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1. Common variant at 16p11.2 conferring risk of psychosis

Author

Steinberg, S, de Jong, S, Mattheisen, M, Costas, J, Demontis, D, Jamain, S, Pietiläinen, O P H, Lin, K, Papiol, S, Huttenlocher, J, Sigurdsson, E, Vassos, E, Giegling, I, Breuer, R, Fraser, G, Walker, N, Melle, I, Djurovic, S, Agartz, I, Tuulio-Henriksson, A, Suvisaari, J, Lönnqvist, J, Paunio, T, Olsen, L, Hansen, T, Ingason, A, Pirinen, M, Strengman, E, Hougaard, D M, Ørntoft, T, Didriksen, M, Hollegaard, M V, Nordentoft, M, Abramova, L, Kaleda, V, Arrojo, M, Sanjuán, J, Arango, C, Etain, B, Bellivier, F, Méary, A, Schürhoff, F, Szoke, A, Ribolsi, M, Magni, V, Siracusano, A, Sperling, S, Rossner, M, Christiansen, C, Kiemeney, L A, Franke, B, van den Berg, L H, Veldink, J, Curran, S, Bolton, P, Poot, M, Staal, W, Rehnstrom, K, Kilpinen, H, Freitag, C M, Meyer, J, Magnusson, P, Saemundsen, E, Martsenkovsky, I, Bikshaieva, I, Martsenkovska, I, Vashchenko, O, Raleva, M, Paketchieva, K, Stefanovski, B, Durmishi, N, Pejovic Milovancevic, M, Lecic Tosevski, D, Silagadze, T, Naneishvili, N, Mikeladze, N, Surguladze, S, Vincent, J B, Farmer, A, Mitchell, P B, Wright, A, Schofield, P R, Fullerton, J M, Montgomery, G W, Martin, N G, Rubino, I A, van Winkel, R, Kenis, G, De Hert, M, Réthelyi, J M, Bitter, I, Terenius, L, Jönsson, E G, Bakker, S, van Os, J, Jablensky, A, Leboyer, M, Bramon, E, Powell, J, Murray, R, Corvin, A, Gill, M, Morris, D, O'Neill, F A, Kendler, K, Riley, B, Craddock, N, Owen, M J, O'Donovan, M C, Thorsteinsdottir, U, Kong, A, Ehrenreich, H, Carracedo, A, Golimbet, V, Andreassen, O A, Børglum, A D, Mors, O, Mortensen, P B, Werge, T, Ophoff, R A, Nöthen, M M, Rietschel, M, Cichon, S, Ruggeri, M, Tosato, S, Palotie, A, St Clair, D, Rujescu, D, Collier, D A, Stefansson, H, and Stefansson, K

Published
2014
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6. Expanding the range of ZNF804A variants conferring risk of psychosis

Author

Steinberg, S, Mors, O, Børglum, A D, Gustafsson, O, Werge, T, Mortensen, P B, Andreassen, O A, Sigurdsson, E, Thorgeirsson, T E, Böttcher, Y, Olason, P, Ophoff, R A, Cichon, S, Gudjonsdottir, I H, Pietiläinen, O P H, Nyegaard, M, Tuulio-Henriksson, A, Ingason, A, Hansen, T, Athanasiu, L, Suvisaari, J, Lonnqvist, J, Paunio, T, Hartmann, A, Jürgens, G, Nordentoft, M, Hougaard, D, Norgaard-Pedersen, B, Breuer, R, Möller, H-J, Giegling, I, Glenthøj, B, Rasmussen, H B, Mattheisen, M, Bitter, I, Réthelyi, J M, Sigmundsson, T, Fossdal, R, Thorsteinsdottir, U, Ruggeri, M, Tosato, S, Strengman, E, Kiemeney, L A, Melle, I, Djurovic, S, Abramova, L, Kaleda, V, Walshe, M, Bramon, E, Vassos, E, Li, T, Fraser, G, Walker, N, Toulopoulou, T, Yoon, J, Freimer, N B, Cantor, R M, Murray, R, Kong, A, Golimbet, V, Jönsson, E G, Terenius, L, Agartz, I, Petursson, H, Nöthen, M M, Rietschel, M, Peltonen, L, Rujescu, D, Collier, D A, Stefansson, H, St Clair, D, and Stefansson, K

Published
2011
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8. Meta-analysis of 32 genome-wide linkage studies of schizophrenia

Author

Ng, M Y M, Levinson, D F, Faraone, S V, Suarez, B K, DeLisi, L E, Arinami, T, Riley, B, Paunio, T, Pulver, A E, Irmansyah, Holmans, P A, Escamilla, M, Wildenauer, D B, Williams, N M, Laurent, C, Mowry, B J, Brzustowicz, L M, Maziade, M, Sklar, P, Garver, D L, Abecasis, G R, Lerer, B, Fallin, M D, Gurling, H M D, Gejman, P V, Lindholm, E, Moises, H W, Byerley, W, Wijsman, E M, Forabosco, P, Tsuang, M T, Hwu, H-G, Okazaki, Y, Kendler, K S, Wormley, B, Fanous, A, Walsh, D, O'Neill, F A, Peltonen, L, Nestadt, G, Lasseter, V K, Liang, K Y, Papadimitriou, G M, Dikeos, D G, Schwab, S G, Owen, M J, O'Donovan, M C, Norton, N, Hare, E, Raventos, H, Nicolini, H, Albus, M, Maier, W, Nimgaonkar, V L, Terenius, L, Mallet, J, Jay, M, Godard, S, Nertney, D, Alexander, M, Crowe, R R, Silverman, J M, Bassett, A S, Roy, M-A, Mérette, C, Pato, C N, Pato, M T, Roos, J Louw, Kohn, Y, Amann-Zalcenstein, D, Kalsi, G, McQuillin, A, Curtis, D, Brynjolfson, J, Sigmundsson, T, Petursson, H, Sanders, A R, Duan, J, Jazin, E, Myles-Worsley, M, Karayiorgou, M, and Lewis, C M

Published
2009
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9. Analysis of 10 independent samples provides evidence for association between schizophrenia and a SNP flanking fibroblast growth factor receptor 2

Author

O'Donovan, M C, Norton, N, Williams, H, Peirce, T, Moskvina, V, Nikolov, I, Hamshere, M, Carroll, L, Georgieva, L, Dwyer, S, Holmans, P, Marchini, J L, Spencer, C C A, Howie, B, Leung, H-T, Giegling, I, Hartmann, A M, Möller, H-J, Morris, D W, Shi, Y, Feng, G, Hoffmann, P, Propping, P, Vasilescu, C, Maier, W, Rietschel, M, Zammit, S, Schumacher, J, Quinn, E M, Schulze, T G, Iwata, N, Ikeda, M, Darvasi, A, Shifman, S, He, L, Duan, J, Sanders, A R, Levinson, D F, Adolfsson, R, Ösby, U, Terenius, L, Jönsson, E G, Cichon, S, Nöthen, M M, Gill, M, Corvin, A P, Rujescu, D, Gejman, P V, Kirov, G, Craddock, N, Williams, N M, and Owen, M J

Published
2009
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12. A systematic genomewide linkage study in 353 sib pairs with schizophrenia

Author

Williams, N.M., Norton, N., Williams, H., Ekholm, B., Hamshere, M.L., Lindblom, Y., Chowdari, K.V., Cardno, A.G., Zammit, S., Jones, L.A., Murphy, K.C., Sanders, R.D., McCarthy, G., Gray, M.Y., Jones, G., Holmans, P., Nimgaonkar, V., Adolfson, R., Osby, U., Terenius, L., Sedvall, G., O'Dnovan, M.C., and Owen, M.J.

Subjects
Human genetics -- Research, Schizophrenia -- Research, Biological sciences
Published
2003

14. Analysis of 10 independent samples provides evidence for association between schizophrenia and a SNP flanking fibroblast growth factor receptor 2

Author

OʼDonovan, M C, Norton, N, Williams, H, Peirce, T, Moskvina, V, Nikolov, I, Hamshere, M, Carroll, L, Georgieva, L, Dwyer, S, Holmans, P, Marchini, J L, Spencer, C CA, Howie, B, Leung, H-T, Giegling, I, Hartmann, A M, Möller, H-J, Morris, D W, Shi, Y, Feng, G, Hoffmann, P, Propping, P, Vasilescu, C, Maier, W, Rietschel, M, Zammit, S, Schumacher, J, Quinn, E M, Schulze, T G, Iwata, N, Ikeda, M, Darvasi, A, Shifman, S, He, L, Duan, J, Sanders, A R, Levinson, D F, Adolfsson, R, Ösby, U, Terenius, L, Jönsson, E G, Cichon, S, Nöthen, M M, Gill, M, Corvin, A P, Rujescu, D, Gejman, P V, Kirov, G, Craddock, N, Williams, N M, and Owen, M J

Published
2009

26. Supplementary Material for: Genetic and Functional Study of L-Type Amino Acid Transporter 1 in Schizophrenia

Author

Comasco, E., Vumma, R., Toffoletto, S., Johansson, J., Flyckt, L., Lewander, T., Oreland, L., Bjerkenstedt, L., Andreou, D., Söderman, E., Terenius, L., Agartz, I., Jönsson, E.G., and Venizelos, N.

Abstract

Schizophrenia involves neural catecholaminergic dysregulation. Tyrosine is the precursor of catecholamines, and its major transporter, according to studies on fibroblasts, in the brain is the L-type amino acid transporter 1 (LAT1). The present study assessed haplotype tag single-nucleotide polymorphisms (SNPs) of the SLC7A5/LAT1 gene in 315 patients with psychosis within the schizophrenia spectrum and 233 healthy controls to investigate genetic vulnerability to the disorder as well as genetic relationships to homovanillic acid (HVA) and 3-methoxy-4-hydroxyphenylglycol (MHPG), the major catecholamine metabolites in the cerebrospinal fluid (CSF). Moreover, the involvement of the different isoforms of the system L in tyrosine uptake and LAT1 tyrosine kinetics were studied in fibroblast cell lines of 10 patients with schizophrenia and 10 healthy controls. The results provide suggestive evidence of individual vulnerability to schizophrenia related to the LAT1 SNP rs9936204 genotype. A number of SNPs were nominally associated with CSF HVA and MHPG concentrations but did not survive correction for multiple testing. The LAT1 isoform was confirmed as the major tyrosine transporter in patients with schizophrenia. However, the kinetic parameters (maximal transport capacity, affinity of the binding sites, and diffusion constant of tyrosine transport through the LAT1 isoform) did not differ between patients with schizophrenia and controls. The present genetic findings call for independent replication in larger samples, while the functional study seems to exclude a role of LAT1 in the aberrant transport of tyrosine in fibroblasts of patients with schizophrenia.

Published
2017
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27. Variability in Working Memory Performance Explained by Epistasis vs Polygenic Scores in the ZNF804A Pathway

Author

Nicodemus, Kk, Hargreaves, A, Morris, D, Anney, R, Gill, M, Corvin, A, Donohoe, G, Ripke, S, Sanders, Ar, Kendler, Ks, Levinson, Df, Sklar, P, Holmans, Pa, Lin, Dy, Duan, J, Ophoff, Ra, Andreassen, Oa, Scolnick, E, Cichon, S, Clair, St, D, Gurling, H, Werge, T, Rujescu, D, Blackwood, Dh, Pato, Cn, Malhotra, Ak, Purcell, S, Dudbridge, F, Neale, Bm, Rossin, L, Visscher, Pm, Posthuma, D, Ruderfer, Dm, Fanous, A, Stefansson, H, Steinberg, S, Mowry, Bj, Golimbet, V, Hert, De, M, Jönsson, Eg, Bitter, I, Pietiläinen, Op, Collier, Da, Tosato, Sarah, Agartz, I, Albus, M, Alexander, M, Amdur, Rl, Amin, F, Bass, N, Bergen, Se, Black, Dw, Børglum, Ad, Brown, Ma, Bruggeman, R, Buccola, Ng, Byerley, Wf, Cahn, W, Cantor, Rm, Carr, Vj, Catts, Sv, Choudhury, K, Cloninger, C, Cormican, P, Craddock, N, Danoy, Pa, Datta, S, Haan, De, L, Demontis, D, Dikeos, D, Djurovic, S, Donnelly, P, Duong, L, Dwyer, S, Fink Jensen, A, Freedman, R, Freimer, Nb, Friedl, M, Georgieva, L, Giegling, I, Glenthøj, B, Godard, S, Hamshere, M, Hansen, M, Hansen, T, Hartmann, Am, Henskens, Fa, Hougaard, Dm, Hultman, Cm, Ingason, A, Jablensky, Av, Jakobsen, Kd, Jay, M, Jürgens, G, Kahn, Rs, Keller, Mc, Kenis, G, Kenny, E, Kim, Y, Kirov, Gk, Konnerth, H, Konte, B, Krabbendam, L, Krasucki, R, Lasseter, Vk, Laurent, C, Lawrence, J, Lencz, T, Lerer, F, Liang, Ky, Lichtenstein, P, Lieberman, Ja, Linszen, Dh, Lönnqvist, J, Loughland, Cm, Maclean, Aw, Maher, Bs, Maier, W, Mallet, J, Malloy, P, Mattheisen, M, Mattingsdal, M, Mcghee, Ka, Mcgrath, Jj, Mcintosh, A, Mclean, De, Mcquillin, A, Melle, I, Michie, Pt, Milanova, V, Morris, Dw, Mors, O, Mortensen, Pb, Moskvina, V, Muglia, P, Myin Germeys, I, Nertney, Da, Nestadt, G, Nielsen, J, Nikolov, I, Nordentoft, M, Norton, N, Nöthen, Mm, O'Dushlaine, Ct, Olincy, A, Olsen, L, O'Neill, F, Ørntoft, Tf, Owen, Mj, Pantelis, C, Papadimitriou, G, Pato, Mt, Peltonen, L, Petursson, H, Pickard, B, Pimm, J, Pulver, Ae, Puri, V, Quested, D, Quinn, Em, Rasmussen, Hb, Réthelyi, Jm, Ribble, R, Rietschel, M, Riley, Bp, Ruggeri, Mirella, Schall, U, Schulze, Tg, Schwab, Sg, Scott, Rj, Shi, J, Sigurdsson, E, Silverman, Jm, Spencer, Cc, Stefansson, K, Strange, A, Strengman, E, Stroup, T, Suvisaari, J, Terenius, L, Thirumalai, S, Thygesen, Jh, Timm, S, Toncheva, D, Van, Den, Oord, E, Van, Os, Van, J, Winkel, R, Veldink, J, Walsh, D, Wang, Ag, Wiersma, D, Wildenauer, Db, Williams, Hj, Williams, Nm, Wormley, B, Zammit, S, Sullivan, Pf, O'Donovan, Mc, Daly, Mj, Gejman, P., Functional Genomics, Complex Trait Genetics, De Hert, Marc, Myin-Germeys, Inez, van Winkel, Ruud, Psychiatrie & Neuropsychologie, RS: MHeNs - R2 - Mental Health, Amsterdam Neuroscience, and Adult Psychiatry

Subjects
epistasis, Male, Multifactorial Inheritance, polygenic, Neuropsychological Tests, involvement, 0302 clinical medicine, Neural Pathways, 2.1 Biological and endogenous factors, Psychology, schizophrenia risk, psychosis variant, Aetiology, 0303 health sciences, susceptibility gene znf804a, medicine.diagnostic_test, phenotypes, Zinc Fingers, Neuropsychological test, Single Nucleotide, Middle Aged, Serious Mental Illness, Psychiatry and Mental health, Memory, Short-Term, Mental Health, Schizophrenia, Major depressive disorder, Female, Cognitive Sciences, social and economic factors, Adult, medicine.medical_specialty, Psychosis, working memory, schizophrenia, IQ, Schizoaffective disorder, Polymorphism, Single Nucleotide, Article, 03 medical and health sciences, Gene interaction, Genetic, Social cognition, Memory, Clinical Research, 2.3 Psychological, Behavioral and Social Science, medicine, Genetics, Humans, Genetic Predisposition to Disease, Bipolar disorder, Polymorphism, Psychiatry, 030304 developmental biology, Other Medical and Health Sciences, Prevention, Wellcome Trust Case Control Consortium 2, Neurosciences, Genetic Variation, Epistasis, Genetic, Schizophrenia Psychiatric Genome-wide Association Study (GWAS) Consortium, medicine.disease, attention, Brain Disorders, deficits, Short-Term, Psychotic Disorders, genome-wide association, Epistasis, healthy controls, identification, Cognition Disorders, 030217 neurology & neurosurgery, Genome-Wide Association Study
Abstract

IMPORTANCE We investigated the variation in neuropsychological function explained by risk alleles at the psychosis susceptibility gene ZNF804A and its interacting partners using single nucleotide polymorphisms (SNPs), polygenic scores, and epistatic analyses. Of particular importance was the relative contribution of the polygenic score vs epistasis in variation explained. OBJECTIVES To (1) assess the association between SNPs in ZNF804A and the ZNF804A polygenic score with measures of cognition in cases with psychosis and (2) assess whether epistasis within the ZNF804A pathway could explain additional variation above and beyond that explained by the polygenic score. DESIGN, SETTING, AND PARTICIPANTS Patients with psychosis (n = 424)were assessed in areas of cognitive ability impaired in schizophrenia including IQ, memory, attention, and social cognition.We used the Psychiatric GWAS Consortium 1 schizophrenia genome-wide association study to calculate a polygenic score based on identified risk variants within this genetic pathway. Cognitive measures significantly associated with the polygenic score were tested for an epistatic component using a training set (n = 170), which was used to develop linear regression models containing the polygenic score and 2-SNP interactions. The best-fitting models were tested for replication in 2 independent test sets of cases: (1) 170 individuals with schizophrenia or schizoaffective disorder and (2) 84 patients with broad psychosis (including bipolar disorder, major depressive disorder, and other psychosis). MAIN OUTCOMES AND MEASURES Participants completed a neuropsychological assessment battery designed to target the cognitive deficits of schizophrenia including general cognitive function, episodic memory, working memory, attentional control, and social cognition. RESULTS Higher polygenic scores were associated with poorer performance among patients on IQ, memory, and social cognition, explaining 1%to 3%of variation on these scores (range, P = .01 to .03). Using a narrow psychosis training set and independent test sets of narrow phenotype psychosis (schizophrenia and schizoaffective disorder), broad psychosis, and control participants (n = 89), the addition of 2 interaction terms containing 2 SNPs each increased the R2 for spatial working memory strategy in the independent psychosis test sets from 1.2%using the polygenic score only to 4.8%(P = .11 and .001, respectively) but did not explain additional variation in control participants. CONCLUSIONS AND RELEVANCE These data support a role for the ZNF804A pathway in IQ, memory, and social cognition in cases. Furthermore, we showed that epistasis increases the variation explained above the contribution of the polygenic score. © 2014 American Medical Association. All rights reserved.

Published
2014

29. Schizophrenia genetic variants are not associated with intelligence

Author

van Scheltinga, Af, Bakker, Sc, van Haren, Ne, Derks, Em, Buizer Voskamp, Je, Cahn, W, Ripke, S, Sanders, A, Kendler, K, Levinson, D, Sklar, P, Holmans, P, Lin, D., Duan, J, Ophoff, R, Andreassen, O, Scolnick, E, Cichon, S, St Clair, D, Corvin, A, Gurling, H, Werge, T, Rujescu, D, Blackwood, D, Pato, C, Malhotra, A, Purcell, S, Dudbridge, F, Neale, B, Rossin, L, Visscher, P, Posthuma, D, Ruderfer, D, Fanous, A, Stefansson, H, Steinberg, S, Mowry, B, Golimbet, V, Hert, De, M, Jonsson, E, Bitter, I, Pietilainen, O, Collier, D, Tosato, Sarah, Agartz, I, Albus, M, Alexander, M, Amdur, R, Amin, F, Bass, N, Bergen, S, Black, D, Børglum, A, Brown, M, Bruggeman, R, Buccola, N, Byerley, W, Cantor, R, Carr, V, Catts, S, Choudhury, K, Cloninger, C, Cormican, P, Craddock, N, Danoy, P, Datta, S, Haan, De, L, Demontis, D, Dikeos, D, Djurovic, S, Donnelly, P, Donohoe, G, Duong, L, Dwyer, S, Fink Jensen, A, Freedman, R, Freimer, N, Friedl, M, Georgieva, L, Giegling, I, Gill, M, Glenthøj, B, Godard, S, Hamshere, M, Hansen, M, Hansen, T, Hartmann, A, Henskens, F, Hougaard, D, Hultman, C, Ingason, A, Jablensky, A, Jakobsen, K, Jay, M, Jurgens, G, Kahn, R, Keller, M, Kenis, G, Kenny, E, Kim, Y, Kirov, G, Konnerth, H, Konte, B, Krabbendam, L, Krasucki, R, Lasseter, V, Laurent, C, Lawrence, J, Lencz, T, Lerer, F, Liang, K, Lichtenstein, P, Lieberman, J, Linszen, D, Lonnqvist, J, Loughland, C, Maclean, A, Maher, B, Maier, W, Mallet, J, Malloy, P, Mattheisen, M, Mattingsdal, M, Mcghee, K, Mcgrath, J, Mcintosh, A, Mclean, D, Mcquillin, A, Melle, I, Michie, P, Milanova, V, Morris, D, Mors, O, Mortensen, P, Moskvina, V, Muglia, P, Myin Germeys, I, Nertney, D, Nestadt, G, Nielsen, J, Nikolov, I, Nordentoft, M, Norton, N, Nothen, M, O'Dushlaine, C, Olincy, A, Olsen, L, O'Neill, F, Ørntoft, T, Owen, M, Pantelis, C, Papadimitriou, G, Pato, M, Peltonen, L, Petursson, H, Pickard, B, Pimm, J, Pulver, A, Puri, V, Quested, D, Quinn, E, Rasmussen, H, Rethelyi, Jm, Ribble, R, Rietschel, M, Riley, B, Ruggeri, Mirella, Schall, U, Schulze, T, Schwab, S, Scott, R, Shi, J, Sigurdsson, E, Silverman, J, Spencer, C, Stefansson, K, Strange, A, Strengman, E, Stroup, T, Suvisaari, J, Terenius, L, Thirumalai, S, Thygesen, J, Timm, S, Toncheva, D, van den Oord, E, van Os, J, van Winkel, R, Veldink, J, Walsh, D, Wang, A, Wiersma, D, Wildenauer, D, Williams, H, Williams, N, Wormley, B, Zammit, S, Sullivan, P, O'Donovan, M, Daly, M, Gejman, P), Ophoff, Ra, Kahn, Rs, Functional Genomics, Neuroscience Campus Amsterdam - Neurobiology of Mental Health, Neuroscience Campus Amsterdam - Brain Mechanisms in Health & Disease, Psychiatrie & Neuropsychologie, RS: MHeNs School for Mental Health and Neuroscience, ANS - Amsterdam Neuroscience, APH - Amsterdam Public Health, and Adult Psychiatry

Subjects
Oncology, Adult, Male, Psychosis, medicine.medical_specialty, Multifactorial Inheritance, DNA Copy Number Variations, Endophenotypes, Schizophrenia (object-oriented programming), Intelligence, SNP, Single-nucleotide polymorphism, Genome-wide association study, polygenic, Polymorphism, Single Nucleotide, behavioral disciplines and activities, Article, Cognition, Internal medicine, mental disorders, medicine, Humans, Genetic Predisposition to Disease, deletion, Cognitive decline, Applied Psychology, Genetic association, Genetics, Wechsler Scales, Wechsler Adult Intelligence Scale, medicine.disease, endophenotype, Psychiatry and Mental health, duplication, IQ, Endophenotype, Schizophrenia, Female, Psychology, cognition, schizophrenia, Genome-Wide Association Study
Abstract

BackgroundSchizophrenia is associated with lower pre-morbid intelligence (IQ) in addition to (pre-morbid) cognitive decline. Both schizophrenia and IQ are highly heritable traits. Therefore, we hypothesized that genetic variants associated with schizophrenia, including copy number variants (CNVs) and a polygenic schizophrenia (risk) score (PSS), may influence intelligence.MethodIQ was estimated with the Wechsler Adult Intelligence Scale (WAIS). CNVs were determined from single nucleotide polymorphism (SNP) data using the QuantiSNP and PennCNV algorithms. For the PSS, odds ratios for genome-wide SNP data were calculated in a sample collected by the Psychiatric Genome-Wide Association Study (GWAS) Consortium (8690 schizophrenia patients and 11 831 controls). These were used to calculate individual PSSs in our independent sample of 350 schizophrenia patients and 322 healthy controls.ResultsAlthough significantly more genes were disrupted by deletions in schizophrenia patients compared to controls (p = 0.009), there was no effect of CNV measures on IQ. The PSS was associated with disease status (R2 = 0.055, p = 2.1 × 10−7) and with IQ in the entire sample (R2 = 0.018, p = 0.0008) but the effect on IQ disappeared after correction for disease status.ConclusionsOur data suggest that rare and common schizophrenia-associated variants do not explain the variation in IQ in healthy subjects or in schizophrenia patients. Thus, reductions in IQ in schizophrenia patients may be secondary to other processes related to schizophrenia risk.

Published
2013

42. Analysis of 10 independent samples provides evidence for association between schizophrenia and a SNP flanking fibroblast growth factor receptor 2

Author

O'Donovan, MC, Norton, N, Williams, H, Peirce, T, Moskvina, V, Nikolov, I, Hamshere, M, Carroll, L, Georgieva, L, Dwyer, S, Holmans, P, Marchini, JL, Spencer, CCA, Howie, B, Leung, H-T, Giegling, I, Hartmann, AM, Möller, H-J, Morris, DW, Shi, Y, Feng, G, Hoffmann, P, Propping, P, Vasilescu, C, Maier, W, Rietschel, M, Zammit, S, Schumacher, J, Quinn, EM, Schulze, TG, Iwata, N, Ikeda, M, Darvasi, A, Shifman, S, He, L, Duan, J, Sanders, AR, Levinson, DF, Adolfsson, R, Ösby, U, Terenius, L, Jönsson, EG, Cichon, S, Nöthen, MM, Gill, M, Corvin, AP, Rujescu, D, Gejman, PV, Kirov, G, Craddock, N, Williams, NM, Owen, MJ, Buccola, NG, Mowry, BJ, Freedman, R, Amin, F, Black, DW, Silverman, JM, Byerley, WJ, and Cloninger, CR

Subjects
Adult, Male, Linkage disequilibrium, Genotype, Genome-wide association study, Single-nucleotide polymorphism, Biology, Polymorphism, Single Nucleotide, Linkage Disequilibrium, Article, Cellular and Molecular Neuroscience, Young Adult, Gene Frequency, Meta-Analysis as Topic, Polymorphism (computer science), SNP, Humans, Genetic Predisposition to Disease, Allele, Receptor, Fibroblast Growth Factor, Type 2, Molecular Biology, Allele frequency, Aged, Genetics, Aged, 80 and over, Fibroblast growth factor receptor 2, Chromosomes, Human, Pair 10, Middle Aged, Psychiatry and Mental health, Schizophrenia, Female, Genome-Wide Association Study
Abstract

We and others have previously reported linkage to schizophrenia on chromosome 10q25-q26 but, to date, a susceptibility gene in the region has not been identified. We examined data from 3606 single-nucleotide polymorphisms (SNPs) mapping to 10q25-q26 that had been typed in a genome-wide association study (GWAS) of schizophrenia (479 UK cases/2937 controls). SNPs with P

Published
2016

43. Genome-wide association study identifies five new schizophrenia loci

Author

Ripke, S., Sanders, A. R., Kendler, K. S., Levinson, D. F., Sklar, P., Holmans, P. A., Lin, D., Duan, J., Ophoff, R. A., Andreassen, O. A., Scolnick, E., Cichon, S., Clair, D. S., Corvin, A., Gurling, H., Werge, T., Rujescu, D., D. H. R., Pato, C. N., Malhotra, A. K., Purcell, S., Dudbridge, F., Neale, B. M., Rossin, L., Visscher, P. M., Posthuma, D., Ruderfer, D. M., Fanous, A., Stefansson, H., Steinberg, S., Mowry, B. J., Golimbet, V., Hert, M. D., Jönsson, E. G., Bitter, I., O. P. H., Collier, D. A., Tosato, Sarah, Agartz, I., Albus, M., Alexander, M., Amdur, R. L., Amin, F., Bass, N., Bergen, S. E., Black, D. W., Børglum, A. D., Brown, M. A., Bruggeman, R., Buccola, N. G., Byerley, W. F., Cahn, W., Cantor, R. M., Carr, V. J., Catts, S. V., Choudhury, K., Cloninger, C. R., Cormican, P., Craddock, N., Danoy, P. A., Datta, S., Haan, L. d., Demontis, D., Dikeos, D., Djurovic, S., Donnelly, P., Donohoe, G., Duong, L., Dwyer, S., Fink Jensen, A., Freedman, R., Freimer, N. B., Friedl, M., Georgieva, L., Giegling, I., Gill, M., Glenthøj, B., Godard, S., Hamshere, M., Hansen, M., Hansen, T., Hartmann, A. M., Henskens, F. A., Hougaard, D. M., Hultman, C. M., Ingason, A., Jablensky, A. V., Jakobsen, K. D., Jay, M., Jürgens, G., Kahn, R. S., Keller, M. C., Kenis, G., Kenny, E., Kim, Y., Kirov, G. K., Konnerth, H., Konte, B., Krabbendam, L., Krasucki, R., Lasseter, V. K., Laurent, C., Lawrence, J., Lencz, T., Lerer, F. B., Liang, K., Lichtenstein, P., Lieberman, J. A., Linszen, D. H., Lönnqvist, J., Loughland, C. M., Maclean, A. W., Maher, B. S., Maier, W., Mallet, J., Malloy, P., Mattheisen, M., Mattingsdal, M., Mcghee, K. A., Mcgrath, J. J., Mcintosh, A., Mclean, D. E., Mcquillin, A., Melle, I., Michie, P. T., Milanova, V., Morris, D. W., Mors, O., Mortensen, P. B., Moskvina, V., Muglia, P., Myin Germeys, I., Nertney, D. A., Nestadt, G., Nielsen, J., Nikolov, I., Nordentoft, M., Norton, N., Nöthen, M. M., O'Dushlaine, C. T., Olincy, A., Olsen, L., O'Neill, F. A., Orntoft, T. F., Owen, M. J., Pantelis, C., Papadimitriou, G., Pato, M. T., Peltonen, L., Petursson, H., Pickard, B., Pimm, J., Pulver, A. E., Puri, V., Quested, D., Quinn, E. M., Rasmussen, H. B., Réthelyi, J. M., Ribble, R., Rietschel, M., Riley, B. P., Ruggeri, Mirella, Schall, U., Schulze, T. G., Schwab, S. G., Scott, R. J., Shi, J., Sigurdsson, E., Silverman, J. M., C. C. A., Stefansson, K., Strange, A., Strengman, E., Stroup, T. S., Suvisaari, J., Terenius, L., Thirumalai, S., Thygesen, J. H., Timm, S., Toncheva, D., Den, E. v., J. v., Os, Winkel, R. v., Veldink, J., Walsh, D., Wang, A. G., Wiersma, D., Wildenauer, D. B., Williams, H. J., Williams, N. M., Wormley, B., Zammit, S., Sullivan, P. F., O'Donovan, M. C., Daly, M. J., Gejman, P. V., Genome Wide, S. P., ANS - Amsterdam Neuroscience, Adult Psychiatry, Functional Genomics, Educational Neuroscience, Clinical Child and Family Studies, Neuroscience Campus Amsterdam - integrative Analysis & Modeling, Neuroscience Campus Amsterdam - Attention & Cognition, LEARN! - Brain, learning and development, Psychiatrie & Neuropsychologie, and RS: MHeNs School for Mental Health and Neuroscience

Subjects
Male, Gene Dosage, Biology, VARIANTS, SUSCEPTIBILITY, ANCESTRY, Polymorphism, Single Nucleotide, Article, Linkage Disequilibrium, White People, 03 medical and health sciences, 0302 clinical medicine, microRNA, Genetics, Humans, Genetic Predisposition to Disease, Alleles, 030304 developmental biology, 0303 health sciences, Genome, Genome, Human, HERITABILITY, MICRORNA, BIPOLAR DISORDER, 3. Good health, schizophrenia, COMMON SNPS EXPLAIN, MicroRNAs, INDIVIDUALS, Logistic Models, Gene Expression Regulation, Haplotypes, LARGE PROPORTION, Genetic Loci, Case-Control Studies, Mutation, Female, HUMAN HEIGHT, 030217 neurology & neurosurgery, Genome-Wide Association Study
Abstract

We examined the role of common genetic variation in schizophrenia in a genome-wide association study of substantial size: a stage 1 discovery sample of 21,856 individuals of European ancestry and a stage 2 replication sample of 29,839 independent subjects. The combined stage 1 and 2 analysis yielded genome-wide significant associations with schizophrenia for seven loci, five of which are new (1p21.3, 2q32.3, 8p23.2, 8q21.3 and 10q24.32-q24.33) and two of which have been previously implicated (6p21.32-p22.1 and 18q21.2). The strongest new finding (P = 1.6 × 10 -11) was with rs1625579 within an intron of a putative primary transcript for MIR137 (microRNA 137), a known regulator of neuronal development. Four other schizophrenia loci achieving genome-wide significance contain predicted targets of MIR137, suggesting MIR137-mediated dysregulation as a previously unknown etiologic mechanism in schizophrenia. In a joint analysis with a bipolar disorder sample (16,374 affected individuals and 14,044 controls), three loci reached genome-wide significance: CACNA1C (rs4765905, P = 7.0 × 10 -9), ANK3 (rs10994359, P = 2.5 × 10 -8) and the ITIH3-ITIH4 region (rs2239547, P = 7.8 × 10 -9). © 2011 Nature America, Inc. All rights reserved.

Published
2011

45. A role for epigenetic mechanisms in the regulation of prodynorphin expression by alcohol

Author

D'Addario C., Ogren SO, Terenius L., Ekstrom T, CAPUTI, FRANCESCA FELICIA, CANDELETTI, SANZIO, ROMUALDI, PATRIZIA, D'Addario C, Caputi FF, Candeletti S, Ogren SO, Terenius L, Ekstrom T, and Romualdi P.

Subjects
alcohol, opioid, epigenetic
Abstract

Background and Aim: Alcohol alters several neurotransmitter systems within the brain and accumulated evidences indicate the endogenous opioid system as an important target of its action. We studied, in vitro and in vivo the molecular alterations occurring in the prodynorphin gene following different exposures to alcohol. Methods: Human neuroblastoma SH-SY5Y cells were exposed to low, clearly not intoxicating, and high etha- 208 European Opioid Conference 2011, Kraków, Poland nol concentrations at different time points. Sprague Dawley rats received alcohol intragastrically trying to mimic human drinking that establishes tolerance and dependence conditions. Real-time RT-PCR was used to assess the abundance of mRNAs of interest. DNA methylation was analyzed by Methylation Specific-Real Time PCR and bisulfite-Pyrosequencing. Specific histone modifications at gene promoters were evaluated by Chromatin ImmunoPrecipitation. Results: In the cellular model we demonstrated a temporal relationship between selective chromatin modifications induced by ethanol or acetaldehyde, and changes in prodynorphin gene expression were demonstrated. In the amygdala complex of alcoholtreated rats differential changes in prodynorphin gene expression changes were observed depending on the time of exposure; consistently, we propose potential epigenetic mechanisms responsible for these alterations, at least upong short ethanol exposure. Conclusion: Our findings indicate a linkage between gene expression alterations and epigenetic modulation in prodynorphin promoter, thus adding novel information on how the opioid system can be affected by alcohol in several ways. Studies are ongoing to evaluate the chromatin remodelling in the neuroplasticity occurring in the progression of alcohol abuse. It will be also of value to study the ability of epigenetic modulators in reverting dynorphin genetic/epigenetic alterations and alcohol abuse-related behaviours. Moreover, opioid drugs already available in alcoholism treatment could also have possible epigenetic modulating properties.

Published
2011

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