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Axelsson, Tomas
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Publications (10 of 39) Show all publications
Wadelius, M., Eriksson, N., Kreutz, R., Bondon-Guitton, E., Ibañez, L., Carvajal, A., . . . Hallberg, P. (2018). Sulfasalazine-Induced Agranulocytosis Is Associated With the Human Leukocyte Antigen Locus.. Clinical Pharmacology and Therapeutics, 103(5), 843-853
Open this publication in new window or tab >>Sulfasalazine-Induced Agranulocytosis Is Associated With the Human Leukocyte Antigen Locus.
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2018 (English)In: Clinical Pharmacology and Therapeutics, ISSN 0009-9236, E-ISSN 1532-6535, Vol. 103, no 5, p. 843-853Article in journal (Refereed) Published
Abstract [en]

Agranulocytosis is a serious, although rare, adverse reaction to sulfasalazine, which is used to treat inflammatory joint and bowel disease. We performed a genome‐wide association study comprising 9,380,034 polymorphisms and 180 HLA alleles in 36 cases of sulfasalazine‐induced agranulocytosis and 5,170 population controls. Sulfasalazine‐induced agranulocytosis was significantly associated with the HLA region on chromosome 6. The top hit (rs9266634) was located close to HLA‐B, odds ratio (OR) 5.36 (95% confidence interval (CI) (2.97, 9.69) P = 2.55 × 10−8). We HLA‐sequenced a second cohort consisting of 40 cases and 142 treated controls, and confirmed significant associations with HLA‐B*08:01, OR = 2.25 (95% CI (1.02, 4.97) P = 0.0439), in particular the HLA‐B*08:01 haplotype HLA‐DQB1*02:01‐DRB1*03:01‐B*08:01‐C*07:01, OR = 3.79 (95% CI (1.63, 8.80) P = 0.0019), and with HLA‐A*31:01, OR = 4.81 (95% CI (1.52, 15.26) P = 0.0077). The number needed to test for HLA‐B*08:01 and HLA‐A*31:01 to avoid one case was estimated to be 1,500. We suggest that intensified monitoring or alternative treatment should be considered for known carriers of HLA‐B*08:01 or HLA‐A*31:01.

National Category
Clinical Laboratory Medicine
Research subject
Clinical Pharmacology
Identifiers
urn:nbn:se:uu:diva-342623 (URN)10.1002/cpt.805 (DOI)000430118300025 ()28762467 (PubMedID)
Projects
Farmakogenomik
Funder
Science for Life Laboratory - a national resource center for high-throughput molecular bioscienceSwedish Research Council, 521-2014-3370; 521-2011-2440Swedish Heart Lung Foundation, 20120557; 20140291
Available from: 2018-02-22 Created: 2018-02-22 Last updated: 2018-06-19Bibliographically approved
Nolte, I. M., Munoz, M. L., Tragante, V., Amare, A. T., Jansen, R., Vaez, A., . . . de Geus, E. J. C. (2017). Genetic loci associated with heart rate variability and their effects on cardiac disease risk. Nature Communications, 8, Article ID 15805.
Open this publication in new window or tab >>Genetic loci associated with heart rate variability and their effects on cardiac disease risk
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2017 (English)In: Nature Communications, ISSN 2041-1723, E-ISSN 2041-1723, Vol. 8, article id 15805Article in journal (Refereed) Published
Abstract [en]

Reduced cardiac vagal control reflected in low heart rate variability (HRV) is associated with greater risks for cardiac morbidity and mortality. In two-stage meta-analyses of genome-wide association studies for three HRV traits in up to 53,174 individuals of European ancestry, we detect 17 genome-wide significant SNPs in eight loci. HRV SNPs tag non-synonymous SNPs (in NDUFA11 and KIAA1755), expression quantitative trait loci (eQTLs) (influencing GNG11, RGS6 and NEO1), or are located in genes preferentially expressed in the sinoatrial node (GNG11, RGS6 and HCN4). Genetic risk scores account for 0.9 to 2.6% of the HRV variance. Significant genetic correlation is found for HRV with heart rate (-0.74 < r(g) < -0.55) and blood pressure (-0.35 < r(g) < -0.20). These findings provide clinically relevant biological insight into heritable variation in vagal heart rhythm regulation, with a key role for genetic variants (GNG11, RGS6) that influence G-protein heterotrimer action in GIRK-channel induced pacemaker membrane hyperpolarization.

Place, publisher, year, edition, pages
NATURE PUBLISHING GROUP, 2017
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:uu:diva-329672 (URN)10.1038/ncomms15805 (DOI)000403216600001 ()28613276 (PubMedID)
Available from: 2017-09-19 Created: 2017-09-19 Last updated: 2019-03-11Bibliographically approved
Hallberg, P., Persson, M., Axelsson, T., Cavalli, M., Norling, P., Johansson, H.-E., . . . Wadelius, M. (2017). Genetic variants associated with angiotensin-converting enzyme inhibitor-induced cough: a genome-wide association study in a Swedish population. Pharmacogenomics (London), 18(3), 201-213
Open this publication in new window or tab >>Genetic variants associated with angiotensin-converting enzyme inhibitor-induced cough: a genome-wide association study in a Swedish population
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2017 (English)In: Pharmacogenomics (London), ISSN 1462-2416, E-ISSN 1744-8042, Vol. 18, no 3, p. 201-213Article in journal (Refereed) Published
Abstract [en]

Aim: We conducted a genome-wide association study on angiotensin-converting enzyme inhibitor-induced cough and used our dataset to replicate candidate genes iden-tified in previous studies. Patients & methods: A total of 124 patients and 1345 treated controls were genotyped using Illumina arrays. The genome-wide significance level was set to p < 5 x 10(-8). Results: We identified nearly genome-wide significant associations in CLASP1, PDE11A, KCNMB2, TGFA, SLC38A6 and MMP16. The strongest association was with rs62151109 in CLASP1 (odds ratio: 3.97; p = 9.44 x 10(-8)). All top hits except two were located in intronic or noncoding DNA regions. None of the candidate genes were significantly associated in our study. Conclusion: Angiotensin-converting enzyme inhibitor-induced cough is potentially associated with genes that are independent of bradykinin pathways.

Place, publisher, year, edition, pages
FUTURE MEDICINE LTD, 2017
Keywords
angiotensin converting enzyme inhibitors, bradykinin, cough, drug-related side effects and adverse reactions, enalapril, genome-wide association study, lisinopril, pharmacogenetics, quinapril, ramipril
National Category
Pharmacology and Toxicology
Identifiers
urn:nbn:se:uu:diva-318602 (URN)10.2217/pgs-2016-0184 (DOI)000393682600002 ()28084903 (PubMedID)
Funder
Swedish Research Council, Medicine 521-2011-2440 521-2014-3370Swedish Heart Lung Foundation, 20120557 20140291Science for Life Laboratory - a national resource center for high-throughput molecular bioscience
Available from: 2017-03-31 Created: 2017-03-31 Last updated: 2018-01-13Bibliographically approved
Hibar, D. P., Adams, H. H. H., Jahanshad, N., Chauhan, G., Stein, J. L., Hofer, E., . . . Ikram, M. A. (2017). Novel genetic loci associated with hippocampal volume. Nature Communications, 8, Article ID 13624.
Open this publication in new window or tab >>Novel genetic loci associated with hippocampal volume
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2017 (English)In: Nature Communications, ISSN 2041-1723, E-ISSN 2041-1723, Vol. 8, article id 13624Article in journal (Refereed) Published
Abstract [en]

The hippocampal formation is a brain structure integrally involved in episodic memory, spatial navigation, cognition and stress responsiveness. Structural abnormalities in hippocampal volume and shape are found in several common neuropsychiatric disorders. To identify the genetic underpinnings of hippocampal structure here we perform a genome-wide association study (GWAS) of 33,536 individuals and discover six independent loci significantly associated with hippocampal volume, four of them novel. Of the novel loci, three lie within genes (ASTN2, DPP4 and MAST4) and one is found 200 kb upstream of SHH. A hippocampal subfield analysis shows that a locus within the MSRB3 gene shows evidence of a localized effect along the dentate gyrus, subiculum, CA1 and fissure. Further, we show that genetic variants associated with decreased hippocampal volume are also associated with increased risk for Alzheimer's disease (r(g) = -0.155). Our findings suggest novel biological pathways through which human genetic variation influences hippocampal volume and risk for neuropsychiatric illness.

National Category
Medical Genetics
Identifiers
urn:nbn:se:uu:diva-316027 (URN)10.1038/ncomms13624 (DOI)000392154900001 ()28098162 (PubMedID)
Available from: 2017-02-27 Created: 2017-02-27 Last updated: 2018-10-16Bibliographically approved
Andreou, D., Soderman, E., Axelsson, T., Sedvall, G. C., Terenius, L., Agartz, I. & Jonsson, E. G. (2016). Associations between a locus downstream DRD1 gene and cerebrospinal fluid dopamine metabolite concentrations in psychosis. Neuroscience Letters, 619, 126-130
Open this publication in new window or tab >>Associations between a locus downstream DRD1 gene and cerebrospinal fluid dopamine metabolite concentrations in psychosis
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2016 (English)In: Neuroscience Letters, ISSN 0304-3940, E-ISSN 1872-7972, Vol. 619, p. 126-130Article in journal (Refereed) Published
Abstract [en]

Dopamine activity, mediated by the catecholaminergic neurotransmitter dopamine, is prominent in the human brain and has been implicated in schizophrenia. Dopamine targets five different receptors and is then degraded to its major metabolite homovanillic acid (HVA). We hypothesized that genes encoding dopamine receptors may be associated with cerebrospinal fluid (CSF) HVA concentrations in patients with psychotic disorder. We searched for association between 67 single nucleotide polymorphisms (SNPs) in the five dopamine receptor genes i.e., DRD1, DRD2, DRD3, DRD4 and DRD5, and the CSF HVA concentrations in 74 patients with psychotic disorder. Nominally associated SNPs were also tested in 111 healthy controls. We identified a locus, located downstream DRD1 gene, where four SNPs, rs11747728, rs11742274, rs265974 and rs11747886, showed association with CSF HVA concentrations in psychotic patients. The associations between rs11747728, which is a regulatory region variant, and rs11742274 with HVA remained significant after correction for multiple testing. These associations were restricted to psychotic patients and were absent in healthy controls. The results suggest that the DRD1 gene is implicated in the pathophysiology of psychosis and support the dopamine hypothesis of schizophrenia.

Keywords
Schizophrenia, Psychiatric genetics, Homovanillic acid (HVA), Dopamine receptor D1 gene (DRD1)
National Category
Neurology
Identifiers
urn:nbn:se:uu:diva-297116 (URN)10.1016/j.neulet.2016.03.005 (DOI)000374624000020 ()26957229 (PubMedID)
Funder
Swedish Research Council, K2007-62X-15077-04-1Swedish Research Council, K2008-62P-20597-01-3Swedish Research Council, K2010-62X-15078-07-2Swedish Research Council, K2012-61X-15078-09-3Stockholm County CouncilThe Karolinska Institutet's Research FoundationKnut and Alice Wallenberg FoundationScience for Life Laboratory - a national resource center for high-throughput molecular bioscienceSwedish Research Council
Available from: 2016-06-22 Created: 2016-06-21 Last updated: 2017-11-28Bibliographically approved
Limbach, M., Saare, M., Tserel, L., Kisand, K., Eglit, T., Sauer, S., . . . Peterson, P. (2016). Epigenetic profiling in CD4+and CD8+T cells from Graves' disease patients reveals changes in genes associated with T cell receptor signaling. Journal of Autoimmunity, 67, 46-56
Open this publication in new window or tab >>Epigenetic profiling in CD4+and CD8+T cells from Graves' disease patients reveals changes in genes associated with T cell receptor signaling
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2016 (English)In: Journal of Autoimmunity, ISSN 0896-8411, E-ISSN 1095-9157, Vol. 67, p. 46-56Article in journal (Refereed) Published
Abstract [en]

In Graves' disease (GD), a combination of genetic, epigenetic and environmental factors causes an autoimmune response to the thyroid gland, characterized by lymphocytic infiltrations and autoantibodies targeting the thyroid stimulating hormone receptor (TSHR) and other thyroid antigens. To identify the epigenetic changes involved in GD, we performed a genome-wide analysis of DNA methylation and enrichment of H3K4me3 and H3K27ac histone marks in sorted CD4+ and CD8+ T cells. We found 365 and 3322 differentially methylated CpG sites in CD4+ and CD8+ T cells, respectively. Among the hypermethylated CpG sites, we specifically found enrichment of genes involved in T cell signaling (CD247, LCK, ZAP70, CD3D, CD3E, CD3G, CTLA4 and CD8A) and decreased expression of CD3 gene family members. The hypermethylation was accompanied with decreased levels of H3K4me3 and H3K27ac marks at several T cell signaling genes in ChIP-seq analysis. In addition, we found hypermethylation of the TSHR gene first intron, where several GD-associated polymorphisms are located. Our results demonstrate an involvement of dysregulated DNA methylation and histone modifications at T cell signaling genes in GD patients.

Keywords
Graves' disease, DNA methylation, Epigenetics, T cell signaling, TSHR
National Category
Immunology in the medical area
Identifiers
urn:nbn:se:uu:diva-282328 (URN)10.1016/j.jaut.2015.09.006 (DOI)000370884900006 ()26459776 (PubMedID)
Funder
EU, European Research Council, 262055 (ESGI)EU, European Research Council
Available from: 2016-04-05 Created: 2016-04-05 Last updated: 2018-01-10Bibliographically approved
Hallberg, P., Eriksson, N., Ibanez, L., Bondon-Guitton, E., Kreutz, R., Carvajal, A., . . . Wadelius, M. (2016). Genetic variants associated with antithyroid drug-induced agranulocytosis: a genome-wide association study in a European population. The Lancet Diabetes and Endocrinology, 4(6), 507-516
Open this publication in new window or tab >>Genetic variants associated with antithyroid drug-induced agranulocytosis: a genome-wide association study in a European population
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2016 (English)In: The Lancet Diabetes and Endocrinology, ISSN 2213-8587, E-ISSN 2213-8595, Vol. 4, no 6, p. 507-516Article in journal (Refereed) Published
Abstract [en]

Background: Drug-induced agranulocytosis is a potentially life-threatening adverse reaction. Genome-wide association studies (GWASs) in ethnic Chinese people in Taiwan and Hong Kong have shown an association between agranulocytosis induced by antithyroid drugs and the HLA alleles HLA-B*38:02 and HLA-DRB1*08:03. We aimed to identify genetic variants associated with antithyroid drug-induced agranulocytosis in a white European population.

Methods: We did a GWAS in 234 European adults with any non-chemotherapy drug-induced agranulocytosis (absolute neutrophil count <= 0.5 x 10(9)/L [<= 500/mu L]) and 5170 population controls. 39 of the 234 patients had agranulocytosis that was induced by antithyroid drugs (thiamazole [methimazole], carbimazole, or propylthiouracil). After imputation and HLA allele prediction, 9 380 034 single nucleotide polymorphisms (SNPs) and 180 HLA alleles were tested for association. The genome-wide significance threshold was p<5 x 10(-8).

Findings: Agranulocytosis induced by non-chemotherapy drugs in general was significantly associated with the HLA region on chromosome 6, with odds ratios (ORs) of 3.24 (95% CI 2.31-4.55, p = 1.20 x 10(-11)) for HLA-B*27:05 and 3.57 (2.61-4.90, p = 2.32 x 10(-15)) for the top SNP (rs114291795). Drug-specific analysis showed that the association with HLA-B*27: 05 was largely driven by cases induced by antithyroid drugs. In a multiple logistic regression model, the OR for HLA-B*27: 05 was 7.30 (3.81-13.96) when antithyroid drug-induced agranulocytosis was compared with population controls (p= 1.91 x 10(-9)) and 16.91 (3.44-83.17) when compared with a small group of hyperthyroid controls (p = 5.04 x 10(-4)). Three SNPs were strongly associated with antithyroid drug-induced agranulocytosis: rs652888 (OR 4.73, 95% CI 3.00-7.44, p= 1.92 x 10(-11)) and rs199564443 (17.42, 7.38-41.12, p = 7.04 x 10(-11)), which were independent of HLA-B*27:05, and rs1071816 (5.27, 3.06-9.10, p = 2.35 x 10(-9)) which was in moderate linkage disequilibrium with HLA-B*27:05. In heterozygous carriers of all three SNPs, the predicted probability of antithyroid drug-induced agranulocytosis was about 30% (OR 753, 95% CI 105-6812). To avoid one case of agranulocytosis, based on the possible risk reduction if all three SNPs are genotyped and carriers are treated or monitored differently from non-carriers, roughly 238 patients would need to be genotyped.

Interpretation: In white European people, antithyroid drug-induced agranulocytosis was associated with HLA-B* 27: 05 and with other SNPs on chromosome 6. In the future, carriers of these variants could be placed under intensified monitoring or offered alternative treatment for hyperthyroidism.

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:uu:diva-302237 (URN)10.1016/S2213-8587(16)00113-3 (DOI)000376462800016 ()27157822 (PubMedID)
External cooperation:
Funder
Vattenfall ABSwedish Heart Lung Foundation
Available from: 2016-09-01 Created: 2016-08-31 Last updated: 2017-11-21Bibliographically approved
Johansson, Å., Eriksson, N., Lindholm, D., Varenhorst, C., James, S., Syvänen, A.-C., . . . Wallentin, L. (2016). Genome-wide association and Mendelian randomization study of NT-proBNP in patients with acute coronary syndrome. Human Molecular Genetics, 25(7), 1447-1456
Open this publication in new window or tab >>Genome-wide association and Mendelian randomization study of NT-proBNP in patients with acute coronary syndrome
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2016 (English)In: Human Molecular Genetics, ISSN 0964-6906, E-ISSN 1460-2083, Vol. 25, no 7, p. 1447-1456Article in journal (Refereed) Published
Abstract [en]

N-terminal pro-B-type natriuretic peptide (NT-proBNP) is a strong predictor of mortality in coronary artery disease and is widely employed as a prognostic biomarker. However, a causal relationship between NT-proBNP and clinical endpoints has not been established. We have performed a genome-wide association and Mendelian randomization study of NT-proBNP. We used a discovery set of 3740 patients from the PLATelet inhibition and patient Outcomes (PLATO) trial, which enrolled 18 624 patients with acute coronary syndrome (ACS). A further set of 5492 patients, from the same trial, was used for replication. Genetic variants at two novel loci (SLC39A8 and POC1B/GALNT4) were associated with NT-proBNP levels and replicated together with the previously known NPPB locus. The most significant SNP (rs198389, pooled P = 1.07 x 10(-15)) in NPPB interrupts an E-box consensus motif in the gene promoter. The association in SLC39A8 is driven by a deleterious variant (rs13107325, pooled P = 5.99 x 10(-10)), whereas the most significant SNP in POC1B/GALNT4 (rs11105306, pooled P = 1.02 x 10(-16)) is intronic. The SLC39A8 SNP was associated with higher risk of cardiovascular (CV) death (HR = 1.39, 95% CI: 1.08-1.79, P = 0.0095), but the other loci were not associated with clinical endpoints. We have identified two novel loci to be associated with NT-proBNP in patients with ACS. Only the SLC39A8 variant, but not the NPPB variant, was associated with a clinical endpoint. Due to pleotropic effects of SLC39A8, these results do not suggest that NT-proBNP levels have a direct effect on mortality in ACS patients. PLATO Clinical Trial Registration: ; NCT00391872.

National Category
Medical Genetics Medical Biotechnology (with a focus on Cell Biology (including Stem Cell Biology), Molecular Biology, Microbiology, Biochemistry or Biopharmacy)
Identifiers
urn:nbn:se:uu:diva-296862 (URN)10.1093/hmg/ddw012 (DOI)000374231000016 ()26908625 (PubMedID)
Funder
Swedish Research Council, 80576801Swedish Research Council, 70374401AstraZeneca
Available from: 2016-06-20 Created: 2016-06-20 Last updated: 2018-07-06Bibliographically approved
Adams, H. H. H., Hibar, D. P., Chouraki, V., Stein, J. L., Nyquist, P. A., Renteria, M. E., . . . Thompson, P. M. (2016). Novel genetic loci underlying human intracranial volume identified through genome-wide association. Nature Neuroscience, 19(12), 1569-1582
Open this publication in new window or tab >>Novel genetic loci underlying human intracranial volume identified through genome-wide association
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2016 (English)In: Nature Neuroscience, ISSN 1097-6256, E-ISSN 1546-1726, Vol. 19, no 12, p. 1569-1582Article in journal (Refereed) Published
Abstract [en]

Intracranial volume reflects the maximally attained brain size during development, and remains stable with loss of tissue in late life. It is highly heritable, but the underlying genes remain largely undetermined. In a genome-wide association study of 32,438 adults, we discovered five previously unknown loci for intracranial volume and confirmed two known signals. Four of the loci were also associated with adult human stature, but these remained associated with intracranial volume after adjusting for height. We found a high genetic correlation with child head circumference (rho(genetic) = 0.748), which indicates a similar genetic background and allowed us to identify four additional loci through meta-analysis (N-combined = 37,345). Variants for intracranial volume were also related to childhood and adult cognitive function, and Parkinson's disease, and were enriched near genes involved in growth pathways, including PI3K-AKT signaling. These findings identify the biological underpinnings of intracranial volume and their link to physiological and pathological traits.

National Category
Medical Genetics
Identifiers
urn:nbn:se:uu:diva-311497 (URN)10.1038/nn.4398 (DOI)000389011900016 ()27694991 (PubMedID)
Funder
NIH (National Institute of Health), N01-AG-1-2100 271201200022C R01MH62873 K99MH102357 R01 HD050735 P30AG10161 RF1AG15819 R01AG17917 R01AG30146 R01AG40039 5R01AG037212 HHSN268200625226C R01D0042157-01A MH081802 1RC2 MH089951 1RC2 MH089995EU, European Research Council, 602450 278948 602805 643051 ERC-230374Knut and Alice Wallenberg FoundationRagnar Söderbergs stiftelseTorsten Söderbergs stiftelseWellcome trust, 084730 082604/2/07/ZSwedish Research Council, K2007-62X-15077-04-1 K2008-62P-20597-01-3 K2010-62X-15078-07-2 K2012-61X-15078-09-3Stockholm County CouncilThe Karolinska Institutet's Research FoundationAustralian Research Council, FT0991634
Available from: 2016-12-28 Created: 2016-12-28 Last updated: 2018-10-16Bibliographically approved
Andreou, D., Soderman, E., Axelsson, T., Sedvall, G. C., Terenius, L., Agartz, I. & Jonsson, E. G. (2015). Cerebrospinal fluid monoamine metabolite concentrations as intermediate phenotypes between glutamate-related genes and psychosis. Psychiatry Research, 229(1-2), 497-504
Open this publication in new window or tab >>Cerebrospinal fluid monoamine metabolite concentrations as intermediate phenotypes between glutamate-related genes and psychosis
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2015 (English)In: Psychiatry Research, ISSN 0165-1781, E-ISSN 1872-7123, Vol. 229, no 1-2, p. 497-504Article in journal (Refereed) Published
Abstract [en]

Glutamate-related genes have been associated with schizophrenia, but the results have been ambiguous and difficult to replicate. Homovanillic acid (HVA), 5-hydroxyindoleacetic acid (5-HIAA) and 3-methoxy-4-hydroxyphenylglycol (MHPG) are the major degradation products of the monoamines dopamine, serotonin and noradrenaline, respectively, and their concentrations in the cerebrospinal fluid (CSF), mainly HVA, have been associated with schizophrenia. In the present study, we hypothesized that CSF HVA, 5-HIAA and MHPG concentrations represent intermediate phenotypes in the association between glutamate-related genes and psychosis. To test this hypothesis, we searched for association between 238 single nucleotide polymorphisms (SNPs) in ten genes shown to be directly or indirectly implicated in glutamate transmission and CSF HVA, 5-HIAA and MHPG concentrations in 74 patients with psychotic disease. Thirty-eight nominally significant associations were found. Further analyses in 111 healthy controls showed that 87% of the nominal associations were restricted to the patients with psychosis. Some of the psychosis-only-associated SNPs found in the D-amino acid oxidase activator (DADA) and the kynurenine 3-monooxygenase (KMO) genes have previously been reported to be associated with schizophrenia. The present results suggest that CSF monoamine metabolite concentrations may represent intermediate phenotypes in the association between glutamate-related genes and psychosis.

Keywords
Schizophrenia, Psychiatric genetics, Homovanillic acid (HVA), 5-hydroxyindoleacetic acid (5-HIAA), 3-methoxy-4-hydroxyphenylglycol (MHPG)
National Category
Psychiatry
Identifiers
urn:nbn:se:uu:diva-264038 (URN)10.1016/j.psychres.2015.06.023 (DOI)000360772600071 ()26142836 (PubMedID)
Funder
Swedish Research Council, K2007-62X-15077-04-1 K2008-62P-20597-01-3. K2010-62X-15078-07-2 K2012-61X-15078-09-3Stockholm County CouncilKnut and Alice Wallenberg Foundation
Available from: 2015-10-06 Created: 2015-10-05 Last updated: 2017-12-01Bibliographically approved
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