mendelian disease: Huntington's disease and the trinucleotide repeat disorders. Human Molecular Genetics 26 (R2), pp.R83-R90. (10.1093/hmg/ddx261)
• Lee, J. et al., 2017. A modifier of Huntington's disease onset at the MLH1 locus. Human Molecular Genetics 26 (19), pp.3859-3867. (10.1093/hmg/ddx286)
• Hensman Moss, D. J. et al., 2017. Identification of genetic variants associated with Huntington's disease progression: a genome-wide association study. Lancet Neurology 16 (9), pp.701-711. (10.1016/S1474-4422(17)30161-8)
• Sims, R. et al. 2017. Rare coding variants in PLCG2, ABI3 and TREM2 implicate microglial-mediated innate immunity in Alzheimer's disease. Nature Genetics 49 , pp.1373-1384. (10.1038/ng.3916)
• Chao, M. J. et al., 2017. Haplotype-based stratification of Huntington's disease. European Journal of Human Genetics 25 , pp.1202-1209. (10.1038/ejhg.2017.125)
• Phillips, T. J. et al., 2017. Treating the placenta to prevent adverse effects of gestational hypoxia on fetal brain development. Scientific Reports 7 , pp.-. 9079. (10.1038/s41598-017-06300-1)
• Allardyce, J. et al. 2017. Psychosis and the level of mood incongruence in bipolar disorder are related to genetic liability for schizophrenia. bioRxiv
• Weiner, D. J. et al., 2017. Polygenic transmission disequilibrium confirms that common and rare variation act additively to create risk for autism spectrum disorders. Nature Genetics 49 (7), pp.978-985. (10.1038/ng.3863)
• Hendricks, A. E. et al., 2017. Rare variant analysis of human and rodent obesity genes in individuals with severe childhood obesity. Scientific Reports 7 4394. (10.1038/s41598-017-03054-8)
• Witt, S. H. et al., 2017. Genome-wide association study of borderline personality disorder reveals genetic overlap with the bipolar disorder, schizophrenia and major depression. Translational Psychiatry 7 e1155.
• The Autism Spectrum Disorders Working Group of The Psychiatric G, , Anney, R. J. L. and Holmans, P. 2017. Meta-analysis of GWAS of over 16,000 individuals with autism spectrum disorder highlights a novel locus at 10q24.32 and a significant overlap with schizophrenia. Molecular Autism 8 21. (10.1186/s13229-017-0137-9)
• Hensman Moss, D. J. et al., 2017. Huntington's disease blood and brain show a common gene expression pattern and share an immune signature with Alzheimer's disease. Scientific Reports 7 , pp.-. 44849. (10.1038/srep44849)
• McLaughlin, R. L. et al., 2017. Genetic correlation between amyotrophic lateral sclerosis and schizophrenia. Nature Communications 8 14774. (10.1038/ncomms14774)
• Bowles, K. R. et al. 2017. SMAD transcription factors are altered in cell models of HD and regulate HTT expression. Cellular Signalling 31 , pp.1-14. (10.1016/j.cellsig.2016.12.005)
• Marshall, C. R. et al., 2017. Contribution of copy number variants to schizophrenia from a genome-wide study of 41,321 subjects. Nature Genetics 49 , pp.27-35. (10.1038/ng.3725)

2016

• Rees, E. et al. 2016. Analysis of intellectual disability copy number variants for association with schizophrenia. JAMA Psychiatry 73 (9), pp.963-969. (10.1001/jamapsychiatry.2016.1831)
• Thapar, A. et al. 2016. Psychiatric gene discoveries shape evidence on ADHD's biology. Molecular Psychiatry 21 , pp.1202-1207. (10.1038/mp.2015.163)
• Tansey, K. E. et al. 2016. Common alleles contribute to schizophrenia in CNV carriers. Molecular Psychiatry 21 , pp.1085-1089. (10.1038/mp.2015.143)
• Pardinas, A. et al. 2016. Common schizophrenia alleles are enriched in mutation-intolerant genes and maintained by background selection. bioRxiv (10.1101/068593)
• Miller, J. R. C. et al., 2016. RNA-Seq of Huntington's disease patient myeloid cells reveals innate transcriptional dysregulation associated with proinflammatory pathway activation. Human Molecular Genetics 25 (14), pp.2893-2904. (10.1093/hmg/ddw142)
• Bettencourt, C. et al., 2016. DNA repair pathways underlie a common genetic mechanism modulating onset in polyglutamine diseases. Annals of Neurology 79 (6), pp.983-990. (10.1002/ana.24656)
• Smith, D. J. et al., 2016. Genome-wide analysis of over 106,000 individuals identifies 9 neuroticism-associated loci. Molecular Psychiatry 21 , pp.749-757. (10.1038/mp.2016.49)
• Han, J. et al. 2016. Gender differences in CNV burden do not confound schizophrenia CNV associations. Scientific Reports 6 25986. (10.1038/srep25986)
• Singh, T. et al., 2016. Rare loss-of-function variants in SETD1A are associated with schizophrenia and developmental disorders. Nature Neuroscience 19 (4), pp.571-577. (10.1038/nn.4267)
• Fry, A. E. et al. 2016. Pathogenic copy number variants and SCN1A mutations in patients with intellectual disability and childhood-onset epilepsy. BMC Medical Genetics 17 , pp.-. 34. (10.1186/s12881-016-0294-2)
• Franke, B. et al., 2016. Genetic influences on schizophrenia and subcortical brain volumes: large-scale proof of concept. Nature Neuroscience 19 (3), pp.420-431. (10.1038/nn.4228)
• Jones, H. J. et al., 2016. Phenotypic manifestation of genetic risk for schizophrenia during adolescence in the general population. JAMA Psychiatry 73 (3), pp.221-228. (10.1001/jamapsychiatry.2015.3058)
• Richards, A. et al. 2016. Exome arrays capture polygenic rare variant contributions to schizophrenia. Human Molecular Genetics 25 (5), pp.1001-1007. (10.1093/hmg/ddv620)
• Keum, J. W. et al., 2016. The HTT CAG expansion mutation determines age at death but not disease duration in Huntington’s Disease. American Journal of Human Genetics 98 (2), pp.287-298. (10.1016/j.ajhg.2015.12.018)
• Deming, Y. et al., 2016. A potential endophenotype for Alzheimer's disease: cerebrospinal fluid clusterin. Neurobiology of Aging 37 , pp.208.e1-208.e9. (10.1016/j.neurobiolaging.2015.09.009)
• Mooney, M. A. et al., 2016. Pathway analysis in attention deficit hyperactivity disorder: an ensemble approach. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics 171 (6), pp.815-826. (10.1002/ajmg.b.32446)

2015

• Escott-Price, V. et al. 2015. Common polygenic variation enhances risk prediction for Alzheimer's disease. Brain 138 (12), pp.3673-3684. (10.1093/brain/awv268)
• Bayram-Weston, Z. et al. 2015. Similar striatal gene expression profiles in the striatum of the YAC128 and HdhQ150 mouse models of Huntington's disease are not reflected in mutant Huntingtin inclusion prevalence. BMC Genomics 16 , pp.-. 1079. (10.1186/s12864-015-2251-4)
• Tansey, K. E. et al. 2015. Common alleles contribute to schizophrenia in CNV carriers [Erratum]. Molecular Psychiatry 21 1153. (10.1038/mp.2015.170)
• Kun-Rodrigues, C. et al., 2015. A systematic screening to identifyde novomutations causing sporadic early-onset Parkinson's disease. Human Molecular Genetics 24 (23), pp.6711-20. (10.1093/hmg/ddv376)
• Lee, S. H. et al., 2015. New data and an old puzzle: the negative association between schizophrenia and rheumatoid arthritis. International Journal of Epidemiology 44 (5), pp.1706-1721. (10.1093/ije/dyv136)
• Vilhjálmsson, B. et al., 2015. Modeling linkage disequilibrium increases accuracy of polygenic risk scores. American Journal of Human Genetics 97 (4), pp.576-592. (10.1016/j.ajhg.2015.09.001)
• Walter, K. et al., 2015. The UK10K project identifies rare variants in health and disease. Nature 526 , pp.82-90. (10.1038/nature14962)
• Huang, J. et al., 2015. Improved imputation of low-frequency and rare variants using the UK10K haplotype reference panel. Nature Communications 6 8111. (10.1038/ncomms9111)
• Leonpacher, A. K. et al., 2015. Distinguishing bipolar from unipolar depression: the importance of clinical symptoms and illness features. Psychological Medicine 45 (11), pp.2437-2446. (10.1017/S0033291715000446)
• Lee, J. M. et al., 2015. Identification of genetic factors that modify clinical onset of Huntington's disease. Cell 162 (3), pp.516-526. (10.1016/j.cell.2015.07.003)
• Jones, L. et al. 2015. Convergent genetic and expression data implicate immunity in Alzheimer's disease. Alzheimer's and Dementia 11 (6), pp.658-671. (10.1016/j.jalz.2014.05.1757)
• Østergaard, S. D. et al., 2015. Associations between potentially modifiable risk factors and Alzheimer disease: A mendelian randomization study. PLOS MEDICINE 12 (6), pp.e1001841. e1001841. (10.1371/journal.pmed.1001841)
• Schmidts, M. et al., 2015. TCTEX1D2 mutations underlie Jeune asphyxiating thoracic dystrophy with impaired retrograde intraflagellar transport. Nature Communications 6 7074. (10.1038/ncomms8074)
• Pocklington, A. et al. 2015. Novel findings from CNVs implicate inhibitory and excitatory signaling complexes in schizophrenia. Neuron 86 (5), pp.1203-1214. (10.1016/j.neuron.2015.04.022)
• Hosp, F. et al., 2015. Quantitative interaction proteomics of neurodegenerative disease proteins. Cell Reports 11 (7), pp.1134-46. (10.1016/j.celrep.2015.04.030)
• Bulik-Sullivan, B. K. et al., 2015. LD Score regression distinguishes confounding from polygenicity in genome-wide association studies. Nature Genetics 47 (3), pp.291-295. (10.1038/ng.3211)
• Taylor, P. N. et al. 2015. Whole-genome sequence-based analysis of thyroid function. Nature Communications 6 5681. (10.1038/ncomms6681)
• O'Dushlaine, C. et al., 2015. Psychiatric genome-wide association study analyses implicate neuronal, immune and histone pathways. Nature Neuroscience 18 (2), pp.199-209. (10.1038/nn.3922)
• Maier, R. et al., 2015. Joint analysis of psychiatric disorders increases accuracy of risk prediction for schizophrenia, bipolar disorder, and major depressive disorder. American Journal of Human Genetics 96 (2), pp.283-294. (10.1016/j.ajhg.2014.12.006)
• Correia, K. et al., 2015. The Genetic Modifiers of Motor OnsetAge (GeM MOA) website: Genome-wide association analysis for genetic modifiers of Huntington's Disease. Journal of Huntington's Disease 4 (3), pp.279-284. (10.3233/JHD-150169)
• Ruderfer, D. et al., 2015. No evidence for rare recessive and compound heterozygous disruptive variants in schizophrenia. European Journal of Human Genetics 23 (4), pp.555. (10.1038/ejhg.2014.228)
• Rees, E. et al. 2015. Analysis of exome sequence in 604 trios for recessive genotypes in schizophrenia. Translational Psychiatry 5 (7) e607. (10.1038/tp.2015.99)

2014

• Georgieva, L. et al. 2014. De novo CNVs in bipolar affective disorder and schizophrenia. Human Molecular Genetics 23 (24), pp.6677-6683. (10.1093/hmg/ddu379)
• Gusev, A. et al., 2014. Partitioning heritability of regulatory and cell-type-specific variants across 11 common diseases. American Journal of Human Genetics 95 (5), pp.535-552. (10.1016/j.ajhg.2014.10.004)
• Ruderfer, D. M. et al., 2014. Polygenic dissection of diagnosis and clinical dimensions of bipolar disorder and schizophrenia. Molecular Psychiatry 19 (9), pp.1017-1024. (10.1038/mp.2013.138)
• Timpson, N. J. et al., 2014. A rare variant in APOC3 is associated with plasma triglyceride and VLDL levels in Europeans. Nature Communications 5 4871. (10.1038/ncomms5871)
• Munafò, M. et al., 2014. Scientific rigor and the art of motorcycle maintenance. Nature Biotechnology 32 (9), pp.871-873. (10.1038/nbt.3004)
• Martin, J. et al. 2014. Biological overlap of attention-deficit/hyperactivity disorder and autism spectrum disorder: evidence from copy number variants. Journal of the American Academy of Child and Adolescent Psychiatry 53 (7), pp.761-770.e26. (10.1016/j.jaac.2014.03.004)
• Ripke, S. et al., 2014. Biological insights from 108 schizophrenia-associated genetic loci. Nature 511 (7510), pp.421-427. (10.1038/nature13595)
• Craddock, N. J. et al. 2014. Identifying gene-environment interactions in schizophrenia: contemporary challenges for integrated, large-scale investigations. Schizophrenia Bulletin 40 (4), pp.729-736. (10.1093/schbul/sbu069)
• Erk, S. et al., 2014. Replication of brain function effects of a genome-wide supported psychiatric risk variant in the CACNA1C gene and new multi-locus effects. NeuroImage 94 , pp.147-154. (10.1016/j.neuroimage.2014.03.007)
• Escott-Price, V. et al. 2014. Gene-wide analysis detects two new susceptibility genes for Alzheimer's Disease. PLoS ONE 9 (6) e94661. (10.1371/journal.pone.0094661)
• Liu, G. et al., 2014. Cardiovascular disease contributes to Alzheimer's disease: evidence from large-scale genome-wide association studies. Neurobiology of Aging 35 (4), pp.786-92. (10.1016/j.neurobiolaging.2013.10.084)
• Fromer, M. et al., 2014. De novo mutations in schizophrenia implicate synaptic networks. Nature 506 , pp.179-184. (10.1038/nature12929)
• Duncan, L. E. et al., 2014. Pathway analyses implicate glial cells in schizophrenia. PLoS ONE 9 (2), pp.-. e89441. (10.1371/journal.pone.0089441)

2013

• Green, E. K. et al. 2013. Replication of bipolar disorder susceptibility alleles and identification of two novel genome-wide significant associations in a new bipolar disorder case-control sample. Molecular Psychiatry 18 (12), pp.1302-1307. (10.1038/mp.2012.142)
• van Scheltinga, A. F. T. et al., 2013. Schizophrenia genetic variants are not associated with intelligence. Psychological Medicine 43 (12), pp.2563-2570. (10.1017/S0033291713000196)
• Ripke, S. et al., 2013. Genome-wide association analysis identifies 13 new risk loci for schizophrenia. Nature Genetics 45 (10), pp.1150-1159. (10.1038/ng.2742)
• Hamshere, M. L. et al. 2013. Genome-wide significant associations in schizophrenia to ITIH3/4, CACNA1C and SDCCAG8, and extensive replication of associations reported by the Schizophrenia PGC. Molecular Psychiatry 18 (6), pp.708-712. (10.1038/mp.2012.67)
• Zou, F. et al., 2013. Linking protective GAB2 variants, increased cortical GAB2 expression and decreased Alzheimer's Disease pathology. PLoS ONE 8 (5) e64802. (10.1371/journal.pone.0064802)
• Terwisscha van Scheltinga, A. F. et al., 2013. Genetic schizophrenia risk variants jointly modulate total brain and white matter volume. Biological Psychiatry 73 (6), pp.525-531. (10.1016/j.biopsych.2012.08.017)
• Chapman, J. et al., 2013. A genome-wide study shows a limited contribution of rare copy number variants to Alzheimer's disease risk. Human Molecular Genetics 22 (4), pp.816-824. (10.1093/hmg/dds476)
• Escott-Price, V. et al. 2013. Analysis of genome-wide association studies of Alzheimer disease and of Parkinson disease to determine if these 2 diseases share a common genetic risk. JAMA Neurology 70 (10), pp.1268-1276. (10.1001/jamaneurol.2013.448)
• Hamshere, M. L. et al. 2013. High loading of polygenic risk for ADHD in children with comorbid aggression. American Journal of Psychiatry 170 (8), pp.909-916. (10.1176/appi.ajp.2013.12081129)
• Hamshere, M. L. et al. 2013. Shared polygenic contribution between childhood attention-deficit hyperactivity disorder and adult schizophrenia. British Journal of Psychiatry 203 (2), pp.107-111. (10.1192/bjp.bp.112.117432)
• Holmans, P. A. et al. 2013. A pathway-based analysis provides additional support for an immune-related genetic susceptibility to Parkinson's disease. Human Molecular Genetics 22 (5), pp.1039-1049. (10.1093/hmg/dds492)
• Lambert, J. et al., 2013. Meta-analysis of 74,046 individuals identifies 11 new susceptibility loci for Alzheimer's disease [Letter]. Nature Genetics 45 (12), pp.1452-1458. (10.1038/ng.2802)
• Lee, S. et al., 2013. Genetic relationship between five psychiatric disorders estimated from genome-wide SNPs. Nature Genetics 45 (9), pp.984-994. (10.1038/ng.2711)
• Yang, L. et al., 2013. Polygenic transmission and complex neuro developmental network for attention deficit hyperactivity disorder: Genome-wide association study of both common and rare variants. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics 162 (5), pp.419-430. (10.1002/ajmg.b.32169)

2012

• Hollingworth, P. et al. 2012. Genome-wide association study of Alzheimer's disease with psychotic symptoms. Molecular Psychiatry 17 (12), pp.1316-1327. (10.1038/mp.2011.125)
• Eyre, S. et al., 2012. High-density genetic mapping identifies new susceptibility loci for rheumatoid arthritis. Nature Genetics 44 (12), pp.1336-1340. (10.1038/ng.2462)
• Goes, F. S. et al., 2012. Genome-wide association of mood-incongruent psychotic bipolar disorder. Translational Psychiatry 2 (10) e180. (10.1038/tp.2012.106)
• Hamilton, G. et al., 2012. The role of ECE1 variants in cognitive ability in old age and Alzheimer's disease risk. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics 159B (6), pp.696-709. (10.1002/ajmg.b.32073)
• Levinson, D. F. et al., 2012. Genome-wide association study of multiplex schizophrenia pedigrees. American Journal of Psychiatry 169 (9), pp.963-973. (10.1176/appi.ajp.2012.11091423)
• Hamilton, G. et al., 2012. Functional and genetic analysis of haplotypic sequence variation at the nicastrin genomic locus. Neurobiology of Aging 33 (8) 1848.e1. (10.1016/j.neurobiolaging.2012.02.005)
• Shi, H. et al., 2012. Genetic variants influencing human aging from late-onset Alzheimer's disease (LOAD) genome-wide association studies (GWAS). Neurobiology of Aging 33 (8) 1849.e5. (10.1016/j.neurobiolaging.2012.02.014)
• Jia, P. et al., 2012. Network-assisted investigation of combined causal signals from genome-wide association studies in schizophrenia. PLoS Computational Biology 8 (7) e1002587. (10.1371/journal.pcbi.1002587)
• Goes, F. S. et al., 2012. Co-morbid anxiety disorders in bipolar disorder and major depression: familial aggregation and clinical characteristics of co-morbid panic disorder, social phobia, specific phobia and obsessive-compulsive disorder. Psychological Medicine 42 (07), pp.1449-1459. (10.1017/S0033291711002637)
• Derks, E. M. et al., 2012. Investigation of the genetic association between quantitative measures of psychosis and schizophrenia: A polygenic risk score analysis. PLoS ONE 7 (6) e37852. (10.1371/journal.pone.0037852)
• Sabunciyan, S. et al., 2012. Genome-Wide DNA methylation scan in major depressive disorder. PLoS ONE 7 (4) e34451. (10.1371/journal.pone.0034451)
• Hudson, G. et al., 2012. No consistent evidence for association between mtDNA variants and Alzheimer disease. Neurology 78 (14), pp.1038-1042. (10.1212/WNL.0b013e31824e8f1d)
• Jia, P. et al., 2012. A bias-reducing pathway enrichment analysis of genome-wide association data confirmed association of the MHC region with schizophrenia. Journal of Medical Genetics 49 (2), pp.96-103. (10.1136/jmedgenet-2011-100397)
• Kirov, G. et al. 2012. De novo CNV analysis implicates specific abnormalities of postsynaptic signalling complexes in the pathogenesis of schizophrenia. Molecular Psychiatry 17 (2), pp.142-153. (10.1038/mp.2011.154)
• Gerrish, A. et al. 2012. The role of variation at AβPP, PSEN1, PSEN2, and MAPT in late onset Alzheimer's Disease. Journal of Alzheimer's Disease 28 (2), pp.377-387. (10.3233/JAD-2011-110824)
• Escott-Price, V. et al. 2012. Permutation-based approaches do not adequately allow for linkage disequilibrium in gene-wide multi-locus association analysis. European Journal of Human Genetics 20 (8), pp.890-896. (10.1038/ejhg.2012.8)
• Keller, M. F. et al., 2012. Using genome-wide complex trait analysis to quantify 'missing heritability' in Parkinson's disease. Human Molecular Genetics 21 (22), pp.4996-5009. (10.1093/hmg/dds335)
• Keller, M. C. et al., 2012. Runs of homozygosity implicate autozygosity as a schizophrenia risk factor. Plos Genetics 8 (4) e1002656. (10.1371/journal.pgen.1002656)
• Le Foll, B. et al., 2012. Correction: ACSL6 is associated with the number of cigarettes smoked and its expression is altered by chronic nicotine exposure. PLoS ONE 7 (8)(10.1371/annotation/071abcbd-6f0c-4c4b-9507-dae42450457e)
• Richards, A. et al. 2012. Schizophrenia susceptibility alleles are enriched for alleles that affect gene expression in adult human brain. Molecular Psychiatry 17 (2), pp.193-201. (10.1038/mp.2011.11)
• Simón-Sánchez, J. et al., 2012. Cooperative genome-wide analysis shows increased homozygosity in early onset Parkinson's Disease. PLoS ONE 7 (3) e28787. (10.1371/journal.pone.0028787)
• Stergiakouli, E. et al. 2012. Investigating the contribution of common genetic variants to the risk and pathogenesis of ADHD. American Journal of Psychiatry 169 (2), pp.186-194. (10.1176/appi.ajp.2011.11040551)
• Tansey, K. E. et al. 2012. Genetic predictors of response to serotonergic and noradrenergic antidepressants in major depressive disorder: a genome-wide analysis of individual-level data and a meta-analysis. Plos Medicine 9 (10) e1001326. (10.1371/journal.pmed.1001326)
• Williams, N. M. et al. 2012. Genome-wide analysis of copy number variants in attention deficit hyperactivity disorder: the role of rare variants and duplications at 15q13.3. American Journal of Psychiatry 169 (2), pp.195-204. (10.1176/appi.ajp.2011.11060822)

2011

• Chen, J. et al., 2011. ACSL6 is associated with the number of cigarettes smoked and its expression is altered by chronic nicotine exposure. PLoS ONE 6 (12) e28790. (10.1371/journal.pone.0028790)
• Cardno, A. G. et al., 2011. A genomewide linkage study of age at onset in schizophrenia. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics 156B (8), pp.929-940. (10.1002/ajmg.1404)
• Hinney, A. et al., 2011. Genome-wide association study in German patients with attention deficit/hyperactivity disorder. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics 156 (8), pp.888-897. (10.1002/ajmg.b.31246)
• Sklar, P. et al., 2011. Large-scale genome-wide association analysis of bipolar disorder identifies a new susceptibility locus near ODZ4 [Letter]. Nature Genetics 43 (10), pp.977-983. (10.1038/ng.943)
• Ripke, S. et al., 2011. Genome-wide association study identifies five new schizophrenia loci [Letter]. Nature Genetics 43 (10), pp.969-976. (10.1038/ng.940)
• Chen, J. et al., 2011. Two non-synonymous markers in PTPN21, identified by genome-wide association study data-mining and replication, are associated with schizophrenia. Schizophrenia Research 131 (1-3), pp.43-51.
• Escott-Price, V. et al. 2011. An examination of single nucleotide polymorphism selection prioritization strategies for tests of gene-gene interaction. Biological Psychiatry 70 (2), pp.198-203. (10.1016/j.biopsych.2011.01.034)
• Chen, J. et al., 2011. Two non-synonymous markers in PTPN21, identified by genome-wide association study data-mining and replication, are associated with schizophrenia. Schizophrenia Research 131 (1-3), pp.43-51. (10.1016/j.schres.2011.06.023)
• Hollingworth, P. et al. 2011. Common variants at ABCA7, MS4A6A/MS4A4E, EPHA1, CD33 and CD2AP are associated with Alzheimer's disease. Nature Genetics 43 (5), pp.429-435. (10.1038/ng.803)
• Williams, H. J. et al. 2011. Fine mapping of ZNF804A and genome-wide significant evidence for its involvement in schizophrenia and bipolar disorder. Molecular Psychiatry 16 (4), pp.429-441. (10.1038/mp.2010.36)
• O'Dushlaine, C. et al., 2011. Molecular pathways involved in neuronal cell adhesion and membrane scaffolding contribute to schizophrenia and bipolar disorder susceptibility. Molecular Psychiatry 16 (3), pp.286-292. (10.1038/mp.2010.7)
• Reilly, M. P. et al., 2011. Identification of ADAMTS7 as a novel locus for coronary atherosclerosis and association of ABO with myocardial infarction in the presence of coronary atherosclerosis: two genome-wide association studies. The Lancet 377 (9763), pp.383-392. (10.1016/S0140-6736(10)61996-4)
• Bridges, M. et al., 2011. Genetic classification of populations using supervised learning. PLoS ONE 6 (5) e14802. (10.1371/journal.pone.0014802)
• Hamshere, M. L. et al. 2011. Polygenic dissection of the bipolar phenotype. British Journal of Psychiatry 198 (4), pp.284-288. (10.1192/bjp.bp.110.087866)
• Williams, H. J. et al. 2011. Most genome-wide significant susceptibility loci for schizophrenia and bipolar disorder reported to date cross-traditional diagnostic boundaries. Human Molecular Genetics 20 (2), pp.387-391. (10.1093/hmg/ddq471)
• Dudbridge, F. , Holmans, P. A. and Wilson, S. G. 2011. A flexible model for association analysis in sibships with missing genotype data. Annals of Human Genetics 75 (3), pp.428-438. (10.1111/j.1469-1809.2010.00636.x)
• Escott-Price, V. et al. 2011. Evaluation of an approximation method for assessment of overall significance of multiple-dependent tests in a genomewide association study. Genetic Epidemiology 35 (8), pp.861-866. (10.1002/gepi.20636)
• Hamshere, M. L. et al. 2011. Phenotype evaluation and genomewide linkage study of clinical variables in schizophrenia. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics 156 (8), pp.929-940. (10.1002/ajmg.b.31240)
• Kendler, K. S. et al., 2011. Genomewide association analysis of symptoms of alcohol dependence in the molecular genetics of schizophrenia (MGS2) control sample. Alcoholism-Clinical and Experimental Research 35 (5), pp.963-975. (10.1111/j.1530-0277.2010.01427.x)
• Langley, K. et al. 2011. Clinical and cognitive characteristics of children with attention-deficit hyperactivity disorder, with and without copy number variants. British Journal of Psychiatry 199 (5), pp.398-403.
• Levinson, D. F. et al., 2011. Copy number variants in schizophrenia: confirmation of five previous findings and new evidence for 3q29 microdeletions and VIPR2 duplications. American Journal of Psychiatry 168 (3), pp.302-316. (10.1176/appi.ajp.2010.10060876)
• Lips, E. S. et al., 2011. Functional gene group analysis identifies synaptic gene groups as risk factor for schizophrenia. Molecular Psychiatry , pp.1-11. (10.1038/mp.2011.117)
• Peterson, R. E. et al., 2011. Genetic risk sum score comprised of common polygenic variation is associated with body mass index. Human Genetics 129 (2), pp.221-230. (10.1007/s00439-010-0917-1)
• Sims, R. et al. 2011. No evidence that extended tracts of homozygosity are associated with Alzheimer's disease. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics 156 (7), pp.764-771. (10.1002/ajmg.b.31216)

2010

• Carroll, L. S. et al. 2010. Evidence for rare and common genetic risk variants for schizophrenia at protein kinase C, alpha. Molecular Psychiatry 15 (11), pp.1101-1111. (10.1038/mp.2009.96)
• Craddock, N. J. et al. 2010. Strong genetic evidence for a selective influence of GABAA receptors on a component of the bipolar disorder phenotype [Corrigendum]. Molecular Psychiatry 15 (11), pp.1121-1121. (10.1038/mp.2010.62)
• Jones, L. et al. 2010. Genetic evidence implicates the immune system and cholesterol metabolism in the aetiology of Alzheimer's disease. PLoS ONE 5 (11) e13950. (10.1371/journal.pone.0013950)
• Williams, N. M. et al. 2010. Rare chromosomal deletions and duplications in attention-deficit hyperactivity disorder: a genome-wide analysis. The Lancet 376 (9750), pp.1401-1408. (10.1016/S0140-6736(10)61109-9)
• Green, E. K. et al. 2010. The bipolar disorder risk allele at CACNA1C also confers risk of recurrent major depression and of schizophrenia. Molecular Psychiatry 15 (10), pp.1016-1022. (10.1038/mp.2009.49)
• Allison, D. B. et al., 2010. Accurately assessing the risk of schizophrenia conferred by rare copy-number variation affecting genes with brain function. PLoS Genetics 6 (9) e1001097. (10.1371/journal.pgen.1001097)
• Escott-Price, V. et al. 2010. Genetic differences between five European populations. Human Heredity 70 (2), pp.141-149. (10.1159/000313854)
• Grozeva, D. et al. 2010. Rare copy number variants: A point of rarity in genetic risk for bipolar disorder and schizophrenia. Archives of General Psychiatry 67 (4), pp.318-327. (10.1001/archgenpsychiatry.2010.25)
• Craddock, N. J. et al. 2010. Strong genetic evidence for a selective influence of GABAA receptors on a component of the bipolar disorder phenotype. Molecular Psychiatry 15 (2), pp.146-153. (10.1038/mp.2008.66)
• Dwyer, S. L. et al. 2010. No evidence that rare coding variants in ZNF804A confer risk of schizophrenia. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics 153B (8), pp.1411-1416. (10.1002/ajmg.b.31117)
• Green, E. K. et al. 2010. Variation at the GABAA receptor gene, Rho 1 (GABRR1) associated with susceptibility to bipolar schizoaffective disorder. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics 153B (7), pp.1347-1349. (10.1002/ajmg.b.31108)
• Holmans, P. A. 2010. Statistical methods for pathway analysis of genome-wide data for association with complex genetic traits. In: Moore, J. H. and Dunlap, J. C. eds. Computational Methods for Genetics of Complex Traits. Advances in Genetics Vol. 72.San Diego, CA: Academic Press. , pp.141-179. (10.1016/B978-0-12-380862-2.00007-2)
• Liu, Y. et al., 2010. Meta-analysis of genome-wide association data of bipolar disorder and major depressive disorder [Letter]. Molecular Psychiatry 16 (1), pp.2-4. (10.1038/mp.2009.107)
• Neale, B. M. et al., 2010. Case-control genome-wide association study of attention-deficit/hyperactivity disorder. Journal of the American Academy of Child & Adolescent Psychiatry 49 (9), pp.906-920. (10.1016/j.jaac.2010.06.007)
• Neale, B. M. et al., 2010. Meta-analysis of genome-wide association studies of attention-deficit/hyperactivity disorder. Journal of the American Academy of Child & Adolescent Psychiatry 49 (9), pp.884-897. (10.1016/j.jaac.2010.06.008)
• Shi, J. et al., 2010. Genome-wide association study of recurrent early-onset major depressive disorder. Molecular Psychiatry 16 (2), pp.193-201. (10.1038/mp.2009.124)

2009

• Harold, D. et al. 2009. Genome-wide association study identifies variants at CLU and PICALM associated with Alzheimer's disease [Letter]. Nature Genetics 41 (10), pp.1088-1093. (10.1038/ng.440)
• Shi, J. et al., 2009. Common variants on chromosome 6p22.1 are associated with schizophrenia [Letter]. Nature 460 (7256), pp.753-757. (10.1038/nature08192)
• Ng, M. Y. M. et al., 2009. Meta-analysis of 32 genome-wide linkage studies of schizophrenia. Molecular Psychiatry 14 (8), pp.774-785. (10.1038/mp.2008.135)
• Orozco, G. et al., 2009. Combined effects of three independent SNPs greatly increase the risk estimate for RA at 6q23. Human Molecular Genetics 18 (14), pp.2693-2699. (10.1093/hmg/ddp193)
• Holmans, P. A. et al. 2009. Gene ontology analysis of GWA study data sets provides insights into the biology of bipolar disorder. American Journal of Human Genetics 85 (1), pp.13-24. (10.1016/j.ajhg.2009.05.011)
• Kirov, G. et al. 2009. Support for the involvement of large copy number variants in the pathogenesis of schizophrenia. Human Molecular Genetics 18 (8), pp.1497-1503. (10.1093/hmg/ddp043)
• Webster, J. A. et al., 2009. Genetic control of human brain transcript expression in Alzheimer Disease. American Journal of Human Genetics 84 (4), pp.445-458. (10.1016/j.ajhg.2009.03.011)
• Escott-Price, V. et al. 2009. Gene-wide analyses of genome-wide association data sets: evidence for multiple common risk alleles for schizophrenia and bipolar disorder and for overlap in genetic risk. Molecular Psychiatry 14 (3), pp.252-260. (10.1038/mp.2008.133)
• Hamshere, M. L. et al. 2009. Genetic utility of broadly defined bipolar schizoaffective disorder as a diagnostic concept. British Journal of Psychiatry 195 (1), pp.23-29. (10.1192/bjp.bp.108.061424)
• Harold, D. et al. 2009. Erratum: Genome-wide association study identifies variants at CLU and PICALM associated with Alzheimer's disease [Corrigendum]. Nature Genetics 41 (10), pp.1156. (10.1038/ng1009-1156d)
• O'Donovan, M. C. et al. 2009. Analysis of 10 independent samples provides evidence for association between schizophrenia and a SNP flanking fibroblast growth factor receptor 2. Molecular Psychiatry 14 (1), pp.30-36. (10.1038/mp.2008.108)
• Purcell, S. M. et al., 2009. Common polygenic variation contributes to risk of schizophrenia and bipolar disorder. Nature 460 (7256), pp.748-752. (10.1038/nature08185)
• Glaser, B. and Holmans, P. A. 2009. Comparison of methods for combining case-control and family-based association studies. Human Heredity 68 (2), pp.106-116. (10.1159/000212503)
• Hamshere, M. L. et al. 2009. Mood-incongruent psychosis in bipolar disorder: conditional linkage analysis shows genome-wide suggestive linkage at 1q32.3, 7p13 and 20q13.31. Bipolar Disorders 11 (6), pp.610-620. (10.1111/j.1399-5618.2009.00736.x)
• Holmans, P. A. et al. 2009. Genomewide linkage scan of schizophrenia in a large multicenter pedigree sample using single nucleotide polymorphisms. Molecular Psychiatry 14 (8), pp.786-795. (10.1038/mp.2009.11)
• Langley, K. et al. 2009. Molecular genetic contribution to the developmental course of attention-deficit hyperactivity disorder. European Child & Adolescent Psychiatry 18 (1), pp.26-32. (10.1007/s00787-008-0698-4)
• Mahon, P. B. et al., 2009. Genome-wide linkage and follow-up association study of postpartum mood symptoms. American Journal of Psychiatry 166 (11), pp.1229-1237. (10.1176/appi.ajp.2009.09030417)
• Shyn, S. I. et al., 2009. Novel loci for major depression identified by genome-wide association study of Sequenced Treatment Alternatives to Relieve Depression and meta-analysis of three studies. Molecular Psychiatry 16 (2), pp.202-215. (10.1038/mp.2009.125)

2008

• Barton, A. et al., 2008. Rheumatoid arthritis susceptibility loci at chromosomes 10p15, 12q13 and 22q13. Nature Genetics 40 (10), pp.1156-1159. (10.1038/ng.218)
• Ferreira, M. A. R. et al., 2008. Collaborative genome-wide association analysis supports a role for ANK3 and CACNA1C in bipolar disorder. Nature Genetics 40 (9), pp.1056-1058. (10.1038/ng.209)
• Barton, A. et al., 2008. Re-evaluation of putative rheumatoid arthritis susceptibility genes in the post-genome wide association study era and hypothesis of a key pathway underlying susceptibility. Human Molecular Genetics 17 (15), pp.2274-2279. (10.1093/hmg/ddn128)
• Fisher, S. A. et al., 2008. Genetic determinants of ulcerative colitis include the ECM1 locus and five loci implicated in Crohn's disease. Nature Genetics 40 (6), pp.710-712. (10.1038/ng.145)
• Loos, R. J. F. et al., 2008. Common variants near MC4R are associated with fat mass, weight and risk of obesity. Nature Genetics 40 (6), pp.768-775. (10.1038/ng.140)
• Hodges, A. K. et al. 2008. Brain gene expression correlates with changes in behavior in the R6/1 mouse model of Huntington's disease. Genes, Brain and Behavior 7 (3), pp.288-299. (10.1111/j.1601-183X.2007.00350.x)
• Stone, J. L. et al., 2008. Rare chromosomal deletions and duplications increase risk of schizophrenia. Nature 455 (7210), pp.237-241. (10.1038/nature07239)
• Blom, E. S. et al., 2008. Does APOE explain the linkage of Alzheimer's disease to chromosome 19q13?. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics 147B (6), pp.778-783. (10.1002/ajmg.b.30681)
• Bray, N. J. et al. 2008. Cis- and trans- loci influence expression of the schizophrenia susceptibility gene DTNBP1. Human Molecular Genetics 17 (8), pp.1169-1174. (10.1093/hmg/ddn006)
• Irmansyah, et al., 2008. Genome-wide scan in 124 Indonesian sib-pair families with Schizophrenia reveals genome-wide significant linkage to a locus on chromosome 3p26-21. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics 147B (7), pp.1245-1252. (10.1002/ajmg.b.30763)
• Langley, K. et al. 2008. Testing for gene × environment interaction effects in attention deficit hyperactivity disorder and associated antisocial behavior. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics 147B (1), pp.49-53. (10.1002/ajmg.b.30571)
• Li, Y. et al., 2008. Evidence that common variation in NEDD9 is associated with susceptibility to late-onset Alzheimer's and Parkinson's disease. Human Molecular Genetics 17 (5), pp.759-767. (10.1093/hmg/ddm348)
• O'Donovan, M. C. et al. 2008. Identification of loci associated with schizophrenia by genome-wide association and follow-up. Nature Genetics 40 (9), pp.1053-1055. (10.1038/ng.201)
• Richards, A. L. et al. 2008. A comparison of four clustering methods for brain expression microarray data. BMC Bioinformatics 9 490. (10.1186/1471-2105-9-490)
• Verma, R. et al., 2008. Linkage disequilibrium mapping of a chromosome 15q25-26 major depression linkage region and sequencing of NTRK3. Biological psychiatry 63 (12), pp.1185-1189. (10.1016/j.biopsych.2008.02.005)

2007

• Glaser, B. et al. 2007. Analyses of single marker and pairwise effects of candidate loci for rheumatoid arthritis using logistic regression and random forests [Conference Proceedings]. BMC Proceedings 1 (S1), pp.S54-S54.
• Hamshere, M. L. et al. 2007. Large-scale linkage analysis of 1302 affected relative pairs with rheumatoid arthritis [Conference Proceedings]. BMC Proceedings 1 (S1), pp.S100-S100.
• Segurado, R. et al. 2007. Combining linkage data sets for meta-analysis and mega-analysis: the GAW15 rheumatoid arthritis data set [Conference Proceedings]. BMC Proceedings 1 (S1), pp.S104-S104.
• Nejentsev, S. et al., 2007. Localization of type 1 diabetes susceptibility to the MHC class I genes HLA-B and HLA-A. Nature 450 (7171), pp.887-892. (10.1038/nature06406)
• Verma, R. et al., 2007. Investigating the role ofp11 (S100A10) sequence variation in susceptibility to major depression. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics 144B (8), pp.1079-1082. (10.1002/ajmg.b.30514)
• Myers, A. J. et al., 2007. A survey of genetic human cortical gene expression. Nature Genetics 39 (12), pp.1494-1499. (10.1038/ng.2007.16)
• Thomson, W. et al., 2007. Rheumatoid arthritis association at 6q23. Nature Genetics 39 (12), pp.1431-1433. (10.1038/ng.2007.32)
• Strand, A. D. et al., 2007. Expression profiling of Huntington's disease models suggests that brain-derived neurotrophic factor depletion plays a major role in striatal degeneration. Journal of Neuroscience 27 (43), pp.11758-11768. (10.1523/JNEUROSCI.2461-07.2007)
• Hollingworth, P. et al., 2007. Increased familial risk and genomewide significant linkage for Alzheimer's disease with psychosis. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics 144B (7), pp.841-848. (10.1002/ajmg.b.30515)
• Hamshere, M. L. et al. 2007. Genome-wide linkage analysis of 723 affected relative pairs with late-onset Alzheimer's disease. Human Molecular Genetics Advanc , pp.1-34. (10.1093/hmg/ddm224)
• Jones, I. R. et al. 2007. Bipolar affective puerperal psychosis: genome-wide significant evidence for linkage to chromosome 16. American journal of psychiatry 164 (7), pp.1099-1104. (10.1176/appi.ajp.164.7.1099)
• Langley, K. et al. 2007. Effects of low birth weight, maternal smoking in pregnancy and social class on the phenotypic manifestation of Attention Deficit Hyperactivity Disorder and associated antisocial behaviour: investigation in a clinical sample. BMC Psychiatry 7 (1), pp.26-26. (10.1186/1471-244X-7-26)
• Burton, P. R. et al., 2007. Genome-wide association study of 14,000 cases of seven common diseases and 3,000 shared controls. Nature 447 (7145), pp.661-678. (10.1038/nature05911)
• Strand, A. D. et al., 2007. Conservation of regional gene expression in mouse and human brain. PLOS Genetics 3 (4) e59. (10.1371/journal.pgen.0030059)
• O'Donovan, M. C. et al. 2007. Convergent evidence that oligodendrocyte lineage transcription factor 2 (OLIG2) and interacting genes influence susceptibility to schizophrenia [Conference Abstract]. Schizophrenia bulletin 33 (2), pp.311-312. (10.1093/schbul/sbm004)
• Grupe, A. et al., 2007. Evidence for novel susceptibility genes for late-onset Alzheimer's disease from a genome-wide association study of putative functional variants. Human Molecular Genetics 16 (8), pp.865-873. (10.1093/hmg/ddm031)
• Holmans, P. A. et al. 2007. Genetics of recurrent early-onset major depression (GenRED): final genome scan report. American Journal of Psychiatry 164 (2), pp.248-258.
• Holmans, P. A. et al. 2007. Genetics of recurrent early-onset major depression (GenRED): final genome scan report. American Journal of Psychiatry 164 (2), pp.248-258. (10.1176/appi.ajp.164.2.248)
• Levinson, D. F. et al., 2007. Genetics of recurrent early-onset major depression (GenRED): significant linkage on chromosome 15q25-q26 after fine mapping with single nucleotide polymorphism markers. American Journal of Psychiatry 164 (2), pp.259-264.
• Ghosh, S. et al., 2007. Linkage analyses of rheumatoid arthritis and related quantitative phenotypes: the GAW15 experience. Genetic Epidemiology 31 (S1), pp.S86-S95. (10.1002/gepi.20284)
• Martin, L. J. et al., 2007. Multiple testing in the genomics era: Findings from Genetic Analysis Workshop 15, Group 15. Genetic Epidemiology 31 (S1), pp.S124-S131. (10.1002/gepi.20289)
• Burton, P. R. et al., 2007. Association scan of 14,500 nonsynonymous SNPs in four diseases identifies autoimmunity variants. Nature Genetics 39 (11), pp.1329-1337. (10.1038/ng.2007.17)
• Thapar, A. et al. 2007. Promoting Measured Genes and Measured Environments: On the Importance of Careful Statistical Analyses and Biological Relevance—Reply [Letter]. Archives of General Psychiatry 64 (3), pp.378-379. (10.1001/archpsyc.64.3.378-b)

2006

• Georgieva, L. et al. 2006. Convergent evidence that oligodendrocyte lineage transcription factor 2 (OLIG2) and interacting genes influence susceptibility to schizophrenia. Proceedings of the National Academy of Sciences of the United States of America (PNAS) ISSN 1091-6490 103 (33), pp.12469-12474. (10.1073/pnas.0603029103)
• Escott-Price, V. et al. 2006. Effects of differential genotyping error rate on the Type 1 error probability of case-control studies. Human heredity 61 (1), pp.55-64. (10.1159/000092553)
• Hodges, A. K. et al. 2006. Regional and cellular gene expression changes in human Huntington's disease brain. Human Molecular Genetics 15 (6), pp.965-977. (10.1093/hmg/ddl013)
• Grupe, A. et al., 2006. A scan of chromosome 10 identifies a novel locus showing strong association with late-onset Alzheimer disease. The American Journal of Human Genetics 78 (1), pp.78-88.
• Smemo, S. et al., 2006. Ubiquilin 1 polymorphisms are not associated with late-onset Alzheimer's disease. Annals of Neurology 59 (1), pp.21-26. (10.1002/ana.20673)
• Bray, N. J. et al. 2006. Cis- and trans-acting loci influence expression of DTNBP1, a susceptibility gene for schizophrenia. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics 141B (7), pp.723-724.
• Hamshere, M. L. et al. 2006. Genome wide significant linkage in schizophrenia conditioning on occurrence of depressive episodes. Journal of Medical Genetics 43 (7), pp.563-567. (10.1136/jmg.2005.035345)
• Macgregor, S. , Craddock, N. J. and Holmans, P. A. 2006. Use of phenotypic covariates in association analysis by sequential addition of cases. European Journal of Human Genetics 14 (5), pp.529-534. (10.1038/sj.ejhg.5201604)

2005

• Hamshere, M. L. et al. 2005. Covariate linkage analysis of GAW14 simulated data incorporating subclinical phenotype, sex, population, parent-of-origin, and interaction. BMC Genetics 6 (1), pp.S45. (10.1186/1471-2156-6-S1-S45)
• Levinson, D. F. and Holmans, P. A. 2005. The effect of linkage disequilibrium on linkage analysis of incomplete pedigrees. BMC Genetics 6 (1), pp.S6-S6. (10.1186/1471-2156-6-S1-S6)
• Hamshere, M. L. et al. 2005. Genomewide linkage scan in schizoaffective disorder: significant evidence for linkage at 1q42 close to DISC1, and suggestive evidence at 22q11 and 19p13. Archives of general psychiatry 62 (10), pp.1081-1088. (10.1001/archpsyc.62.10.1081)
• Nowotny, P. et al., 2005. Association studies between risk for late-onset Alzheimer's disease and variants in insulin degrading enzyme. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics 136B (1), pp.62-68. (10.1002/ajmg.b.30186)
• Holmans, P. A. et al. 2005. Genome screen for loci influencing age at onset and rate of decline in late onset Alzheimer's disease. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics 135B (1), pp.24-32. (10.1002/ajmg.b.30114)
• Lambert, D. et al., 2005. Stage 2 of the Wellcome Trust UK-Irish bipolar affective disorder sibling-pair genome screen: evidence for linkage on chromosomes 6q16-q21, 4q12-q21, 9p21, 10p14-p12 and 18q22. Molecular psychiatry 10 (9), pp.831-841. (10.1038/sj.mp.4001684)
• Cope, N. A. et al., 2005. Strong evidence that KIAA0319 on chromosome 6p is a susceptibility gene for developmental dyslexia. American Journal of Human Genetics 76 (4), pp.581-591. (10.1086/429131)
• Li, Y. et al., 2005. Genetic association of the APP binding protein 2 gene (APBB2) with late onset Alzheimer disease. Human Mutation 25 (3), pp.270-277. (10.1002/humu.20138)
• Escott-Price, V. et al. 2005. Design of Case-controls Studies with Unscreened Controls. Annals of Human Genetics 69 (5), pp.566-576. (10.1111/j.1529-8817.2005.00175.x)
• Seaman, S. R. and Holmans, P. A. 2005. Effect of genotyping error on type-I error rate of affected sib pair studies with genotyped parents. Human Heredity 59 (3), pp.157-164. (10.1159/000085939)
• Escott-Price, V. et al. 2005. Streamlined analysis of pooled genotype data in SNP-based association studies. Genetic Epidemiology 28 (3), pp.273-282. (10.1002/gepi.20062)
• Hodges, A. et al., 2005. Regional specificity of transcriptional changes in early grade Huntington's disease brain. Journal of Neurology, Neurosurgery and Psychiatry 76 , pp.A16-A16.
• Hughes, G. P. et al., 2005. Integrating behaviour and brain gene expression in Huntington's disease transgenic mouse models. Journal of Neurology, Neurosurgery and Psychiatry 76 , pp.A41-A41.

2004

• Li, Y. et al., 2004. Association of late-onset Alzheimer's disease with genetic variation in multiple members of the GAPD gene family. Proceedings of the National Academy of Sciences 101 (44), pp.15688-15693. (10.1073/pnas.0403535101)
• Li, Y. et al., 2004. Association of ABCA1 with late-onset Alzheimer?s disease is not observed in a case-control study. Neuroscience Letters 366 (3), pp.268-271. (10.1016/j.neulet.2004.05.047)
• Mowry, B. J. et al., 2004. Multicenter linkage study of schizophrenia loci on chromosome 22q. Molecular Psychiatry 9 (8), pp.784-795. (10.1038/sj.mp.4001481)
• Holmans, P. A. et al. 2004. Genomewide significant linkage to recurrent, early-onset major depressive disorder on chromosome 15q. The American Journal of Human Genetics 74 (6), pp.1154-1167. (10.1086/421333)
• Bernardinelli, L. et al., 2004. Bayesian trio models for association in the presence of genotyping errors. Genetic Epidemiology 26 (1), pp.70-80. (10.1002/gepi.10291)
• Busby, V. et al., 2004. Alpha-T-Catenin Is Expressed in Human Brain and Interacts With the Wnt Signaling Pathway But Is Not Responsible for Linkage to Chromosome 10 in Alzheimer's Disease. Neuromolecular Medicine 5 (2), pp.133-146. (10.1385/NMM:5:2:133)
• Myers, A. J. et al., 2004. Variation in the urokinase-plasminogen activator gene does not explain the chromosome 10 linkage signal for late onset AD. American Journal of Medical Genetics 124B (1), pp.29-37. (10.1002/ajmg.b.20036)

2003

• Williams, N. M. et al. 2003. A systematic genomewide linkage study in 353 sib pairs with schizophrenia. The American journal of human genetics 73 (6), pp.1355-1367. (10.1086/380206)
• Levinson, D. F. et al., 2003. Genetics of recurrent early-onset depression (GenRED): Design and preliminary clinical characteristics of a repository sample for genetic linkage studies. American Journal of Medical Genetics 119B (1), pp.118-130. (10.1002/ajmg.b.20009)
• Hensiek, A. et al., 2003. Updated results of the United Kingdom linkage-based genome screen in multiple sclerosis. Journal of Neuroimmunology 143 (1-2), pp.25-30. (10.1016/j.jneuroim.2003.08.007)
• McInnis, M. G. et al., 2003. Genome-wide scan of bipolar disorder in 65 pedigrees: supportive evidence for linkage at 8q24, 18q22, 4q32, 2p12, and 13q12. Molecular Psychiatry 8 (3), pp.288-298. (10.1038/sj.mp.4001277)
• Rice, K. M. and Holmans, P. A. 2003. Allowing for Genotyping Error in Analysis of Unmatched Case-Control Studies. Annals of Human Genetics 67 (2), pp.165-174. (10.1046/j.1469-1809.2003.00020.x)

2002

• Levinson, D. et al., 2002. Is schizophrenia linked to chromosome 1q? Response. Science 298 (5602), pp.2277-2279.
• Richards, A. J. et al., 2002. Vitreoretinopathy with phalangeal epiphyseal dysplasia, a type II collagenopathy resulting from a novel mutation in the C-propeptide region of the molecule. Journal of Medical Genetics 39 (9), pp.661-665. (10.1136/jmg.39.9.661)
• Akesson, E. et al., 2002. A genome-wide screen for linkage in Nordic sib-pairs with multiple sclerosis. Genes and Immunity 3 (5), pp.279-285. (10.1038/sj.gene.6363866)
• Levinson, D. F. et al., 2002. No major schizophrenia locus detected on chromosome 1q in a large multicenter sample. Science 296 (5568), pp.739-741. (10.1126/science.1069914)
• Myers, A. et al., 2002. Full genome screen for Alzheimer disease: Stage II analysis. American Journal Of Medical Genetics Part A 114 (2), pp.235-244. (10.1002/ajmg.10183)
• Holmans, P. A. 2002. Detecting gene-gene interactions using affected sib pair analysis with covariates. Human Heredity 53 (2), pp.92-102. (10.1159/000057987)
• Bennett, P. et al., 2002. The Wellcome trust UK-Irish bipolar affective disorder sibling-pair genome screen: first stage report. Molecular Psychiatry 7 (2), pp.189-200. (10.1038/sj.mp.4000957)

2001

• Holmans, P. A. 2001. Likelihood-ratio affected sib-pair tests applied to multiply affected sibships: issues of power and type I error rate. Genetic Epidemiology 20 (1), pp.44-56. (10.1002/1098-2272(200101))

2000

• Myers, A. et al., 2000. Susceptibility locus for Alzheimer's disease on chromosome 10. Science 290 (5500), pp.2304-2305. (10.1126/science.290.5500.2304)
• Levinson, D. F. et al., 2000. Multicenter linkage study of schizophrenia candidate regions on chromosomes 5q, 6q, 10p, and 13q: schizophrenia linkage collaborative group III. American Journal of Human Genetics 67 (3), pp.652-663. (10.1086/303041)
• Murphy, K. C. et al., 2000. Chromosome 22q, velo-cardio-facial syndrome (VCFS) and schizophrenia. Journal of Medical Genetics 37 , pp.S58-S58.
• Bandmann, O. et al., 2000. Detailed genotyping demonstrates association between the slow acetylator genotype for N-acetyltransferase 2 (NAT2) and familial Parkinson's disease. Movement Disorders 15 (1), pp.30-35. (10.1002/1531-8257(200001)15:13.0.CO;2-V)
• Neuman, R. J. et al., 2000. Clustering methods applied to allele sharing data. Genetic Epidemiology 19 (1), pp.57-63. (10.1002/1098-2272(2000)19:1+<::AID-GEPI9>3.0.CO;2-D)

1999

• Williams, N. M. et al. 1999. A two-stage genome scan for schizophrenia susceptibility genes in 196 affected sibling pairs. Human Molecular Genetics 8 (9), pp.1729-1739. (10.1093/hmg/8.9.1729)
• Wavrant-De Vrieze, F. et al., 1999. Genetic variability at the amyloid-beta precursor protein locus may contribute to the risk of late-onset Alzheimer's disease. Neuroscience Letters 269 (2), pp.67-70.
• Hateboer, N. et al., 1999. Familial phenotype differences in PKD11. Kidney International 56 (1), pp.34-40. (10.1046/j.1523-1755.1999.00541.x)
• Rees, M. I. et al., 1999. Autosome search for schizophrenia susceptibility genes in multiply affected families. Molecular Psychiatry 4 (4), pp.353-359. (10.1038/sj.mp.4000521)
• Wavrant-DeVrieze, F. et al., 1999. No association between the alpha-2 macroglobulin I1000V polymorphism and Alzheimer's disease. Neuroscience Letters 262 (2), pp.137-139. (10.1016/S0304-3940(99)00035-X)
• Kehoe, P. et al., 1999. A full genome scan for late onset Alzheimer's disease. Human Molecular Genetics 8 (2), pp.237-245. (10.1093/hmg/8.2.237)
• Bandmann, O. et al., 1999. Toxins, genetics, and Parkinson's disease: the role of N-acetyltransferase 2. Advances in Neurology -New York- Raven Press- 80 , pp.199-204.

1998

• Holmans, P. A. 1998. Affected sib-pair methods for detecting linkage to dichotomous traits: review of the methodology. Human biology 70 (6), pp.1025-1040.
• Kehoe, P. G. et al., 1998. The butyrylcholinesterase K variant and susceptibility to Alzheimer's disease. Journal of Medical Genetics 35 (12), pp.1034-1035. (10.1136/jmg.35.12.1034)
• Bandmann, O. et al., 1998. Dopa-responsive dystonia: a clinical and molecular genetic study. Annals of Neurology 44 (4), pp.649-656. (10.1002/ana.410440411)
• Wu, W. S. et al., 1998. Genetic studies on chromosome 12 in late-onset Alzheimer disease. JAMA - The Journal of the American Medical Association 280 (7), pp.619-622. (10.1001/jama.280.7.619)
• Daniels, J. et al., 1998. A simple method for analyzing microsatellite allele image patterns generated from DNA pools and its application to allelic association studies. American Journal of Human Genetics 62 (5), pp.1189-1197. (10.1086/301816)
• Williams, J. et al. 1998. A meta-analysis and transmission disequilibrium study of association between the dopamine D3 receptor gene and schizophrenia. Molecular Psychiatry 3 (2), pp.141-149.
• Hateboer, N. et al., 1998. Inter-family variability of phenotype in autosomal dominant polycystic kidney disease type 1. European Journal of Human Genetics 6 (1), pp.71-71.
• Holmans, P. A. and Craddock, N. J. 1998. Efficient strategies for genome scanning with affected sib pairs - Reply. American Journal of Human Genetics 62 (1), pp.205-207. (10.1086/301683)
• Murphy, K. C. et al., 1998. A linkage study of chromosome 22q in SIB-pairs with schizophrenia. Schizophrenia Research 29 (1-2), pp.131-132. (10.1016/S0920-9964(97)88632-X)
• Spurlock, G. et al. 1998. A family based association study of T102C polymorphism in 5HT2A and schizophrenia plus identification of new polymorphisms in the promoter. Molecular Psychiatry 3 (1), pp.42-49. (10.1038/sj.mp.4000342)

1997

• Bandmann, O. et al., 1997. Association of slow acetylator genotype for N-acetyltransferase 2 with familial Parkinson's disease. The Lancet 350 (9085), pp.1136-1139. (10.1016/S0140-6736(97)03495-8)
• Hateboer, N. et al., 1997. PKD2: The phenotype defined. Kidney International 52 (4), pp.1122-1122.
• Baboolal, K. et al., 1997. Association of the angiotensin I converting enzyme gene deletion polymorphism with early onset of ESRF in PKD1 adult polycystic kidney disease. Kidney International 52 (3), pp.607-613. (10.1038/ki.1997.373)
• Hateboer, N. et al., 1997. Phenotype PKD2 vs. PKD1; results from the European concerted action.. Journal of the American Society of Nephrology 8 , pp.A1722-A1722.
• Owen, M. J. , Holmans, P. A. and McGuffin, P. 1997. Association studies in psychiatric genetics. Molecular Psychiatry 2 (4), pp.270-273. (10.1038/sj.mp.4000292)
• Daniels, J. K. et al., 1997. Linkage study of chromosome 6p in sib-pairs with schizophrenia. American Journal of Medical Genetics 74 (3), pp.319-323. (10.1002/(SICI)1096-8628(19970531)74:3<319::AID-AJMG14>3.0.CO;2-R)
• Holmans, P. A. and Craddock, N. J. 1997. Efficient strategies for genome scanning using maximum-likelihood affected-sib-pair analysis. American Journal of Human Genetics 60 (3), pp.657-666.
• Rees, M. et al., 1997. Association studies of bipolar disorder at the human serotonin transporter gene (hSERT; 5HTT). Molecular Psychiatry 2 (5), pp.398-402. (10.1038/sj.mp.4000256)

1996

• Levinson, D. F. et al., 1996. Additional support for schizophrenia linkage on chromosomes 6 and 8: a multicenter study. Schizophrenia Linkage Collaborative Group for Chromosomes 3, 6 and 8. American Journal of Medical Genetics 67 (6), pp.580-594. (10.1002/(SICI)1096-8628(19961122)67:6<580::AID-AJMG11>3.0.CO;2-P)
• Kehoe, P. et al., 1996. Association between a PS-1 intronic polymorphism and late onset Alzheimer's disease. NeuroReport 7 (13), pp.2155-2158. (10.1097/00001756-199609020-00019)
• Asherson, P. et al., 1996. Linkage, association and mutational analysis of the dopamine D3 receptor gene in schizophrenia. Molecular Psychiatry 1 (2), pp.125-132.
• Gill, M. et al., 1996. A combined analysis of D22S278 marker alleles in affected sib-pairs: support for a susceptibility locus for schizophrenia at chromosome 22q12. Schizophrenia Collaborative Linkage Group (Chromosome 22).. American Journal of Medical Genetics 67 (1), pp.40-45. (10.1002/(SICI)1096-8628(19960216)67:1<40::AID-AJMG6>3.0.CO;2-W)
• Cardno, A. et al., 1996. Factor-derived subsyndromes of schizophrenia and familial morbid risks. Schizophrenia Research 18 (2-3), pp.IVA2-IVA2.
• Craddock, N. J. et al. 1996. Increasing the efficiency of genomic searches for linkage in complex disorders by DNA pooling of affected sib-pairs. Molecular Psychiatry 1 (1), pp.59-64.

1995

• Roberts, A. G. et al., 1995. Partial characterization and assignment of the gene for protoporphyrinogen oxidase and variegate porphyria to human chromosome 1q23. Human Molecular Genetics 4 (12), pp.2387-2390. (10.1093/hmg/4.12.2387)
• Holmans, P. A. and Clayton, D. 1995. Efficiency of typing unaffected relatives in an affected-sib-pair linkage study with single-locus and multiple tightly linked markers. American Journal of Human Genetics 57 (5), pp.1221-1232.
• Wood, N. W. et al., 1995. Susceptibility to multiple sclerosis and the immunoglobulin heavy chain variable region. Journal of Neurology 242 (10), pp.677-682. (10.1007/BF00866919)
• Wood, N. W. et al., 1995. The T-cell receptor beta locus and susceptibility to multiple sclerosis. Neurology 45 (10), pp.1859-1863. (10.1212/WNL.45.10.1859)
• Kellar-Wood, H. F. et al., 1995. Multiple sclerosis and the HLA-D region: linkage and association studies. Journal of Neuroimmunology 58 (2), pp.183-190. (10.1016/0165-5728(95)00015-T)
• Holmans, P. A. , McGuffin, P. and Clayton, D. 1995. Genome scan for association and linkage. Genetic Epidemiology 12 (6), pp.613-618. (10.1002/gepi.1370120615)
• Robertson, N. et al. 1995. Strategies for the identification of susceptibility genes in multiple sclerosis [Editorial]. The International Ms Journal 2 , pp.19-28.

1994

• Wood, N. W. et al., 1994. No linkage or association between multiple sclerosis and the myelin basic protein gene in affected sibling pairs. Journal of Neurology, Neurosurgery & Psychiatry 57 (10), pp.1191-1194. (10.1136/jnnp.57.10.1191)
• Eoli, M. et al., 1994. No linkage between multiple sclerosis and the T cell receptor alpha chain locus. Journal of the Neurological Sciences 124 (1), pp.32. (10.1016/0022-510X(94)90007-8)

1993

• Holmans, P. A. 1993. Asymptotic properties of affected-sib-pair linkage analysis. American journal of human genetics 52 (2), pp.362-374.