The aim of my research group is to identify how different layers of genetics, epigenetics and gene expression can be involved together in the development of mental disorders, their outcome and how they are modulated by the environment.
I am a core researcher at the NORMENT, a Norwegian Centre of Excellence for Research on Mental Health. The NORMENT is described here: http://www.med.uio.no/norment/english/ In Bergen I am situated at the Dr Martens group for research on biological psychiatry, our research activity is described here: http://www.uib.no/en/rg/geneticsgroup/106397/martens-group#at-a-glance
Description of our group in the NORMENT centre:
Epigenetics and multi-omicsAbout the group
The group consists of people with background in genetics, statistics, medicine and informatics who together bring their complementary expertise to try understand the interaction between genetic and environmental risk in mental disorders. We work in close collaboration with clinicians.
We use datasets generated in house or publicly available that combine genetic, epigenetic and gene expression datasets for mental disorders (mostly schizophrenia and bipolar disorders) that are in addition well annotated for environmental factors.Aims
Genetic studies of psychiatric disorders have identified numerous genomic regions that harbor genetic variants which explain some of the risk to develop illness. In addition to the genetic risk, many environmental risks (drug use, trauma, migration, etc) can affect the development and the outcome of mental disorders.
Our aim is to identify how the different layers of genetics, epigenetics and gene expression can be involved together in the development of mental disorders, their outcome and how they are modulated by the environment.Projects
- Molecular mechanisms of exposure to cannabis in patients with schizophrenia: We are looking at the difference between cannabis users and non users in DNA methylation and modelling these differences in cell models.
- The 3D sample: In a set of patients and controls we have genetic information, epigenetic information and gene expression. We are combining these 3 datasets to try identify common effects across the 3 dimensions.
- DNA methylation in psychiatric disorders, and mediation of gene by environment effects, from birth to adulthood. We are examining the variations on DNA methylation associated with mental disorders.
- An evolutionary epigenetics approach to schizophrenia: We examine if regions differentially methylated in the recent human evolution can be implicated in schizophrenia.
- van der Meer D, et al. (2018) Brain scans from 21,297 individuals reveal the genetic architecture of hippocampal subfield volumes. Mol Psychiatry.
- Banerjee N, et al. (2018) Recently evolved human-specific methylated regions are enriched in schizophrenia signals. Bmc Evol Biol 18.
- Hughes T, et al. (2018) Elevated expression of a minor isoform of ANK3 is a risk factor for bipolar disorder. Transl Psychiatry 8(1):210.
- Banerjee N, et al. (2018) Analysis of differentially methylated regions in great apes and extinct hominids provides support for the evolutionary hypothesis of schizophrenia. Schizophr Res.
- Davies G, et al. (2018) Study of 300,486 individuals identifies 148 independent genetic loci influencing general cognitive function. Nature Communications 9.
I teach Genetics and Evolution to medical students in their 3rd semester, at the Faculty of Medicine, UiB.
I also participate in the IGSIN course for PhD students, UiB, and the Master course in Genetics of Cognitive Neuroscience at the University of Oslo.
- 2019. Common brain disorders are associated with heritable patterns of apparent aging of the brain. Nature Neuroscience.
- 2019. Genome-wide association study identifies eight risk loci and implicates metabo-psychiatric origins for anorexia nervosa. Nature Genetics. 51: 1207-1214. doi: 10.1038/s41588-019-0439-2
- 2018. Recently evolved human-specific methylated regions are enriched in schizophrenia signals. BMC Evolutionary Biology. 18:63: 1-11. doi: 10.1186/s12862-018-1177-2
- 2018. Analysis of differentially methylated regions in great apes and extinct hominids provides support for the evolutionary hypothesis of schizophrenia. Schizophrenia Research. 8 pages. doi: 10.1016/j.schres.2018.11.025
- 2018. Study of 300,486 individuals identifies 148 independent genetic loci influencing general cognitive function. Nature Communications. 9: 1-16. doi: 10.1038/s41467-018-04362-x
- 2018. Williams Syndrome neuroanatomical score associates with GTF2IRD1 in large-scale magnetic resonance imaging cohorts: A proof of concept for multivariate endophenotypes. Translational psychiatry. 8:114: 1-8. doi: 10.1038/s41398-018-0166-y
- 2018. Elevated expression of a minor isoform of ANK3 is a risk factor for bipolar disorder. Translational psychiatry. 8: 1-10. doi: 10.1038/s41398-018-0175-x
- 2018. Multi-Trait analysis of gwas and biological insights into cognition: A response to Hill (2018). Twin Research and Human Genetics. 21: 394-397. doi: 10.1017/thg.2018.46
- 2018. Genome-wide association meta-analysis in 269,867 individuals identifies new genetic and functional links to intelligence. Nature Genetics. 50: 912-919. doi: 10.1038/s41588-018-0152-6
- 2018. Genetic variation in 117 myelination-related genes in schizophrenia: Replication of association to lipid biosynthesis genes. Scientific Reports. 8: 1-8. Published 2018-05-02. doi: 10.1038/s41598-018-25280-4
- 2018. Genetic and transcriptional analysis of inflammatory bowel disease-associated pathways in patients with GUCY2C-linked familial diarrhea. Scandinavian Journal of Gastroenterology. 53: 1264-1273. doi: 10.1080/00365521.2018.1521867
- 2018. Meta-analysis of Alzheimer’s disease on 9,751 samples from Norway and IGAP study identifies four risk loci. Scientific Reports. 8. 8 pages. doi: 10.1038/s41598-018-36429-6
- 2018. Brain scans from 21,297 individuals reveal the genetic architecture of hippocampal subfield volumes. Molecular Psychiatry. 1-13. doi: 10.1038/s41380-018-0262-7
- 2017. Psychotic patients who used cannabis frequently before illness onset have higher genetic predisposition to schizophrenia than those who did not. Psychological Medicine. 48: 43-49. Published 2017-10-03. doi: 10.1017/S0033291717001209
- 2017. A genetic association study of CSMD1 and CSMD2 with cognitive function. Brain, behavior, and immunity. 61: 209-216. doi: 10.1016/j.bbi.2016.11.026
- 2017. Novel genetic loci associated with hippocampal volume. Nature Communications. 8:13624: 1-12. doi: 10.1038/ncomms13624
- 2017. Assembly and analysis of 100 full MHC haplotypes from the Danish population. Genome Research. 27: 1597-1607. doi: 10.1101/gr.218891.116
- 2017. Large-scale cognitive GWAS meta-analysis reveals tissue-specific neural expression and potential nootropic drug targets. Cell reports. 21: 2597-2613. doi: 10.1016/j.celrep.2017.11.028
- 2017. Identification of gene loci that overlap between schizophrenia and educational attainment. Schizophrenia Bulletin. 43: 654-664. doi: 10.1093/schbul/sbw085
- 2017. A genome-wide association study of anorexia nervosa suggests a risk locus implicated in dysregulated leptin signaling. Scientific Reports. 7:3847: 1-9. doi: 10.1038/s41598-017-01674-8
- 2017. Sequencing and de novo assembly of 150 genomes from Denmark as a population reference. Nature. 548: 87-91. doi: 10.1038/nature23264
- 2017. Analysis of the joint effect of SNPs to identify independent loci and allelic heterogeneity in schizophrenia GWAS data. Translational psychiatry. 7. doi: 10.1038/s41398-017-0033-2
- 2017. GWAS meta-analysis reveals novel loci and genetic correlates for general cognitive function: a report form the COGENT consortium. Molecular Psychiatry. 22: 336-345. doi: 10.1038/mp.2016.244
- 2016. Novel genetic loci underlying human intracranial volume identified through genome-wide association. Nature Neuroscience. 19: 1569-1582. doi: 10.1038/nn.4398
- 2016. Nationwide genomic study in Denmark reveals remarkable population homogeneity. Genetics. 204: 711-722. doi: 10.1534/genetics.116.189241
- 2016. Genetics of structural connectivity and information processing in the brain. Brain Structure and Function. 221: 4643-4661. doi: 10.1007/s00429-016-1194-0
- 2016. Genome-wide autozygosity is associated with lower general cognitive ability. Molecular Psychiatry. 21: 837-843. doi: 10.1038/mp.2015.120
- 2016. Conservation of Distinct Genetically-Mediated Human Cortical Pattern. PLoS Genetics. 12:e1006143. 18 pages. doi: 10.1371/journal.pgen.1006143
- 2016. Genetic evidence for a role of the SREBP transcription system and lipid biosynthesis in schizophrenia and antipsychotic treatment. European Neuropsychopharmacology. 27: 589-598. doi: 10.1016/j.euroneuro.2016.07.011
- 2016. Circadian clock gene variants and insomnia, sleepiness, and shift work disorder. Sleep and Biological Rhythms. 14: 55-62. doi: 10.1007/s41105-015-0023-9
- 2015. Large-scale genomics unveil polygenic architecture of human cortical surface area. Nature Communications. 6:7549. doi: 10.1038/ncomms8549
- 2015. Genetic contributions to variation in general cognitive function: a meta-analysis of genome-wide association studies in the CHARGE consortium (N=53 949). Molecular Psychiatry. 20: 183-192. doi: 10.1038/mp.2014.188
- 2015. Genetic basis of a cognitive complexity metric. PLoS ONE. 10:e0123886. doi: 10.1371/journal.pone.0123886
- 2015. Common genetic variants influence human subcortical brain structures. Nature. 520: 224-229. doi: 10.1038/nature14101
- 2015. Common variants in the ARC gene are not associated with cognitive abilities. Brain and Behavior. 5. 8 pages. doi: 10.1002/brb3.376
- 2015. Independent evidence for an association between general cognitive ability and a genetic locus for educational attainment. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics. 168: 363-373. doi: 10.1002/ajmg.b.32319
- 2014. GWAS-based pathway analysis differentiates between fluid and crystallized intelligence. Genes, Brain and Behavior. 13. doi: 10.1111/gbb.12152
- 2014. Lack of association of the rs1344706 ZNF804A variant with cognitive functions and DTI indices of white matter microstructure in two independent healthy populations. Psychiatry Research : Neuroimaging. 222: 60-66. doi: 10.1016/j.pscychresns.2014.02.009
- 2014. Human cognitive ability is influenced by genetic variation in components of postsynaptic signalling complexes assembled by NMDA receptors and MAGUK proteins. Translational psychiatry. 4:e341. doi: 10.1038/tp.2013.114
- 2014. Genetic architecture of cognitive traits. Scandinavian Journal of Psychology. 55: 255-262. doi: 10.1111/sjop.12112
- 2014. Molecular genetic evidence for overlap between general cognitive ability and risk for schizophrenia: A report from the Cognitive Genomics consorTium (COGENT). Molecular Psychiatry. 19: 168-174. doi: 10.1038/mp.2013.166
- 2014. A possible genetic association with chronic fatigue in primary Sjögren’s syndrome: a candidate gene study. Rheumatology International. 34: 191-197. doi: 10.1007/s00296-013-2850-9
- 2014. A genome-wide association study of anorexia nervosa. Molecular Psychiatry. 19: 1085-1094. doi: 10.1038/mp.2013.187
- 2014. The ENIGMA Consortium: Large-scale collaborative analyses of neuroimaging and genetic data. Brain Imaging and Behavior. 8: 153-182. doi: 10.1007/s11682-013-9269-5
- 2013. A genetic deconstruction of neurocognitive traits in schizophrenia and bipolar disorder. PLoS ONE. 8. 9 pages. doi: 10.1371/journal.pone.0081052
- 2013. No association of primary Sjögren's syndrome with Fcγ receptor gene variants. Genes and Immunity. 14: 234-237. doi: 10.1038/gene.2013.12
- 2013. Human cognitive ability is influenced by genetic variation in components of postsynaptic signaling complexes assembled by MAGUK proteins. Behavior Genetics. 43: 521-522.
- 2012. Association between genetic variants in the tumour necrosis factor/lymphotoxin alpha/lymphotoxin beta locus and primary Sjogren's syndrome in Scandinavian samples. Annals of the Rheumatic Diseases. 71: 981-988. doi: 10.1136/annrheumdis-2011-200446
- 2012. Linkage-disequilibrium-based binning affects the interpretation of GWASs. American Journal of Human Genetics. 90: 727-733. doi: 10.1016/j.ajhg.2012.02.025
- 2012. Response to Zhu et al. American Journal of Human Genetics. 91: 969-970.
- 2012. Linkage-Disequilibrium-Based Binning Misleads the Interpretation of Genome-wide Association Studies Response. American Journal of Human Genetics. 91: 969-970. doi: 10.1016/j.ajhg.2012.08.028
- 2012. Gene-based analysis of regionally enriched cortical genes in GWAS data sets of cognitive traits and psychiatric disorders. PLoS ONE. 7. 14 pages. doi: 10.1371/journal.pone.0031687
- 2012. Imaging and cognitive genetics: the Norwegian Cognitive NeuroGenetics Sample. Twin Research and Human Genetics. 15: 442-452. doi: 10.1017/thg.2012.8
- 2012. No association of primary Sjögren's Syndrome with Fc gamma? Receptor gene variants. Scandinavian Journal of Immunology. 76: 198-198.
- 2012. DCLK1 variants are associated across schizophrenia and attention deficit/hyperactivity disorder. PLoS ONE. 7. 12 pages. doi: 10.1371/journal.pone.0035424
- 2012. The Imaging and Cognition Genetics Conference 2011, ICG 2011: A Meeting of Minds. Frontiers in Neuroscience. 6. Published 2012-06-03. doi: 10.3389/fnins.2012.00074
- 2012. Identification of common variants associated with human hippocampal and intracranial volumes. Nature Genetics. 44: 552-561. doi: 10.1038/ng.2250
- 2011. Potential association of muscarinic receptor 3 gene variants with primary Sjögren's syndrome. Annals of the Rheumatic Diseases. 70: 1327-1329. doi: 10.1136/ard.2010.138966
- 2011. Genome-wide association studies establish that human intelligence is highly heritable and polygenic. Molecular Psychiatry. 16: 996-1005. doi: 10.1038/mp.2011.85
- 2011. Lipogenic effects of psychotropic drugs: focus on the SREBP system. Frontiers in Bioscience. 16: 49-60. doi: 10.2741/3675
- 2011. The Complement Control-Related Genes CSMD1 and CSMD2 Associate to Schizophrenia. Biological Psychiatry. 70: 35-42. doi: 10.1016/j.biopsych.2011.01.030
- 2011. Association study of energy homeostasis genes and antipsychotic-induced weight gain in patients with schizophrenia. Pharmacopsychiatry. 44: 15-20. doi: 10.1055/s-0030-1263174
- 2010. Fc gamma receptor IIA, IIIA and IIIB single nucleotide polymorphisms and Fc gamma receptor IIIB copy number variation: No association with primary Sjögren's syndrome. Scandinavian Journal of Rheumatology. 39: 36-36.
- 2010. Polymorphisms in SREBF1 and SREBF2, two antipsychotic-activated transcription factors controlling cellular lipogenesis, are associated with schizophrenia in German and Scandinavian samples. Molecular Psychiatry. 15: 463-472. doi: 10.1038/mp.2008.110
- 2009. A possible association between schizophrenia and GRIK3 polymorphisms in a multicenter sample of Scandinavian origin (SCOPE). Schizophrenia Research. 107: 242-248. doi: 10.1016/j.schres.2008.10.010
- 2009. Association of MCTP2 gene variants with schizophrenia in three independent samples of Scandinavian origin (SCOPE). Psychiatry Research. 168: 256-258. doi: 10.1016/j.psychres.2008.08.007
- 2009. Variants in doublecortin- and calmodulin kinase like 1, a gene up-regulated by BDNF, are Associated with memory and general cognitive abilities. PLoS ONE. 4. doi: 10.1371/journal.pone.0007534
- 2009. Association between the insulin-induced gene 2 (INSIG2) and weight gain in a German sample of antipsychotic-treated schizophrenic patients: perturbation of SREBP-controlled lipogenesis in drug-related metabolic adverse effects? Molecular Psychiatry. 14: 308-317. doi: 10.1038/sj.mp.4002133
- 2008. A possible association between schizophrenia and GRIK3 polymorphisms in a multicenter sample of Scandinavian origin (SCOPE). Schizophrenia Research.
- 2008. Polymorphisms in SREBF1 and SREBF2, two antipsychotic-activated transcription factors controlling cellular lipogenesis, are associated with schizophrenia in German and Scandinavian samples. Molecular Psychiatry.
- 2008. Association between the insulin-induced gene 2 (INSIG2) and weight gain in a German sample of antipsychotic-treated schizophrenic patients: pertubation of SREBP-controlled lipogenesis in drug-realted metabolic adverse effects? Molecular Psychiatry. 14: 308-317. Published 2008-01-15.
See my ORCID page: https://orcid.org/0000-0002-8085-051X