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1. Large-scale analysis of structural brain asymmetries in schizophrenia via the ENIGMA consortium.

Author

Schijven, Dick, Postema, M.C., Fukunaga, M., Matsumoto, J., Miura, K., Zwarte, S.M.C. de, Haren, N.E.M. van, Cahn, W., Hulshoff Pol, H.E., Kahn, R.S., Ayesa-Arriola, R., Ortoz-García de la Foz, V., Tordesillas-Gutierrez, D., Vázquez-Bourgon, J., Crespo-Facorro, B., Alnæs, D., Dahl, A., Westlye, L.T., Agartz, I., Andreassen, O.A., Jönsson, E.G., Kochunov, P., Bruggemann, J.M., Catts, S.V., Michie, P.T., Mowry, B.J., Quidé, Y., Rasser, P.E., Schall, U., Scott, R.J., Carr, V.J., Green, M.J., Henskens, F.A., Loughland, C.M., Pantelis, C., Weickert, C.S., Weickert, T.W., Haan, L. de, Brosch, K., Pfarr, J.K., Ringwald, K.G., Stein, F., Jansen, Andreas, Kircher, T.T.J., Nenadić, I., Krämer, Bernd, Gruber, O., Satterthwaite, T.D., Bustillo, J., Mathalon, D.H., Preda, A., Calhoun, V.D., Ford, J.M., Potkin, S.G., Chen, Jingxu, Tan, Yunlong, Wang, Zhiren, Xiang, Hong, Fan, Fengmei, Bernardoni, F., Ehrlich, S., Fuentes-Claramonte, P., Garcia-Leon, M.A., Guerrero-Pedraza, A., Salvador, R., Sarró, S., Pomarol-Clotet, E., Ciullo, V., Piras, F., Vecchio, D., Banaj, N., Spalletta, G., Michielse, S., Amelsvoort, T. van, Dickie, E.W., Voineskos, A.N., Sim, K., Ciufolini, S., Dazzan, P., Murray, R.M., Kim, W.S., Chung, Y.C., Andreou, C., Schmidt, A, Borgwardt, S., McIntosh, A.M., Whalley, H.C., Lawrie, S.M., Plessis, S. du, Luckhoff, H.K., Scheffler, F., Emsley, R., Grotegerd, D., Lencer, R., Dannlowski, U., Edmond, J.T., Rootes-Murdy, K., Stephen, J.M., Mayer, A.R., Antonucci, L.A., Fazio, L., Pergola, G., Bertolino, A., Díaz-Caneja, C.M., Janssen, J, Lois, N.G., Arango, C., Tomyshev, A.S., Lebedeva, I., Cervenka, S., Sellgren, C.M., Georgiadis, F., Kirschner, M., Kaiser, S., Hajek, T., Skoch, A., Spaniel, F., Kim, M., Kwak, Y.B., Oh, S., Kwon, J.S., James, A., Bakker, G., Knöchel, C., Stäblein, M., Oertel, V., Uhlmann, A., Howells, F.M., Stein, D.J., Temmingh, H.S., Diaz-Zuluaga, A.M., Pineda-Zapata, J.A., López-Jaramillo, C., Homan, S., Ji, E., Surbeck, W., Homan, P., Fisher, S.E., Franke, B., Glahn, D.C., Gur, R.C., Hashimoto, R., Jahanshad, N., Luders, E., Medland, S.E., Thompson, P.M., Turner, J.A., Erp, T.G. van, Francks, C., Schijven, Dick, Postema, M.C., Fukunaga, M., Matsumoto, J., Miura, K., Zwarte, S.M.C. de, Haren, N.E.M. van, Cahn, W., Hulshoff Pol, H.E., Kahn, R.S., Ayesa-Arriola, R., Ortoz-García de la Foz, V., Tordesillas-Gutierrez, D., Vázquez-Bourgon, J., Crespo-Facorro, B., Alnæs, D., Dahl, A., Westlye, L.T., Agartz, I., Andreassen, O.A., Jönsson, E.G., Kochunov, P., Bruggemann, J.M., Catts, S.V., Michie, P.T., Mowry, B.J., Quidé, Y., Rasser, P.E., Schall, U., Scott, R.J., Carr, V.J., Green, M.J., Henskens, F.A., Loughland, C.M., Pantelis, C., Weickert, C.S., Weickert, T.W., Haan, L. de, Brosch, K., Pfarr, J.K., Ringwald, K.G., Stein, F., Jansen, Andreas, Kircher, T.T.J., Nenadić, I., Krämer, Bernd, Gruber, O., Satterthwaite, T.D., Bustillo, J., Mathalon, D.H., Preda, A., Calhoun, V.D., Ford, J.M., Potkin, S.G., Chen, Jingxu, Tan, Yunlong, Wang, Zhiren, Xiang, Hong, Fan, Fengmei, Bernardoni, F., Ehrlich, S., Fuentes-Claramonte, P., Garcia-Leon, M.A., Guerrero-Pedraza, A., Salvador, R., Sarró, S., Pomarol-Clotet, E., Ciullo, V., Piras, F., Vecchio, D., Banaj, N., Spalletta, G., Michielse, S., Amelsvoort, T. van, Dickie, E.W., Voineskos, A.N., Sim, K., Ciufolini, S., Dazzan, P., Murray, R.M., Kim, W.S., Chung, Y.C., Andreou, C., Schmidt, A, Borgwardt, S., McIntosh, A.M., Whalley, H.C., Lawrie, S.M., Plessis, S. du, Luckhoff, H.K., Scheffler, F., Emsley, R., Grotegerd, D., Lencer, R., Dannlowski, U., Edmond, J.T., Rootes-Murdy, K., Stephen, J.M., Mayer, A.R., Antonucci, L.A., Fazio, L., Pergola, G., Bertolino, A., Díaz-Caneja, C.M., Janssen, J, Lois, N.G., Arango, C., Tomyshev, A.S., Lebedeva, I., Cervenka, S., Sellgren, C.M., Georgiadis, F., Kirschner, M., Kaiser, S., Hajek, T., Skoch, A., Spaniel, F., Kim, M., Kwak, Y.B., Oh, S., Kwon, J.S., James, A., Bakker, G., Knöchel, C., Stäblein, M., Oertel, V., Uhlmann, A., Howells, F.M., Stein, D.J., Temmingh, H.S., Diaz-Zuluaga, A.M., Pineda-Zapata, J.A., López-Jaramillo, C., Homan, S., Ji, E., Surbeck, W., Homan, P., Fisher, S.E., Franke, B., Glahn, D.C., Gur, R.C., Hashimoto, R., Jahanshad, N., Luders, E., Medland, S.E., Thompson, P.M., Turner, J.A., Erp, T.G. van, and Francks, C.

Abstract

Item does not contain fulltext, Left-right asymmetry is an important organizing feature of the healthy brain that may be altered in schizophrenia, but most studies have used relatively small samples and heterogeneous approaches, resulting in equivocal findings. We carried out the largest case-control study of structural brain asymmetries in schizophrenia, with MRI data from 5,080 affected individuals and 6,015 controls across 46 datasets, using a single image analysis protocol. Asymmetry indexes were calculated for global and regional cortical thickness, surface area, and subcortical volume measures. Differences of asymmetry were calculated between affected individuals and controls per dataset, and effect sizes were meta-analyzed across datasets. Small average case-control differences were observed for thickness asymmetries of the rostral anterior cingulate and the middle temporal gyrus, both driven by thinner left-hemispheric cortices in schizophrenia. Analyses of these asymmetries with respect to the use of antipsychotic medication and other clinical variables did not show any significant associations. Assessment of age- and sex-specific effects revealed a stronger average leftward asymmetry of pallidum volume between older cases and controls. Case-control differences in a multivariate context were assessed in a subset of the data (N = 2,029), which revealed that 7% of the variance across all structural asymmetries was explained by case-control status. Subtle case-control differences of brain macrostructural asymmetry may reflect differences at the molecular, cytoarchitectonic, or circuit levels that have functional relevance for the disorder. Reduced left middle temporal cortical thickness is consistent with altered left-hemisphere language network organization in schizophrenia.

Published
2023

2. What we learn about bipolar disorder from large-scale neuroimaging: Findings and future directions from the ENIGMA Bipolar Disorder Working Group

Author

Ching, C.R., Hibar, D.P., Gurholt, T.P., Nunes, A., Thomopoulos, S.I., Abé, C., Agartz, I., Brouwer, R.M., Cannon, D.M., Zwarte, S.M.C. de, Eyler, L.T., Favre, P., Hajek, T., Haukvik, U.K., Houenou, J., Landén, M., Lett, T.A., McDonald, C., Nabulsi, L., Patel, Y., Pauling, M.E., Paus, T., Radua, J., Soeiro-de-Souza, M.G., Tronchin, G., Haren, N.E.M. van, Vieta, E., Walter, H., Zeng, L.L., Alda, M., Almeida, J., Alnaes, D., Alonso-Lana, S., Altimus, C., Bauer, M, Baune, B.T., Bearden, C.E., Bellani, M., Benedetti, F. De, Berk, M., Bilderbeck, A.C., Blumberg, H.P., Bøen, E., Bollettini, I., Bonnin, C. Del Mar, Brambilla, P., Canales-Rodríguez, E.J., Caseras, X., Dandash, O., Dannlowski, U., Delvecchio, G., Díaz-Zuluaga, A.M., Dima, D., Duchesnay, É., Elvsåshagen, T., Fears, S.C., Frangou, S., Fullerton, J.M., Glahn, D.C., Goikolea, J.M., Green, M.J., Grotegerd, D., Gruber, O., Haarman, B.C.M., Henry, C., Howells, F.M., Ives-Deliperi, V., Jansen, Andreas, Kircher, T.T.J., Knöchel, C., Kramer, B., Lafer, B., López-Jaramillo, C., Machado-Vieira, R., MacIntosh, B.J., Melloni, E.M.T., Mitchell, P.B., Nenadic, I., Nery, F., Nugent, A.C., Oertel, V., Ophoff, R.A., Ota, M., Overs, B.J., Pham, D.L., Phillips, M.L., Pineda-Zapata, J.A., Poletti, S., Polosan, M., Pomarol-Clotet, E., Pouchon, A., Quidé, Y., Rive, M.M., Roberts, G., Ruhe, H.G., Salvador, R., Sarró, S., Satterthwaite, T.D., Schene, A.H., Sim, K., Thompson, P.M., Andreassen, O.A., Ching, C.R., Hibar, D.P., Gurholt, T.P., Nunes, A., Thomopoulos, S.I., Abé, C., Agartz, I., Brouwer, R.M., Cannon, D.M., Zwarte, S.M.C. de, Eyler, L.T., Favre, P., Hajek, T., Haukvik, U.K., Houenou, J., Landén, M., Lett, T.A., McDonald, C., Nabulsi, L., Patel, Y., Pauling, M.E., Paus, T., Radua, J., Soeiro-de-Souza, M.G., Tronchin, G., Haren, N.E.M. van, Vieta, E., Walter, H., Zeng, L.L., Alda, M., Almeida, J., Alnaes, D., Alonso-Lana, S., Altimus, C., Bauer, M, Baune, B.T., Bearden, C.E., Bellani, M., Benedetti, F. De, Berk, M., Bilderbeck, A.C., Blumberg, H.P., Bøen, E., Bollettini, I., Bonnin, C. Del Mar, Brambilla, P., Canales-Rodríguez, E.J., Caseras, X., Dandash, O., Dannlowski, U., Delvecchio, G., Díaz-Zuluaga, A.M., Dima, D., Duchesnay, É., Elvsåshagen, T., Fears, S.C., Frangou, S., Fullerton, J.M., Glahn, D.C., Goikolea, J.M., Green, M.J., Grotegerd, D., Gruber, O., Haarman, B.C.M., Henry, C., Howells, F.M., Ives-Deliperi, V., Jansen, Andreas, Kircher, T.T.J., Knöchel, C., Kramer, B., Lafer, B., López-Jaramillo, C., Machado-Vieira, R., MacIntosh, B.J., Melloni, E.M.T., Mitchell, P.B., Nenadic, I., Nery, F., Nugent, A.C., Oertel, V., Ophoff, R.A., Ota, M., Overs, B.J., Pham, D.L., Phillips, M.L., Pineda-Zapata, J.A., Poletti, S., Polosan, M., Pomarol-Clotet, E., Pouchon, A., Quidé, Y., Rive, M.M., Roberts, G., Ruhe, H.G., Salvador, R., Sarró, S., Satterthwaite, T.D., Schene, A.H., Sim, K., Thompson, P.M., and Andreassen, O.A.

Abstract

Contains fulltext : 252204.pdf (Publisher’s version ) (Open Access), MRI-derived brain measures offer a link between genes, the environment and behavior and have been widely studied in bipolar disorder (BD). However, many neuroimaging studies of BD have been underpowered, leading to varied results and uncertainty regarding effects. The Enhancing Neuro Imaging Genetics through Meta-Analysis (ENIGMA) Bipolar Disorder Working Group was formed in 2012 to empower discoveries, generate consensus findings and inform future hypothesis-driven studies of BD. Through this effort, over 150 researchers from 20 countries and 55 institutions pool data and resources to produce the largest neuroimaging studies of BD ever conducted. The ENIGMA Bipolar Disorder Working Group applies standardized processing and analysis techniques to empower large-scale meta- and mega-analyses of multimodal brain MRI and improve the replicability of studies relating brain variation to clinical and genetic data. Initial BD Working Group studies reveal widespread patterns of lower cortical thickness, subcortical volume and disrupted white matter integrity associated with BD. Findings also include mapping brain alterations of common medications like lithium, symptom patterns and clinical risk profiles and have provided further insights into the pathophysiological mechanisms of BD. Here we discuss key findings from the BD working group, its ongoing projects and future directions for large-scale, collaborative studies of mental illness.

Published
2022

3. Simvastatin Augmentation for Patients With Early-Phase Schizophrenia-Spectrum Disorders: A Double-Blind, Randomized Placebo-Controlled Trial

Author

Sommer, I.E., Gangadin, S.S., Witte, L.D. de, Koops, S., Baal, C. van, Bahn, S., Drexhage, H., Haren, N.E.M. van, Veling, W., Bruggeman, R., Martens, P., Wiersma, S., Veerman, S.R.T., Grootens, K.P., Beveren, N. van, Kahn, R.S., Begemann, M.J.H., Sommer, I.E., Gangadin, S.S., Witte, L.D. de, Koops, S., Baal, C. van, Bahn, S., Drexhage, H., Haren, N.E.M. van, Veling, W., Bruggeman, R., Martens, P., Wiersma, S., Veerman, S.R.T., Grootens, K.P., Beveren, N. van, Kahn, R.S., and Begemann, M.J.H.

Abstract

Contains fulltext : 244699.pdf (Publisher’s version ) (Open Access), Schizophrenia-spectrum disorders (SSD) are associated with increased inflammatory markers, both in brain and periphery. Augmentation with drugs that lower this pro-inflammatory status may improve clinical presentation. Simvastatin crosses the blood-brain barrier, has anti- inflammatory and neuroprotective effects and reduces metabolic syndrome. In this study, we investigated if 12 months of simvastatin augmentation can improve symptoms and cognition in patients with early SSD. This double-blind placebo-controlled trial included 127 SSD patients across the Netherlands, <3 years after their diagnosis. From these, 119 were randomly assigned 1:1 to simvastatin 40 mg (n = 61) or placebo (n = 58), stratified for sex and study site. Primary outcomes were symptom severity and cognition after 12 months of treatment. Depression, symptom subscores, general functioning, metabolic syndrome, movement disorders, and safety were secondary outcomes. Intention to treat analyses were performed using linear mixed models and ANCOVA. No main effect of simvastatin treatment was found on total symptom severity after 12 months of treatment as compared to placebo (X2(1) = 0.01, P = .90). Group differences varied over time (treatment*time X2(4) = 11.2; P = .025), with significantly lower symptom severity in the simvastatin group after 6 months (mean difference = -4.8; P = .021; 95% CI: -8.8 to -0.7) and at 24 months follow-up (mean difference = -4.7; P = .040; 95% CI: -9.3 to -0.2). No main treatment effect was found for cognition (F(1,0.1) = 0.37, P = .55) or secondary outcomes. SAEs occurred more frequently with placebo (19%) than with simvastatin (6.6%). This negative finding corroborates other large scale studies on aspirin, minocycline, and celecoxib that could not replicate positive findings of smaller studies, and suggests that anti-inflammatory augmentation does not improve the clinical presentation of SSD.

Published
2021

4. Functional connectome differences in individuals with hallucinations across the psychosis continuum

Author

Schutte, M.J.L., Bohlken, M.M., Collin, G., Abramovic, L., Boks, M.P., Cahn, W., Dauwan, M., Dellen, E. van, Haren, N.E.M. van, Hugdahl, K., Koops, S., Mandl, R.C.W., Sommer, I.E., Schutte, M.J.L., Bohlken, M.M., Collin, G., Abramovic, L., Boks, M.P., Cahn, W., Dauwan, M., Dellen, E. van, Haren, N.E.M. van, Hugdahl, K., Koops, S., Mandl, R.C.W., and Sommer, I.E.

Abstract

Contains fulltext : 238642.pdf (Publisher’s version ) (Open Access), Hallucinations may arise from an imbalance between sensory and higher cognitive brain regions, reflected by alterations in functional connectivity. It is unknown whether hallucinations across the psychosis continuum exhibit similar alterations in functional connectivity, suggesting a common neural mechanism, or whether different mechanisms link to hallucinations across phenotypes. We acquired resting-state functional MRI scans of 483 participants, including 40 non-clinical individuals with hallucinations, 99 schizophrenia patients with hallucinations, 74 bipolar-I disorder patients with hallucinations, 42 bipolar-I disorder patients without hallucinations, and 228 healthy controls. The weighted connectivity matrices were compared using network-based statistics. Non-clinical individuals with hallucinations and schizophrenia patients with hallucinations exhibited increased connectivity, mainly among fronto-temporal and fronto-insula/cingulate areas compared to controls (P < 0.001 adjusted). Differential effects were observed for bipolar-I disorder patients with hallucinations versus controls, mainly characterized by decreased connectivity between fronto-temporal and fronto-striatal areas (P = 0.012 adjusted). No connectivity alterations were found between bipolar-I disorder patients without hallucinations and controls. Our results support the notion that hallucinations in non-clinical individuals and schizophrenia patients are related to altered interactions between sensory and higher-order cognitive brain regions. However, a different dysconnectivity pattern was observed for bipolar-I disorder patients with hallucinations, which implies a different neural mechanism across the psychosis continuum.

Published
2021

5. Simvastatin Augmentation for Patients With Early-Phase Schizophrenia-Spectrum Disorders: A Double-Blind, Randomized Placebo-Controlled Trial

Author

Sommer, I.E., Gangadin, S.S., Witte, L.D. de, Koops, S., Baal, C. van, Bahn, S., Drexhage, H., Haren, N.E.M. van, Veling, W., Bruggeman, R., Martens, P., Wiersma, S., Veerman, S.R.T., Grootens, K.P., Beveren, N. van, Kahn, R.S., Begemann, M.J.H., Sommer, I.E., Gangadin, S.S., Witte, L.D. de, Koops, S., Baal, C. van, Bahn, S., Drexhage, H., Haren, N.E.M. van, Veling, W., Bruggeman, R., Martens, P., Wiersma, S., Veerman, S.R.T., Grootens, K.P., Beveren, N. van, Kahn, R.S., and Begemann, M.J.H.

Abstract

Contains fulltext : 244699.pdf (Publisher’s version ) (Open Access), Schizophrenia-spectrum disorders (SSD) are associated with increased inflammatory markers, both in brain and periphery. Augmentation with drugs that lower this pro-inflammatory status may improve clinical presentation. Simvastatin crosses the blood-brain barrier, has anti- inflammatory and neuroprotective effects and reduces metabolic syndrome. In this study, we investigated if 12 months of simvastatin augmentation can improve symptoms and cognition in patients with early SSD. This double-blind placebo-controlled trial included 127 SSD patients across the Netherlands, <3 years after their diagnosis. From these, 119 were randomly assigned 1:1 to simvastatin 40 mg (n = 61) or placebo (n = 58), stratified for sex and study site. Primary outcomes were symptom severity and cognition after 12 months of treatment. Depression, symptom subscores, general functioning, metabolic syndrome, movement disorders, and safety were secondary outcomes. Intention to treat analyses were performed using linear mixed models and ANCOVA. No main effect of simvastatin treatment was found on total symptom severity after 12 months of treatment as compared to placebo (X2(1) = 0.01, P = .90). Group differences varied over time (treatment*time X2(4) = 11.2; P = .025), with significantly lower symptom severity in the simvastatin group after 6 months (mean difference = -4.8; P = .021; 95% CI: -8.8 to -0.7) and at 24 months follow-up (mean difference = -4.7; P = .040; 95% CI: -9.3 to -0.2). No main treatment effect was found for cognition (F(1,0.1) = 0.37, P = .55) or secondary outcomes. SAEs occurred more frequently with placebo (19%) than with simvastatin (6.6%). This negative finding corroborates other large scale studies on aspirin, minocycline, and celecoxib that could not replicate positive findings of smaller studies, and suggests that anti-inflammatory augmentation does not improve the clinical presentation of SSD.

Published
2021

6. Functional connectome differences in individuals with hallucinations across the psychosis continuum

Author

Schutte, M.J.L., Bohlken, M.M., Collin, G., Abramovic, L., Boks, M.P., Cahn, W., Dauwan, M., Dellen, E. van, Haren, N.E.M. van, Hugdahl, K., Koops, S., Mandl, R.C.W., Sommer, I.E., Schutte, M.J.L., Bohlken, M.M., Collin, G., Abramovic, L., Boks, M.P., Cahn, W., Dauwan, M., Dellen, E. van, Haren, N.E.M. van, Hugdahl, K., Koops, S., Mandl, R.C.W., and Sommer, I.E.

Abstract

Contains fulltext : 238642.pdf (Publisher’s version ) (Open Access), Hallucinations may arise from an imbalance between sensory and higher cognitive brain regions, reflected by alterations in functional connectivity. It is unknown whether hallucinations across the psychosis continuum exhibit similar alterations in functional connectivity, suggesting a common neural mechanism, or whether different mechanisms link to hallucinations across phenotypes. We acquired resting-state functional MRI scans of 483 participants, including 40 non-clinical individuals with hallucinations, 99 schizophrenia patients with hallucinations, 74 bipolar-I disorder patients with hallucinations, 42 bipolar-I disorder patients without hallucinations, and 228 healthy controls. The weighted connectivity matrices were compared using network-based statistics. Non-clinical individuals with hallucinations and schizophrenia patients with hallucinations exhibited increased connectivity, mainly among fronto-temporal and fronto-insula/cingulate areas compared to controls (P < 0.001 adjusted). Differential effects were observed for bipolar-I disorder patients with hallucinations versus controls, mainly characterized by decreased connectivity between fronto-temporal and fronto-striatal areas (P = 0.012 adjusted). No connectivity alterations were found between bipolar-I disorder patients without hallucinations and controls. Our results support the notion that hallucinations in non-clinical individuals and schizophrenia patients are related to altered interactions between sensory and higher-order cognitive brain regions. However, a different dysconnectivity pattern was observed for bipolar-I disorder patients with hallucinations, which implies a different neural mechanism across the psychosis continuum.

Published
2021

7. Simvastatin Augmentation for Patients With Early-Phase Schizophrenia-Spectrum Disorders: A Double-Blind, Randomized Placebo-Controlled Trial

Author

Sommer, I.E., Gangadin, S.S., Witte, L.D. de, Koops, S., Baal, C. van, Bahn, S., Drexhage, H., Haren, N.E.M. van, Veling, W., Bruggeman, R., Martens, P., Wiersma, S., Veerman, S.R.T., Grootens, K.P., Beveren, N. van, Kahn, R.S., Begemann, M.J.H., Sommer, I.E., Gangadin, S.S., Witte, L.D. de, Koops, S., Baal, C. van, Bahn, S., Drexhage, H., Haren, N.E.M. van, Veling, W., Bruggeman, R., Martens, P., Wiersma, S., Veerman, S.R.T., Grootens, K.P., Beveren, N. van, Kahn, R.S., and Begemann, M.J.H.

Abstract

Contains fulltext : 244699.pdf (Publisher’s version ) (Open Access), Schizophrenia-spectrum disorders (SSD) are associated with increased inflammatory markers, both in brain and periphery. Augmentation with drugs that lower this pro-inflammatory status may improve clinical presentation. Simvastatin crosses the blood-brain barrier, has anti- inflammatory and neuroprotective effects and reduces metabolic syndrome. In this study, we investigated if 12 months of simvastatin augmentation can improve symptoms and cognition in patients with early SSD. This double-blind placebo-controlled trial included 127 SSD patients across the Netherlands, <3 years after their diagnosis. From these, 119 were randomly assigned 1:1 to simvastatin 40 mg (n = 61) or placebo (n = 58), stratified for sex and study site. Primary outcomes were symptom severity and cognition after 12 months of treatment. Depression, symptom subscores, general functioning, metabolic syndrome, movement disorders, and safety were secondary outcomes. Intention to treat analyses were performed using linear mixed models and ANCOVA. No main effect of simvastatin treatment was found on total symptom severity after 12 months of treatment as compared to placebo (X2(1) = 0.01, P = .90). Group differences varied over time (treatment*time X2(4) = 11.2; P = .025), with significantly lower symptom severity in the simvastatin group after 6 months (mean difference = -4.8; P = .021; 95% CI: -8.8 to -0.7) and at 24 months follow-up (mean difference = -4.7; P = .040; 95% CI: -9.3 to -0.2). No main treatment effect was found for cognition (F(1,0.1) = 0.37, P = .55) or secondary outcomes. SAEs occurred more frequently with placebo (19%) than with simvastatin (6.6%). This negative finding corroborates other large scale studies on aspirin, minocycline, and celecoxib that could not replicate positive findings of smaller studies, and suggests that anti-inflammatory augmentation does not improve the clinical presentation of SSD.

Published
2021

8. Functional connectome differences in individuals with hallucinations across the psychosis continuum

Author

Schutte, M.J.L., Bohlken, M.M., Collin, G., Abramovic, L., Boks, M.P., Cahn, W., Dauwan, M., Dellen, E. van, Haren, N.E.M. van, Hugdahl, K., Koops, S., Mandl, R.C.W., Sommer, I.E., Schutte, M.J.L., Bohlken, M.M., Collin, G., Abramovic, L., Boks, M.P., Cahn, W., Dauwan, M., Dellen, E. van, Haren, N.E.M. van, Hugdahl, K., Koops, S., Mandl, R.C.W., and Sommer, I.E.

Abstract

Contains fulltext : 238642.pdf (Publisher’s version ) (Open Access), Hallucinations may arise from an imbalance between sensory and higher cognitive brain regions, reflected by alterations in functional connectivity. It is unknown whether hallucinations across the psychosis continuum exhibit similar alterations in functional connectivity, suggesting a common neural mechanism, or whether different mechanisms link to hallucinations across phenotypes. We acquired resting-state functional MRI scans of 483 participants, including 40 non-clinical individuals with hallucinations, 99 schizophrenia patients with hallucinations, 74 bipolar-I disorder patients with hallucinations, 42 bipolar-I disorder patients without hallucinations, and 228 healthy controls. The weighted connectivity matrices were compared using network-based statistics. Non-clinical individuals with hallucinations and schizophrenia patients with hallucinations exhibited increased connectivity, mainly among fronto-temporal and fronto-insula/cingulate areas compared to controls (P < 0.001 adjusted). Differential effects were observed for bipolar-I disorder patients with hallucinations versus controls, mainly characterized by decreased connectivity between fronto-temporal and fronto-striatal areas (P = 0.012 adjusted). No connectivity alterations were found between bipolar-I disorder patients without hallucinations and controls. Our results support the notion that hallucinations in non-clinical individuals and schizophrenia patients are related to altered interactions between sensory and higher-order cognitive brain regions. However, a different dysconnectivity pattern was observed for bipolar-I disorder patients with hallucinations, which implies a different neural mechanism across the psychosis continuum.

Published
2021

9. Structural brain abnormalities in first-degree relatives of patients with bipolar disorder or schizophrenia

Author

Bosch, E.W., Haren, N.E.M. van (Thesis Advisor), Bosch, E.W., and Haren, N.E.M. van (Thesis Advisor)

Abstract

Patients suffering from either the severe mental disorder bipolar disorder (BD) or schizophrenia (SCZ) show resemblance in cognitive impairments, genetic etiology and structural brain abnormalities. Mapping the structural brain abnormalities in first-degree relatives of BD and SCZ patients can be valuable in order to elucidate the causes of brain abnormalities observed in the patients themselves. The first aim of this thesis is to provide an overview of brain volume abnormalities found in first-degree relatives of BD and SCZ patients. It will also be studied whether there are differences in structural brain abnormalities between siblings, parents, co-twins and offspring of either BD or SCZ probands. Furthermore, the differences in brain volume abnormalities of first-degree relatives of BD patients and first-degree relatives of SCZ patients will be studied. Thirty-two studies investigating structural brain abnormalities in first-degree relatives of BD patients, and three reviews and two meta-analyses investigating structural brain abnormalities in first-degree relatives of SCZ were examined here. From the overview that arose from these articles a list is made of brain regions that were in more than one study found to have an abnormal volume in first-degree relatives compared to healthy controls. It appeared that in first-degree relatives of BD patients there is little consistency in the findings of these studies, with the exception of a rather consistent reported decrease in prefrontal cortex volume. Differences in structural brain abnormalities between siblings, parents, co-twins and offspring of BD probands could not be identified. Decreased hippocampus and prefrontal cortex volumes and increased third ventricle volumes have been consistently reported in all sub-groups of first-degree relatives of SCZ patients. Parents of SCZ patients are also likely to have decreased insula volumes. Although not all results are consistently found, it can be stated that there are m

Published
2015

10. Structural brain abnormalities in first-degree relatives of patients with bipolar disorder or schizophrenia

Author

Bosch, E.W., Haren, N.E.M. van (Thesis Advisor), Bosch, E.W., and Haren, N.E.M. van (Thesis Advisor)

Abstract

Patients suffering from either the severe mental disorder bipolar disorder (BD) or schizophrenia (SCZ) show resemblance in cognitive impairments, genetic etiology and structural brain abnormalities. Mapping the structural brain abnormalities in first-degree relatives of BD and SCZ patients can be valuable in order to elucidate the causes of brain abnormalities observed in the patients themselves. The first aim of this thesis is to provide an overview of brain volume abnormalities found in first-degree relatives of BD and SCZ patients. It will also be studied whether there are differences in structural brain abnormalities between siblings, parents, co-twins and offspring of either BD or SCZ probands. Furthermore, the differences in brain volume abnormalities of first-degree relatives of BD patients and first-degree relatives of SCZ patients will be studied. Thirty-two studies investigating structural brain abnormalities in first-degree relatives of BD patients, and three reviews and two meta-analyses investigating structural brain abnormalities in first-degree relatives of SCZ were examined here. From the overview that arose from these articles a list is made of brain regions that were in more than one study found to have an abnormal volume in first-degree relatives compared to healthy controls. It appeared that in first-degree relatives of BD patients there is little consistency in the findings of these studies, with the exception of a rather consistent reported decrease in prefrontal cortex volume. Differences in structural brain abnormalities between siblings, parents, co-twins and offspring of BD probands could not be identified. Decreased hippocampus and prefrontal cortex volumes and increased third ventricle volumes have been consistently reported in all sub-groups of first-degree relatives of SCZ patients. Parents of SCZ patients are also likely to have decreased insula volumes. Although not all results are consistently found, it can be stated that there are m

Published
2015

11. Association study of fibroblast growth factor genes and brain volumes in schizophrenic patients and healthy controls

Author

Terwisscha van Scheltinga, A.F., Bakker, S.C., Haren, N.E.M. van, Boos, H.B., Schnack, H.G., Cahn, W., Hoogman, M., Zwiers, M.P., Fernandez, G.S.E., Franke, B., Hulshoff Pol, H.E., Kahn, R.S., Terwisscha van Scheltinga, A.F., Bakker, S.C., Haren, N.E.M. van, Boos, H.B., Schnack, H.G., Cahn, W., Hoogman, M., Zwiers, M.P., Fernandez, G.S.E., Franke, B., Hulshoff Pol, H.E., and Kahn, R.S.

Abstract

Item does not contain fulltext

Published
2014

12. Association study of fibroblast growth factor genes and brain volumes in schizophrenic patients and healthy controls

Author

Terwisscha van Scheltinga, A.F., Bakker, S.C., Haren, N.E.M. van, Boos, H.B., Schnack, H.G., Cahn, W., Hoogman, M., Zwiers, M.P., Fernandez, G.S.E., Franke, B., Pol, H.E., Kahn, R.S., Terwisscha van Scheltinga, A.F., Bakker, S.C., Haren, N.E.M. van, Boos, H.B., Schnack, H.G., Cahn, W., Hoogman, M., Zwiers, M.P., Fernandez, G.S.E., Franke, B., Pol, H.E., and Kahn, R.S.

Abstract

Item does not contain fulltext

Published
2014

13. Association study of fibroblast growth factor genes and brain volumes in schizophrenic patients and healthy controls

Author

Terwisscha van Scheltinga, A.F., Bakker, S.C., Haren, N.E.M. van, Boos, H.B., Schnack, H.G., Cahn, W., Hoogman, M., Zwiers, M.P., Fernandez, G.S.E., Franke, B., Hulshoff Pol, H.E., Kahn, R.S., Terwisscha van Scheltinga, A.F., Bakker, S.C., Haren, N.E.M. van, Boos, H.B., Schnack, H.G., Cahn, W., Hoogman, M., Zwiers, M.P., Fernandez, G.S.E., Franke, B., Hulshoff Pol, H.E., and Kahn, R.S.

Abstract

Item does not contain fulltext

Published
2014

14. Association study of fibroblast growth factor genes and brain volumes in schizophrenic patients and healthy controls

Author

Terwisscha van Scheltinga, A.F., Bakker, S.C., Haren, N.E.M. van, Boos, H.B., Schnack, H.G., Cahn, W., Hoogman, M., Zwiers, M.P., Fernandez, G.S.E., Franke, B., Hulshoff Pol, H.E., Kahn, R.S., Terwisscha van Scheltinga, A.F., Bakker, S.C., Haren, N.E.M. van, Boos, H.B., Schnack, H.G., Cahn, W., Hoogman, M., Zwiers, M.P., Fernandez, G.S.E., Franke, B., Hulshoff Pol, H.E., and Kahn, R.S.

Abstract

Item does not contain fulltext

Published
2014

15. Association study of fibroblast growth factor genes and brain volumes in schizophrenic patients and healthy controls

Author

Terwisscha van Scheltinga, A.F., Bakker, S.C., Haren, N.E.M. van, Boos, H.B., Schnack, H.G., Cahn, W., Hoogman, M., Zwiers, M.P., Fernandez, G.S.E., Franke, B., Pol, H.E., Kahn, R.S., Terwisscha van Scheltinga, A.F., Bakker, S.C., Haren, N.E.M. van, Boos, H.B., Schnack, H.G., Cahn, W., Hoogman, M., Zwiers, M.P., Fernandez, G.S.E., Franke, B., Pol, H.E., and Kahn, R.S.

Abstract

Item does not contain fulltext

Published
2014

16. Association study of fibroblast growth factor genes and brain volumes in schizophrenic patients and healthy controls

Author

Terwisscha van Scheltinga, A.F., Bakker, S.C., Haren, N.E.M. van, Boos, H.B., Schnack, H.G., Cahn, W., Hoogman, M., Zwiers, M.P., Fernandez, G.S.E., Franke, B., Pol, H.E., Kahn, R.S., Terwisscha van Scheltinga, A.F., Bakker, S.C., Haren, N.E.M. van, Boos, H.B., Schnack, H.G., Cahn, W., Hoogman, M., Zwiers, M.P., Fernandez, G.S.E., Franke, B., Pol, H.E., and Kahn, R.S.

Abstract

Contains fulltext : 136068.pdf (Publisher’s version ) (Closed access)

Published
2014

17. Association study of fibroblast growth factor genes and brain volumes in schizophrenic patients and healthy controls

Author

Terwisscha van Scheltinga, A.F., Bakker, S.C., Haren, N.E.M. van, Boos, H.B., Schnack, H.G., Cahn, W., Hoogman, M., Zwiers, M.P., Fernandez, G.S.E., Franke, B., Hulshoff Pol, H.E., Kahn, R.S., Terwisscha van Scheltinga, A.F., Bakker, S.C., Haren, N.E.M. van, Boos, H.B., Schnack, H.G., Cahn, W., Hoogman, M., Zwiers, M.P., Fernandez, G.S.E., Franke, B., Hulshoff Pol, H.E., and Kahn, R.S.

Abstract

Item does not contain fulltext

Published
2014

18. Identification of common variants associated with human hippocampal and intracranial volumes.

Author

Stein, J.L., Medland, S.E., Arias Vasquez, A., Hibar, D.P., Senstad, R.E., Winkler, A.M., Toro, R., Appel, K., Bartecek, R., Bergmann, O., Bernard, M., Brown, A.A., Cannon, D.M., Chakravarty, M.M., Christoforou, A., Domin, M., Grimm, O., Hollinshead, M., Holmes, A.J., Homuth, G., Hottenga, J.J., Langan, C., Lopez, L.M., Hansell, N.K., Hwang, K.S., Kim, S., Laje, G., Lee, P.H., Liu, X., Loth, E., Lourdusamy, A., Mattingsdal, M., Mohnke, S., Maniega, S.M., Nho, K., Nugent, A.C., O'Brien, C., Papmeyer, M., Putz, B., Ramasamy, A., Rasmussen, J., Rijpkema, M.J.P., Risacher, S.L., Roddey, J.C., Rose, E.J., Ryten, M., Shen, L., Sprooten, E., Strengman, E., Teumer, A., Trabzuni, D., Turner, J., Eijk, K. van, Erp, T.G. van, Tol, M.J. van, Wittfeld, K., Wolf, C. de, Woudstra, S., Aleman, A., Alhusaini, S., Almasy, L., Binder, E.B., Brohawn, D.G., Cantor, R.M., Carless, M.A., Corvin, A., Czisch, M., Curran, J.E., Davies, G., Almeida, M.A. de, Delanty, N., Depondt, C., Duggirala, R., Dyer, T.D., Erk, S., Fagerness, J., Fox, P.T., Freimer, N.B., Gill, M., Goring, H.H., Hagler, D.J., Hoehn, D., Holsboer, F., Hoogman, M., Hosten, N., Jahanshad, N., Johnson, M.P., Kasperaviciute, D., Kent Jr., J.W., Kochunov, P., Lancaster, J.L., Lawrie, S.M., Liewald, D.C., Mandl, R.C.W., Matarin, M., Mattheisen, M., Meisenzahl, E., Melle, I., Moses, E.K., Muhleisen, T.W., Nauck, M., Nothen, Markus, Olvera, R.L., Pandolfo, M., Pike, G.B., Puls, R., Reinvang, I., Renteria, M.E., Rietschel, M., Roffman, J.L., Royle, N.A., Rujescu, D., Savitz, J., Schnack, H.G., Schnell, K., Seiferth, N., Smith, C., Steen, V.M., Valdes Hernandez, M.C., Heuvel, M. van den, Wee, N.J.A. van der, Haren, N.E.M. van, Veltman, J.A., Volzke, H., Walker, R., Westlye, L.T., Whelan, C.D., Agartz, I., Boomsma, D.I., Cavalleri, G.L., Dale, A.M., Djurovic, S., Drevets, W.C., Hagoort, P., Hall, J., Heinz, A., Jack Jr., C.R., Foroud, T.M., Hellard, S. Le, Macciardi, F., Montgomery, G.W., Poline, J.B., Porteous, D.J., Sisodiya, S.M., Starr, J.M., Sussmann, J., Toga, A.W., Veltman, D.J., Walter, H., Weiner, M.W., Bis, J.C., Ikram, M.A., Smith, A.V., Gudnason, V., Tzourio, C., Vernooij, M.W., Launer, L.J., DeCarli, C., Seshadri, S., Andreassen, O.A., Apostolova, L.G., Bastin, M.E., Blangero, J., Brunner, H.G., Buckner, R.L., Cichon, S., Coppola, G., Zubicaray, G.I. de, Deary, I.J., Donohoe, G., Geus, E.J. de, Espeseth, T., Fernandez, G.S.E., Glahn, D.C., Grabe, H.J., Hardy, J., Hulshoff Pol, H.E., Jenkinson, M., Kahn, R.S., McDonald, C., McIntosh, A.M., McMahon, F.J., McMahon, K.L., Meyer-Lindenberg, A., Morris, D.W., Muller-Myhsok, B., Nichols, T.E., Ophoff, R.A., Paus, T., Pausova, Z., Penninx, B.W.J.H., Potkin, S.G., Samann, P.G., Saykin, A.J., Schumann, G., Smoller, J.W., Wardlaw, J.M., Weale, M.E., Martin, N.G., Franke, B., Wright, M.J., Thompson, P.M., Klaasen, A., et al., Stein, J.L., Medland, S.E., Arias Vasquez, A., Hibar, D.P., Senstad, R.E., Winkler, A.M., Toro, R., Appel, K., Bartecek, R., Bergmann, O., Bernard, M., Brown, A.A., Cannon, D.M., Chakravarty, M.M., Christoforou, A., Domin, M., Grimm, O., Hollinshead, M., Holmes, A.J., Homuth, G., Hottenga, J.J., Langan, C., Lopez, L.M., Hansell, N.K., Hwang, K.S., Kim, S., Laje, G., Lee, P.H., Liu, X., Loth, E., Lourdusamy, A., Mattingsdal, M., Mohnke, S., Maniega, S.M., Nho, K., Nugent, A.C., O'Brien, C., Papmeyer, M., Putz, B., Ramasamy, A., Rasmussen, J., Rijpkema, M.J.P., Risacher, S.L., Roddey, J.C., Rose, E.J., Ryten, M., Shen, L., Sprooten, E., Strengman, E., Teumer, A., Trabzuni, D., Turner, J., Eijk, K. van, Erp, T.G. van, Tol, M.J. van, Wittfeld, K., Wolf, C. de, Woudstra, S., Aleman, A., Alhusaini, S., Almasy, L., Binder, E.B., Brohawn, D.G., Cantor, R.M., Carless, M.A., Corvin, A., Czisch, M., Curran, J.E., Davies, G., Almeida, M.A. de, Delanty, N., Depondt, C., Duggirala, R., Dyer, T.D., Erk, S., Fagerness, J., Fox, P.T., Freimer, N.B., Gill, M., Goring, H.H., Hagler, D.J., Hoehn, D., Holsboer, F., Hoogman, M., Hosten, N., Jahanshad, N., Johnson, M.P., Kasperaviciute, D., Kent Jr., J.W., Kochunov, P., Lancaster, J.L., Lawrie, S.M., Liewald, D.C., Mandl, R.C.W., Matarin, M., Mattheisen, M., Meisenzahl, E., Melle, I., Moses, E.K., Muhleisen, T.W., Nauck, M., Nothen, Markus, Olvera, R.L., Pandolfo, M., Pike, G.B., Puls, R., Reinvang, I., Renteria, M.E., Rietschel, M., Roffman, J.L., Royle, N.A., Rujescu, D., Savitz, J., Schnack, H.G., Schnell, K., Seiferth, N., Smith, C., Steen, V.M., Valdes Hernandez, M.C., Heuvel, M. van den, Wee, N.J.A. van der, Haren, N.E.M. van, Veltman, J.A., Volzke, H., Walker, R., Westlye, L.T., Whelan, C.D., Agartz, I., Boomsma, D.I., Cavalleri, G.L., Dale, A.M., Djurovic, S., Drevets, W.C., Hagoort, P., Hall, J., Heinz, A., Jack Jr., C.R., Foroud, T.M., Hellard, S. Le, Macciardi, F., Montgomery, G.W., Poline, J.B., Porteous, D.J., Sisodiya, S.M., Starr, J.M., Sussmann, J., Toga, A.W., Veltman, D.J., Walter, H., Weiner, M.W., Bis, J.C., Ikram, M.A., Smith, A.V., Gudnason, V., Tzourio, C., Vernooij, M.W., Launer, L.J., DeCarli, C., Seshadri, S., Andreassen, O.A., Apostolova, L.G., Bastin, M.E., Blangero, J., Brunner, H.G., Buckner, R.L., Cichon, S., Coppola, G., Zubicaray, G.I. de, Deary, I.J., Donohoe, G., Geus, E.J. de, Espeseth, T., Fernandez, G.S.E., Glahn, D.C., Grabe, H.J., Hardy, J., Hulshoff Pol, H.E., Jenkinson, M., Kahn, R.S., McDonald, C., McIntosh, A.M., McMahon, F.J., McMahon, K.L., Meyer-Lindenberg, A., Morris, D.W., Muller-Myhsok, B., Nichols, T.E., Ophoff, R.A., Paus, T., Pausova, Z., Penninx, B.W.J.H., Potkin, S.G., Samann, P.G., Saykin, A.J., Schumann, G., Smoller, J.W., Wardlaw, J.M., Weale, M.E., Martin, N.G., Franke, B., Wright, M.J., Thompson, P.M., Klaasen, A., and et al.

Abstract

01 mei 2012, Contains fulltext : 108202.pdf (publisher's version ) (Closed access), Identifying genetic variants influencing human brain structures may reveal new biological mechanisms underlying cognition and neuropsychiatric illness. The volume of the hippocampus is a biomarker of incipient Alzheimer's disease and is reduced in schizophrenia, major depression and mesial temporal lobe epilepsy. Whereas many brain imaging phenotypes are highly heritable, identifying and replicating genetic influences has been difficult, as small effects and the high costs of magnetic resonance imaging (MRI) have led to underpowered studies. Here we report genome-wide association meta-analyses and replication for mean bilateral hippocampal, total brain and intracranial volumes from a large multinational consortium. The intergenic variant rs7294919 was associated with hippocampal volume (12q24.22; N = 21,151; P = 6.70 x 10(-16)) and the expression levels of the positional candidate gene TESC in brain tissue. Additionally, rs10784502, located within HMGA2, was associated with intracranial volume (12q14.3; N = 15,782; P = 1.12 x 10(-12)). We also identified a suggestive association with total brain volume at rs10494373 within DDR2 (1q23.3; N = 6,500; P = 5.81 x 10(-7)).

Published
2012

19. Positive priming and intentional binding: Eye-blink rate predicts reward information effects on the sense of agency

Author

Aarts, H.A.G., Bijleveld, E., Custers, R., Dogge, M., Deelder, M., Schutter, D.J.L.G., Haren, N.E.M. van, Aarts, H.A.G., Bijleveld, E., Custers, R., Dogge, M., Deelder, M., Schutter, D.J.L.G., and Haren, N.E.M. van

Abstract

Item does not contain fulltext, Human society is strongly rooted in people's experiences of agency; that is, the pervasive feeling that one engages in voluntary behavior and causes one's own actions and resulting outcomes. Rewards and positive affect play an important role in the control of voluntary action. However, the role of positive reward signals in the sense of agency is poorly understood. This study examined effects of reward-related information on the sense of agency by employing the intentional binding paradigm. This paradigm measures the extent to which actions and their effects subjectively shift together across time, reflecting a crucial component of people's sense of agency. Results showed that intentional binding is stronger when participants are primed with reward-related information via brief exposure to positive pictures. Interestingly, this positive priming effect was moderated by baseline eye-blink rates (an indirect marker of striatal dopaminergic functioning); reward-related information increased intentional binding mainly for participants displaying higher baseline eye-blink rates. These findings suggest a possible role for striatal dopamine activity in the process by which reward-related information shapes the way people see themselves as agents.

Published
2012

20. Identification of common variants associated with human hippocampal and intracranial volumes.

Author

Stein, J.L., Medland, S.E., Arias Vasquez, A., Hibar, D.P., Senstad, R.E., Winkler, A.M., Toro, R., Appel, K., Bartecek, R., Bergmann, O., Bernard, M., Brown, A.A., Cannon, D.M., Chakravarty, M.M., Christoforou, A., Domin, M., Grimm, O., Hollinshead, M., Holmes, A.J., Homuth, G., Hottenga, J.J., Langan, C., Lopez, L.M., Hansell, N.K., Hwang, K.S., Kim, S., Laje, G., Lee, P.H., Liu, X., Loth, E., Lourdusamy, A., Mattingsdal, M., Mohnke, S., Maniega, S.M., Nho, K., Nugent, A.C., O'Brien, C., Papmeyer, M., Putz, B., Ramasamy, A., Rasmussen, J., Rijpkema, M.J.P., Risacher, S.L., Roddey, J.C., Rose, E.J., Ryten, M., Shen, L., Sprooten, E., Strengman, E., Teumer, A., Trabzuni, D., Turner, J., Eijk, K. van, Erp, T.G. van, Tol, M.J. van, Wittfeld, K., Wolf, C. de, Woudstra, S., Aleman, A., Alhusaini, S., Almasy, L., Binder, E.B., Brohawn, D.G., Cantor, R.M., Carless, M.A., Corvin, A., Czisch, M., Curran, J.E., Davies, G., Almeida, M.A. de, Delanty, N., Depondt, C., Duggirala, R., Dyer, T.D., Erk, S., Fagerness, J., Fox, P.T., Freimer, N.B., Gill, M., Goring, H.H., Hagler, D.J., Hoehn, D., Holsboer, F., Hoogman, M., Hosten, N., Jahanshad, N., Johnson, M.P., Kasperaviciute, D., Kent Jr., J.W., Kochunov, P., Lancaster, J.L., Lawrie, S.M., Liewald, D.C., Mandl, R.C.W., Matarin, M., Mattheisen, M., Meisenzahl, E., Melle, I., Moses, E.K., Muhleisen, T.W., Nauck, M., Nothen, Markus, Olvera, R.L., Pandolfo, M., Pike, G.B., Puls, R., Reinvang, I., Renteria, M.E., Rietschel, M., Roffman, J.L., Royle, N.A., Rujescu, D., Savitz, J., Schnack, H.G., Schnell, K., Seiferth, N., Smith, C., Steen, V.M., Valdes Hernandez, M.C., Heuvel, M. van den, Wee, N.J.A. van der, Haren, N.E.M. van, Veltman, J.A., Volzke, H., Walker, R., Westlye, L.T., Whelan, C.D., Agartz, I., Boomsma, D.I., Cavalleri, G.L., Dale, A.M., Djurovic, S., Drevets, W.C., Hagoort, P., Hall, J., Heinz, A., Jack Jr., C.R., Foroud, T.M., Hellard, S. Le, Macciardi, F., Montgomery, G.W., Poline, J.B., Porteous, D.J., Sisodiya, S.M., Starr, J.M., Sussmann, J., Toga, A.W., Veltman, D.J., Walter, H., Weiner, M.W., Bis, J.C., Ikram, M.A., Smith, A.V., Gudnason, V., Tzourio, C., Vernooij, M.W., Launer, L.J., DeCarli, C., Seshadri, S., Andreassen, O.A., Apostolova, L.G., Bastin, M.E., Blangero, J., Brunner, H.G., Buckner, R.L., Cichon, S., Coppola, G., Zubicaray, G.I. de, Deary, I.J., Donohoe, G., Geus, E.J. de, Espeseth, T., Fernandez, G.S.E., Glahn, D.C., Grabe, H.J., Hardy, J., Hulshoff Pol, H.E., Jenkinson, M., Kahn, R.S., McDonald, C., McIntosh, A.M., McMahon, F.J., McMahon, K.L., Meyer-Lindenberg, A., Morris, D.W., Muller-Myhsok, B., Nichols, T.E., Ophoff, R.A., Paus, T., Pausova, Z., Penninx, B.W.J.H., Potkin, S.G., Samann, P.G., Saykin, A.J., Schumann, G., Smoller, J.W., Wardlaw, J.M., Weale, M.E., Martin, N.G., Franke, B., Wright, M.J., Thompson, P.M., Klaasen, A., et al., Stein, J.L., Medland, S.E., Arias Vasquez, A., Hibar, D.P., Senstad, R.E., Winkler, A.M., Toro, R., Appel, K., Bartecek, R., Bergmann, O., Bernard, M., Brown, A.A., Cannon, D.M., Chakravarty, M.M., Christoforou, A., Domin, M., Grimm, O., Hollinshead, M., Holmes, A.J., Homuth, G., Hottenga, J.J., Langan, C., Lopez, L.M., Hansell, N.K., Hwang, K.S., Kim, S., Laje, G., Lee, P.H., Liu, X., Loth, E., Lourdusamy, A., Mattingsdal, M., Mohnke, S., Maniega, S.M., Nho, K., Nugent, A.C., O'Brien, C., Papmeyer, M., Putz, B., Ramasamy, A., Rasmussen, J., Rijpkema, M.J.P., Risacher, S.L., Roddey, J.C., Rose, E.J., Ryten, M., Shen, L., Sprooten, E., Strengman, E., Teumer, A., Trabzuni, D., Turner, J., Eijk, K. van, Erp, T.G. van, Tol, M.J. van, Wittfeld, K., Wolf, C. de, Woudstra, S., Aleman, A., Alhusaini, S., Almasy, L., Binder, E.B., Brohawn, D.G., Cantor, R.M., Carless, M.A., Corvin, A., Czisch, M., Curran, J.E., Davies, G., Almeida, M.A. de, Delanty, N., Depondt, C., Duggirala, R., Dyer, T.D., Erk, S., Fagerness, J., Fox, P.T., Freimer, N.B., Gill, M., Goring, H.H., Hagler, D.J., Hoehn, D., Holsboer, F., Hoogman, M., Hosten, N., Jahanshad, N., Johnson, M.P., Kasperaviciute, D., Kent Jr., J.W., Kochunov, P., Lancaster, J.L., Lawrie, S.M., Liewald, D.C., Mandl, R.C.W., Matarin, M., Mattheisen, M., Meisenzahl, E., Melle, I., Moses, E.K., Muhleisen, T.W., Nauck, M., Nothen, Markus, Olvera, R.L., Pandolfo, M., Pike, G.B., Puls, R., Reinvang, I., Renteria, M.E., Rietschel, M., Roffman, J.L., Royle, N.A., Rujescu, D., Savitz, J., Schnack, H.G., Schnell, K., Seiferth, N., Smith, C., Steen, V.M., Valdes Hernandez, M.C., Heuvel, M. van den, Wee, N.J.A. van der, Haren, N.E.M. van, Veltman, J.A., Volzke, H., Walker, R., Westlye, L.T., Whelan, C.D., Agartz, I., Boomsma, D.I., Cavalleri, G.L., Dale, A.M., Djurovic, S., Drevets, W.C., Hagoort, P., Hall, J., Heinz, A., Jack Jr., C.R., Foroud, T.M., Hellard, S. Le, Macciardi, F., Montgomery, G.W., Poline, J.B., Porteous, D.J., Sisodiya, S.M., Starr, J.M., Sussmann, J., Toga, A.W., Veltman, D.J., Walter, H., Weiner, M.W., Bis, J.C., Ikram, M.A., Smith, A.V., Gudnason, V., Tzourio, C., Vernooij, M.W., Launer, L.J., DeCarli, C., Seshadri, S., Andreassen, O.A., Apostolova, L.G., Bastin, M.E., Blangero, J., Brunner, H.G., Buckner, R.L., Cichon, S., Coppola, G., Zubicaray, G.I. de, Deary, I.J., Donohoe, G., Geus, E.J. de, Espeseth, T., Fernandez, G.S.E., Glahn, D.C., Grabe, H.J., Hardy, J., Hulshoff Pol, H.E., Jenkinson, M., Kahn, R.S., McDonald, C., McIntosh, A.M., McMahon, F.J., McMahon, K.L., Meyer-Lindenberg, A., Morris, D.W., Muller-Myhsok, B., Nichols, T.E., Ophoff, R.A., Paus, T., Pausova, Z., Penninx, B.W.J.H., Potkin, S.G., Samann, P.G., Saykin, A.J., Schumann, G., Smoller, J.W., Wardlaw, J.M., Weale, M.E., Martin, N.G., Franke, B., Wright, M.J., Thompson, P.M., Klaasen, A., and et al.

Abstract

01 mei 2012, Contains fulltext : 108202.pdf (publisher's version ) (Closed access), Identifying genetic variants influencing human brain structures may reveal new biological mechanisms underlying cognition and neuropsychiatric illness. The volume of the hippocampus is a biomarker of incipient Alzheimer's disease and is reduced in schizophrenia, major depression and mesial temporal lobe epilepsy. Whereas many brain imaging phenotypes are highly heritable, identifying and replicating genetic influences has been difficult, as small effects and the high costs of magnetic resonance imaging (MRI) have led to underpowered studies. Here we report genome-wide association meta-analyses and replication for mean bilateral hippocampal, total brain and intracranial volumes from a large multinational consortium. The intergenic variant rs7294919 was associated with hippocampal volume (12q24.22; N = 21,151; P = 6.70 x 10(-16)) and the expression levels of the positional candidate gene TESC in brain tissue. Additionally, rs10784502, located within HMGA2, was associated with intracranial volume (12q14.3; N = 15,782; P = 1.12 x 10(-12)). We also identified a suggestive association with total brain volume at rs10494373 within DDR2 (1q23.3; N = 6,500; P = 5.81 x 10(-7)).

Published
2012

21. Positive priming and intentional binding: Eye-blink rate predicts reward information effects on the sense of agency

Author

Aarts, H.A.G., Bijleveld, E., Custers, R., Dogge, M., Deelder, M., Schutter, D.J.L.G., Haren, N.E.M. van, Aarts, H.A.G., Bijleveld, E., Custers, R., Dogge, M., Deelder, M., Schutter, D.J.L.G., and Haren, N.E.M. van

Abstract

Item does not contain fulltext, Human society is strongly rooted in people's experiences of agency; that is, the pervasive feeling that one engages in voluntary behavior and causes one's own actions and resulting outcomes. Rewards and positive affect play an important role in the control of voluntary action. However, the role of positive reward signals in the sense of agency is poorly understood. This study examined effects of reward-related information on the sense of agency by employing the intentional binding paradigm. This paradigm measures the extent to which actions and their effects subjectively shift together across time, reflecting a crucial component of people's sense of agency. Results showed that intentional binding is stronger when participants are primed with reward-related information via brief exposure to positive pictures. Interestingly, this positive priming effect was moderated by baseline eye-blink rates (an indirect marker of striatal dopaminergic functioning); reward-related information increased intentional binding mainly for participants displaying higher baseline eye-blink rates. These findings suggest a possible role for striatal dopamine activity in the process by which reward-related information shapes the way people see themselves as agents.

Published
2012

22. Positive priming and intentional binding: Eye-blink rate predicts reward information effects on the sense of agency

Author

Aarts, H.A.G., Bijleveld, E., Custers, R., Dogge, M., Deelder, M., Schutter, D.J.L.G., Haren, N.E.M. van, Aarts, H.A.G., Bijleveld, E., Custers, R., Dogge, M., Deelder, M., Schutter, D.J.L.G., and Haren, N.E.M. van

Abstract

Item does not contain fulltext, Human society is strongly rooted in people's experiences of agency; that is, the pervasive feeling that one engages in voluntary behavior and causes one's own actions and resulting outcomes. Rewards and positive affect play an important role in the control of voluntary action. However, the role of positive reward signals in the sense of agency is poorly understood. This study examined effects of reward-related information on the sense of agency by employing the intentional binding paradigm. This paradigm measures the extent to which actions and their effects subjectively shift together across time, reflecting a crucial component of people's sense of agency. Results showed that intentional binding is stronger when participants are primed with reward-related information via brief exposure to positive pictures. Interestingly, this positive priming effect was moderated by baseline eye-blink rates (an indirect marker of striatal dopaminergic functioning); reward-related information increased intentional binding mainly for participants displaying higher baseline eye-blink rates. These findings suggest a possible role for striatal dopamine activity in the process by which reward-related information shapes the way people see themselves as agents.

Published
2012

23. Identification of common variants associated with human hippocampal and intracranial volumes.

Author

Stein, J.L., Medland, S.E., Arias Vasquez, A., Hibar, D.P., Senstad, R.E., Winkler, A.M., Toro, R., Appel, K., Bartecek, R., Bergmann, O., Bernard, M., Brown, A.A., Cannon, D.M., Chakravarty, M.M., Christoforou, A., Domin, M., Grimm, O., Hollinshead, M., Holmes, A.J., Homuth, G., Hottenga, J.J., Langan, C., Lopez, L.M., Hansell, N.K., Hwang, K.S., Kim, S., Laje, G., Lee, P.H., Liu, X., Loth, E., Lourdusamy, A., Mattingsdal, M., Mohnke, S., Maniega, S.M., Nho, K., Nugent, A.C., O'Brien, C., Papmeyer, M., Putz, B., Ramasamy, A., Rasmussen, J., Rijpkema, M.J.P., Risacher, S.L., Roddey, J.C., Rose, E.J., Ryten, M., Shen, L., Sprooten, E., Strengman, E., Teumer, A., Trabzuni, D., Turner, J., Eijk, K. van, Erp, T.G. van, Tol, M.J. van, Wittfeld, K., Wolf, C. de, Woudstra, S., Aleman, A., Alhusaini, S., Almasy, L., Binder, E.B., Brohawn, D.G., Cantor, R.M., Carless, M.A., Corvin, A., Czisch, M., Curran, J.E., Davies, G., Almeida, M.A. de, Delanty, N., Depondt, C., Duggirala, R., Dyer, T.D., Erk, S., Fagerness, J., Fox, P.T., Freimer, N.B., Gill, M., Goring, H.H., Hagler, D.J., Hoehn, D., Holsboer, F., Hoogman, M., Hosten, N., Jahanshad, N., Johnson, M.P., Kasperaviciute, D., Kent Jr., J.W., Kochunov, P., Lancaster, J.L., Lawrie, S.M., Liewald, D.C., Mandl, R.C.W., Matarin, M., Mattheisen, M., Meisenzahl, E., Melle, I., Moses, E.K., Muhleisen, T.W., Nauck, M., Nothen, Markus, Olvera, R.L., Pandolfo, M., Pike, G.B., Puls, R., Reinvang, I., Renteria, M.E., Rietschel, M., Roffman, J.L., Royle, N.A., Rujescu, D., Savitz, J., Schnack, H.G., Schnell, K., Seiferth, N., Smith, C., Steen, V.M., Valdes Hernandez, M.C., Heuvel, M. van den, Wee, N.J.A. van der, Haren, N.E.M. van, Veltman, J.A., Volzke, H., Walker, R., Westlye, L.T., Whelan, C.D., Agartz, I., Boomsma, D.I., Cavalleri, G.L., Dale, A.M., Djurovic, S., Drevets, W.C., Hagoort, P., Hall, J., Heinz, A., Jack Jr., C.R., Foroud, T.M., Hellard, S. Le, Macciardi, F., Montgomery, G.W., Poline, J.B., Porteous, D.J., Sisodiya, S.M., Starr, J.M., Sussmann, J., Toga, A.W., Veltman, D.J., Walter, H., Weiner, M.W., Bis, J.C., Ikram, M.A., Smith, A.V., Gudnason, V., Tzourio, C., Vernooij, M.W., Launer, L.J., DeCarli, C., Seshadri, S., Andreassen, O.A., Apostolova, L.G., Bastin, M.E., Blangero, J., Brunner, H.G., Buckner, R.L., Cichon, S., Coppola, G., Zubicaray, G.I. de, Deary, I.J., Donohoe, G., Geus, E.J. de, Espeseth, T., Fernandez, G.S.E., Glahn, D.C., Grabe, H.J., Hardy, J., Hulshoff Pol, H.E., Jenkinson, M., Kahn, R.S., McDonald, C., McIntosh, A.M., McMahon, F.J., McMahon, K.L., Meyer-Lindenberg, A., Morris, D.W., Muller-Myhsok, B., Nichols, T.E., Ophoff, R.A., Paus, T., Pausova, Z., Penninx, B.W.J.H., Potkin, S.G., Samann, P.G., Saykin, A.J., Schumann, G., Smoller, J.W., Wardlaw, J.M., Weale, M.E., Martin, N.G., Franke, B., Wright, M.J., Thompson, P.M., Klaasen, A., et al., Stein, J.L., Medland, S.E., Arias Vasquez, A., Hibar, D.P., Senstad, R.E., Winkler, A.M., Toro, R., Appel, K., Bartecek, R., Bergmann, O., Bernard, M., Brown, A.A., Cannon, D.M., Chakravarty, M.M., Christoforou, A., Domin, M., Grimm, O., Hollinshead, M., Holmes, A.J., Homuth, G., Hottenga, J.J., Langan, C., Lopez, L.M., Hansell, N.K., Hwang, K.S., Kim, S., Laje, G., Lee, P.H., Liu, X., Loth, E., Lourdusamy, A., Mattingsdal, M., Mohnke, S., Maniega, S.M., Nho, K., Nugent, A.C., O'Brien, C., Papmeyer, M., Putz, B., Ramasamy, A., Rasmussen, J., Rijpkema, M.J.P., Risacher, S.L., Roddey, J.C., Rose, E.J., Ryten, M., Shen, L., Sprooten, E., Strengman, E., Teumer, A., Trabzuni, D., Turner, J., Eijk, K. van, Erp, T.G. van, Tol, M.J. van, Wittfeld, K., Wolf, C. de, Woudstra, S., Aleman, A., Alhusaini, S., Almasy, L., Binder, E.B., Brohawn, D.G., Cantor, R.M., Carless, M.A., Corvin, A., Czisch, M., Curran, J.E., Davies, G., Almeida, M.A. de, Delanty, N., Depondt, C., Duggirala, R., Dyer, T.D., Erk, S., Fagerness, J., Fox, P.T., Freimer, N.B., Gill, M., Goring, H.H., Hagler, D.J., Hoehn, D., Holsboer, F., Hoogman, M., Hosten, N., Jahanshad, N., Johnson, M.P., Kasperaviciute, D., Kent Jr., J.W., Kochunov, P., Lancaster, J.L., Lawrie, S.M., Liewald, D.C., Mandl, R.C.W., Matarin, M., Mattheisen, M., Meisenzahl, E., Melle, I., Moses, E.K., Muhleisen, T.W., Nauck, M., Nothen, Markus, Olvera, R.L., Pandolfo, M., Pike, G.B., Puls, R., Reinvang, I., Renteria, M.E., Rietschel, M., Roffman, J.L., Royle, N.A., Rujescu, D., Savitz, J., Schnack, H.G., Schnell, K., Seiferth, N., Smith, C., Steen, V.M., Valdes Hernandez, M.C., Heuvel, M. van den, Wee, N.J.A. van der, Haren, N.E.M. van, Veltman, J.A., Volzke, H., Walker, R., Westlye, L.T., Whelan, C.D., Agartz, I., Boomsma, D.I., Cavalleri, G.L., Dale, A.M., Djurovic, S., Drevets, W.C., Hagoort, P., Hall, J., Heinz, A., Jack Jr., C.R., Foroud, T.M., Hellard, S. Le, Macciardi, F., Montgomery, G.W., Poline, J.B., Porteous, D.J., Sisodiya, S.M., Starr, J.M., Sussmann, J., Toga, A.W., Veltman, D.J., Walter, H., Weiner, M.W., Bis, J.C., Ikram, M.A., Smith, A.V., Gudnason, V., Tzourio, C., Vernooij, M.W., Launer, L.J., DeCarli, C., Seshadri, S., Andreassen, O.A., Apostolova, L.G., Bastin, M.E., Blangero, J., Brunner, H.G., Buckner, R.L., Cichon, S., Coppola, G., Zubicaray, G.I. de, Deary, I.J., Donohoe, G., Geus, E.J. de, Espeseth, T., Fernandez, G.S.E., Glahn, D.C., Grabe, H.J., Hardy, J., Hulshoff Pol, H.E., Jenkinson, M., Kahn, R.S., McDonald, C., McIntosh, A.M., McMahon, F.J., McMahon, K.L., Meyer-Lindenberg, A., Morris, D.W., Muller-Myhsok, B., Nichols, T.E., Ophoff, R.A., Paus, T., Pausova, Z., Penninx, B.W.J.H., Potkin, S.G., Samann, P.G., Saykin, A.J., Schumann, G., Smoller, J.W., Wardlaw, J.M., Weale, M.E., Martin, N.G., Franke, B., Wright, M.J., Thompson, P.M., Klaasen, A., and et al.

Abstract

01 mei 2012, Contains fulltext : 108202.pdf (Publisher’s version ) (Closed access), Identifying genetic variants influencing human brain structures may reveal new biological mechanisms underlying cognition and neuropsychiatric illness. The volume of the hippocampus is a biomarker of incipient Alzheimer's disease and is reduced in schizophrenia, major depression and mesial temporal lobe epilepsy. Whereas many brain imaging phenotypes are highly heritable, identifying and replicating genetic influences has been difficult, as small effects and the high costs of magnetic resonance imaging (MRI) have led to underpowered studies. Here we report genome-wide association meta-analyses and replication for mean bilateral hippocampal, total brain and intracranial volumes from a large multinational consortium. The intergenic variant rs7294919 was associated with hippocampal volume (12q24.22; N = 21,151; P = 6.70 x 10(-16)) and the expression levels of the positional candidate gene TESC in brain tissue. Additionally, rs10784502, located within HMGA2, was associated with intracranial volume (12q14.3; N = 15,782; P = 1.12 x 10(-12)). We also identified a suggestive association with total brain volume at rs10494373 within DDR2 (1q23.3; N = 6,500; P = 5.81 x 10(-7)).

Published
2012

24. Brain morphology in schizophrenia and bipolar disorder and the overlap

Author

Meij, N.L. van der, Cahn, W. (Thesis Advisor), Haren, N.E.M. van, Meij, N.L. van der, Cahn, W. (Thesis Advisor), and Haren, N.E.M. van

Abstract

With the development of MRI, brain volumes can be measured in vivo nowadays. MRI research on structure alterations in patients with schizophrenia led to new theories about the etiology of the disease. Reductions in brain volume were shown to be present in early stages of the disease, when most of the symptomatic change and loss of function also occur. What was regarded a neuro-degenerative disease, schizophrenia could be a consequence of a developmental malfunction as well. Next to schizophrenia, more insight can be gained on the nature of bipolar disorder. The overlap between these very heterogeneous mental disorders remains to be elucidated. This review summarizes studies which investigated structure alterations in schizophrenia and bipolar disorder with use of sMRI techniques, with the aim to gain information on the brain morphology of these illnesses. Furthermore, a possible relation of structure alterations with symptoms and functioning of patients is discussed. Current research so far point to main differences between schizophrenia and bipolar disorder. In schizophrenia, more pronounced reductions in brain volume are seen, which are likely to relate to symptoms and functioning of patients. More research, controlled for confounders like medication and subtype of disease is needed, however, to further establish the relevancy of structure alterations found. This is especially the case for research on bipolar disorder, which is scarce compared to research on schizophrenia.

Published
2009

25. Brain morphology in schizophrenia and bipolar disorder and the overlap

Author

Meij, N.L. van der, Cahn, W. (Thesis Advisor), Haren, N.E.M. van, Meij, N.L. van der, Cahn, W. (Thesis Advisor), and Haren, N.E.M. van

Abstract

With the development of MRI, brain volumes can be measured in vivo nowadays. MRI research on structure alterations in patients with schizophrenia led to new theories about the etiology of the disease. Reductions in brain volume were shown to be present in early stages of the disease, when most of the symptomatic change and loss of function also occur. What was regarded a neuro-degenerative disease, schizophrenia could be a consequence of a developmental malfunction as well. Next to schizophrenia, more insight can be gained on the nature of bipolar disorder. The overlap between these very heterogeneous mental disorders remains to be elucidated. This review summarizes studies which investigated structure alterations in schizophrenia and bipolar disorder with use of sMRI techniques, with the aim to gain information on the brain morphology of these illnesses. Furthermore, a possible relation of structure alterations with symptoms and functioning of patients is discussed. Current research so far point to main differences between schizophrenia and bipolar disorder. In schizophrenia, more pronounced reductions in brain volume are seen, which are likely to relate to symptoms and functioning of patients. More research, controlled for confounders like medication and subtype of disease is needed, however, to further establish the relevancy of structure alterations found. This is especially the case for research on bipolar disorder, which is scarce compared to research on schizophrenia.

Published
2009

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