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15 results on '"Brouwer, R"'

1. Exome-sequencing in a large population-based study reveals a rare Asn396Ser variant in the LIPG gene associated with depressive symptoms

Author

Amin, N, Jovanova, O, Adams, H H H, Dehghan, A, Kavousi, M, Vernooij, M W, Peeters, R P, de Vrij, F M S, van der Lee, S J, van Rooij, J G J, van Leeuwen, E M, Chaker, L, Demirkan, A, Hofman, A, Brouwer, R W W, Kraaij, R, Willems van Dijk, K, Hankemeier, T, van Ijcken, W F J, Uitterlinden, A G, Niessen, W J, Franco, O H, Kushner, S A, Ikram, M A, Tiemeier, H, and van Duijn, C M

Published
2017
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3. Employed family-based genetic discovery combining linkage analysis and exome sequencing to identify RCL1 as a novel candidate gene for depression, with independent replication in a population-based cohort

Author

Amin, N, de Vrij, F M S, Baghdadi, M, Brouwer, R W W, van Rooij, J G J, Jovanova, O, Uitterlinden, A G, Hofman, A, Janssen, H L A, Murad, S Darwish, Kraaij, R, Stedehouder, J, van den Hout, M C G N, Kros, J M, van IJcken, W F J, Tiemeier, H, Kushner, S A, and van Duijn, C M

Published
2018
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4. Erratum: Exome-sequencing in a large population-based study reveals a rare Asn396Ser variant in the LIPG gene associated with depressive symptoms

Author

Amin, N, Jovanova, O, Adams, H H H, Dehghan, A, Kavousi, M, Vernooij, M W, Peeters, R P, de Vrij, F M S, van der Lee, S J, van Rooij, J G J, van Leeuwen, E M, Chaker, L, Demirkan, A, Hofman, A, Brouwer, R W W, Kraaij, R, Willems van Dijk, K, Hankemeier, T, van Ijcken, W F J, Uitterlinden, A G, Niessen, W J, Franco, O H, Kushner, S A, Ikram, M A, Tiemeier, H, and van Duijn, C M

Published
2017
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6. Widespread white matter microstructural differences in schizophrenia across 4322 individuals: results from the ENIGMA Schizophrenia DTI Working Group

Author

Kelly, S, primary, Jahanshad, N, additional, Zalesky, A, additional, Kochunov, P, additional, Agartz, I, additional, Alloza, C, additional, Andreassen, O A, additional, Arango, C, additional, Banaj, N, additional, Bouix, S, additional, Bousman, C A, additional, Brouwer, R M, additional, Bruggemann, J, additional, Bustillo, J, additional, Cahn, W, additional, Calhoun, V, additional, Cannon, D, additional, Carr, V, additional, Catts, S, additional, Chen, J, additional, Chen, J-x, additional, Chen, X, additional, Chiapponi, C, additional, Cho, Kl K, additional, Ciullo, V, additional, Corvin, A S, additional, Crespo-Facorro, B, additional, Cropley, V, additional, De Rossi, P, additional, Diaz-Caneja, C M, additional, Dickie, E W, additional, Ehrlich, S, additional, Fan, F-m, additional, Faskowitz, J, additional, Fatouros-Bergman, H, additional, Flyckt, L, additional, Ford, J M, additional, Fouche, J-P, additional, Fukunaga, M, additional, Gill, M, additional, Glahn, D C, additional, Gollub, R, additional, Goudzwaard, E D, additional, Guo, H, additional, Gur, R E, additional, Gur, R C, additional, Gurholt, T P, additional, Hashimoto, R, additional, Hatton, S N, additional, Henskens, F A, additional, Hibar, D P, additional, Hickie, I B, additional, Hong, L E, additional, Horacek, J, additional, Howells, F M, additional, Hulshoff Pol, H E, additional, Hyde, C L, additional, Isaev, D, additional, Jablensky, A, additional, Jansen, P R, additional, Janssen, J, additional, Jönsson, E G, additional, Jung, L A, additional, Kahn, R S, additional, Kikinis, Z, additional, Liu, K, additional, Klauser, P, additional, Knöchel, C, additional, Kubicki, M, additional, Lagopoulos, J, additional, Langen, C, additional, Lawrie, S, additional, Lenroot, R K, additional, Lim, K O, additional, Lopez-Jaramillo, C, additional, Lyall, A, additional, Magnotta, V, additional, Mandl, R C W, additional, Mathalon, D H, additional, McCarley, R W, additional, McCarthy-Jones, S, additional, McDonald, C, additional, McEwen, S, additional, McIntosh, A, additional, Melicher, T, additional, Mesholam-Gately, R I, additional, Michie, P T, additional, Mowry, B, additional, Mueller, B A, additional, Newell, D T, additional, O'Donnell, P, additional, Oertel-Knöchel, V, additional, Oestreich, L, additional, Paciga, S A, additional, Pantelis, C, additional, Pasternak, O, additional, Pearlson, G, additional, Pellicano, G R, additional, Pereira, A, additional, Pineda Zapata, J, additional, Piras, F, additional, Potkin, S G, additional, Preda, A, additional, Rasser, P E, additional, Roalf, D R, additional, Roiz, R, additional, Roos, A, additional, Rotenberg, D, additional, Satterthwaite, T D, additional, Savadjiev, P, additional, Schall, U, additional, Scott, R J, additional, Seal, M L, additional, Seidman, L J, additional, Shannon Weickert, C, additional, Whelan, C D, additional, Shenton, M E, additional, Kwon, J S, additional, Spalletta, G, additional, Spaniel, F, additional, Sprooten, E, additional, Stäblein, M, additional, Stein, D J, additional, Sundram, S, additional, Tan, Y, additional, Tan, S, additional, Tang, S, additional, Temmingh, H S, additional, Westlye, L T, additional, Tønnesen, S, additional, Tordesillas-Gutierrez, D, additional, Doan, N T, additional, Vaidya, J, additional, van Haren, N E M, additional, Vargas, C D, additional, Vecchio, D, additional, Velakoulis, D, additional, Voineskos, A, additional, Voyvodic, J Q, additional, Wang, Z, additional, Wan, P, additional, Wei, D, additional, Weickert, T W, additional, Whalley, H, additional, White, T, additional, Whitford, T J, additional, Wojcik, J D, additional, Xiang, H, additional, Xie, Z, additional, Yamamori, H, additional, Yang, F, additional, Yao, N, additional, Zhang, G, additional, Zhao, J, additional, van Erp, T G M, additional, Turner, J, additional, Thompson, P M, additional, and Donohoe, G, additional

Published
2017
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7. A rare missense variant in RCL1 segregates with depression in extended families

Author

Amin, N, primary, de Vrij, F M S, additional, Baghdadi, M, additional, Brouwer, R W W, additional, van Rooij, J G J, additional, Jovanova, O, additional, Uitterlinden, A G, additional, Hofman, A, additional, Janssen, H L A, additional, Darwish Murad, S, additional, Kraaij, R, additional, Stedehouder, J, additional, van den Hout, M C G N, additional, Kros, J M, additional, van IJcken, W F J, additional, Tiemeier, H, additional, Kushner, S A, additional, and van Duijn, C M, additional

Published
2017
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8. Erratum: Exome-sequencing in a large population-based study reveals a rare Asn396Ser variant in the LIPG gene associated with depressive symptoms

Author

Amin, N, primary, Jovanova, O, additional, Adams, H H H, additional, Dehghan, A, additional, Kavousi, M, additional, Vernooij, M W, additional, Peeters, R P, additional, de Vrij, F M S, additional, van der Lee, S J, additional, van Rooij, J G J, additional, van Leeuwen, E M, additional, Chaker, L, additional, Demirkan, A, additional, Hofman, A, additional, Brouwer, R W W, additional, Kraaij, R, additional, Willems van Dijk, K, additional, Hankemeier, T, additional, van Ijcken, W F J, additional, Uitterlinden, A G, additional, Niessen, W J, additional, Franco, O H, additional, Kushner, S A, additional, Ikram, M A, additional, Tiemeier, H, additional, and van Duijn, C M, additional

Published
2016
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9. Exome-sequencing in a large population-based study reveals a rare Asn396Ser variant in the LIPG gene associated with depressive symptoms

Author

Amin, N, primary, Jovanova, O, additional, Adams, H H H, additional, Dehghan, A, additional, Kavousi, M, additional, Vernooij, M W, additional, Peeters, R P, additional, de Vrij, F M S, additional, van der Lee, S J, additional, van Rooij, J G J, additional, van Leeuwen, E M, additional, Chaker, L, additional, Demirkan, A, additional, Hofman, A, additional, Brouwer, R W W, additional, Kraaij, R, additional, Willems van Dijk, K, additional, Hankemeier, T, additional, van Ijcken, W F J, additional, Uitterlinden, A G, additional, Niessen, W J, additional, Franco, O H, additional, Kushner, S A, additional, Ikram, M A, additional, Tiemeier, H, additional, and van Duijn, C M, additional

Published
2016
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10. Reciprocal causation models of cognitive vs volumetric cerebral intermediate phenotypes for schizophrenia in a pan-European twin cohort

Author

Toulopoulou, T, primary, van Haren, N, additional, Zhang, X, additional, Sham, P C, additional, Cherny, S S, additional, Campbell, D D, additional, Picchioni, M, additional, Murray, R, additional, Boomsma, D I, additional, Pol, H H, additional, Brouwer, R, additional, Schnack, H, additional, Fañanás, L, additional, Sauer, H, additional, Nenadic, I, additional, Weisbrod, M, additional, Cannon, T D, additional, and Kahn, R S, additional

Published
2014
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11. Widespread white matter microstructural differences in schizophrenia across 4322 individuals: results from the ENIGMA Schizophrenia DTI Working Group

Author

Kelly, S, Jahanshad, N, Zalesky, A, Kochunov, P, Agartz, I, Alloza, C, Andreassen, O A, Arango, C, Banaj, N, Bouix, S, Bousman, C A, Brouwer, R M, Bruggemann, J, Bustillo, J, Cahn, W, Calhoun, V, Cannon, D, Carr, V, Catts, S, Chen, J, Chen, J-x, Chen, X, Chiapponi, C, Cho, Kl K, Ciullo, V, Corvin, A S, Crespo-Facorro, B, Cropley, V, De Rossi, P, Diaz-Caneja, C M, Dickie, E W, Ehrlich, S, Fan, F-m, Faskowitz, J, Fatouros-Bergman, H, Flyckt, L, Ford, J M, Fouche, J-P, Fukunaga, M, Gill, M, Glahn, D C, Gollub, R, Goudzwaard, E D, Guo, H, Gur, R E, Gur, R C, Gurholt, T P, Hashimoto, R, Hatton, S N, Henskens, F A, Hibar, D P, Hickie, I B, Hong, L E, Horacek, J, Howells, F M, Hulshoff Pol, H E, Hyde, C L, Isaev, D, Jablensky, A, Jansen, P R, Janssen, J, Jönsson, E G, Jung, L A, Kahn, R S, Kikinis, Z, Liu, K, Klauser, P, Knöchel, C, Kubicki, M, Lagopoulos, J, Langen, C, Lawrie, S, Lenroot, R K, Lim, K O, Lopez-Jaramillo, C, Lyall, A, Magnotta, V, Mandl, R C W, Mathalon, D H, McCarley, R W, McCarthy-Jones, S, McDonald, C, McEwen, S, McIntosh, A, Melicher, T, Mesholam-Gately, R I, Michie, P T, Mowry, B, Mueller, B A, Newell, D T, O'Donnell, P, Oertel-Knöchel, V, Oestreich, L, Paciga, S A, Pantelis, C, Pasternak, O, Pearlson, G, Pellicano, G R, Pereira, A, Pineda Zapata, J, Piras, F, Potkin, S G, Preda, A, Rasser, P E, Roalf, D R, Roiz, R, Roos, A, Rotenberg, D, Satterthwaite, T D, Savadjiev, P, Schall, U, Scott, R J, Seal, M L, Seidman, L J, Shannon Weickert, C, Whelan, C D, Shenton, M E, Kwon, J S, Spalletta, G, Spaniel, F, Sprooten, E, Stäblein, M, Stein, D J, Sundram, S, Tan, Y, Tan, S, Tang, S, Temmingh, H S, Westlye, L T, Tønnesen, S, Tordesillas-Gutierrez, D, Doan, N T, Vaidya, J, van Haren, N E M, Vargas, C D, Vecchio, D, Velakoulis, D, Voineskos, A, Voyvodic, J Q, Wang, Z, Wan, P, Wei, D, Weickert, T W, Whalley, H, White, T, Whitford, T J, Wojcik, J D, Xiang, H, Xie, Z, Yamamori, H, Yang, F, Yao, N, Zhang, G, Zhao, J, van Erp, T G M, Turner, J, Thompson, P M, and Donohoe, G

Abstract

The regional distribution of white matter (WM) abnormalities in schizophrenia remains poorly understood, and reported disease effects on the brain vary widely between studies. In an effort to identify commonalities across studies, we perform what we believe is the first ever large-scale coordinated study of WM microstructural differences in schizophrenia. Our analysis consisted of 2359 healthy controls and 1963 schizophrenia patients from 29 independent international studies; we harmonized the processing and statistical analyses of diffusion tensor imaging (DTI) data across sites and meta-analyzed effects across studies. Significant reductions in fractional anisotropy (FA) in schizophrenia patients were widespread, and detected in 20 of 25 regions of interest within a WM skeleton representing all major WM fasciculi. Effect sizes varied by region, peaking at (d=0.42) for the entire WM skeleton, driven more by peripheral areas as opposed to the core WM where regions of interest were defined. The anterior corona radiata (d=0.40) and corpus callosum (d=0.39), specifically its body (d=0.39) and genu (d=0.37), showed greatest effects. Significant decreases, to lesser degrees, were observed in almost all regions analyzed. Larger effect sizes were observed for FA than diffusivity measures; significantly higher mean and radial diffusivity was observed for schizophrenia patients compared with controls. No significant effects of age at onset of schizophrenia or medication dosage were detected. As the largest coordinated analysis of WM differences in a psychiatric disorder to date, the present study provides a robust profile of widespread WM abnormalities in schizophrenia patients worldwide. Interactive three-dimensional visualization of the results is available at www.enigma-viewer.org.

Published
2018
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12. A rare missense variant in RCL1 segregates with depression in extended families

Author

Amin, N, de Vrij, F M S, Baghdadi, M, Brouwer, R W W, van Rooij, J G J, Jovanova, O, Uitterlinden, A G, Hofman, A, Janssen, H L A, Darwish Murad, S, Kraaij, R, Stedehouder, J, van den Hout, M C G N, Kros, J M, van IJcken, W F J, Tiemeier, H, Kushner, S A, and van Duijn, C M

Abstract

Depression is the most prevalent psychiatric disorder with a complex and elusive etiology that is moderately heritable. Identification of genes would greatly facilitate the elucidation of the biological mechanisms underlying depression, however, its complex etiology has proved to be a major bottleneck in the identification of its genetic risk factors, especially in genome-wide association-like studies. In this study, we exploit the properties of a genetic isolate and its family-based structure to explore whether relatively rare exonic variants influence the burden of depressive symptoms in families. Using a multistep approach involving linkage and haplotype analyses followed by exome sequencing in the Erasmus Rucphen Family (ERF) study, we identified a rare (minor allele frequency (MAF)=1%) missense c.1114C>T mutation (rs115482041) in the RCL1 gene segregating with depression across multiple generations. Rs115482041 showed significant association with depressive symptoms (N=2393, βT-allele=2.33, P-value=1 × 10−4) and explained 2.9% of the estimated genetic variance of depressive symptoms (22%) in ERF. Despite being twice as rare (MAF<0.5%), c.1114C>T showed similar effect and significant association with depressive symptoms in samples from the independent population-based Rotterdam study (N=1604, βT-allele=3.60, P-value=3 × 10−2). A comparison of RCL1 expression in human and mouse brain revealed a striking co-localization of RCL1 with the layer 1 interlaminar subclass of astrocytes found exclusively in higher-order primates. Our findings identify RCL1 as a novel candidate gene for depression and offer insights into mechanisms through which RCL1 may be relevant for depression.

Published
2018
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13. Exome-sequencing in a large population-based study reveals a rare Asn396Servariant in the LIPGgene associated with depressive symptoms

Author

Amin, N, Jovanova, O, Adams, H H H, Dehghan, A, Kavousi, M, Vernooij, M W, Peeters, R P, de Vrij, F M S, van der Lee, S J, van Rooij, J G J, van Leeuwen, E M, Chaker, L, Demirkan, A, Hofman, A, Brouwer, R W W, Kraaij, R, Willems van Dijk, K, Hankemeier, T, van Ijcken, W F J, Uitterlinden, A G, Niessen, W J, Franco, O H, Kushner, S A, Ikram, M A, Tiemeier, H, and van Duijn, C M

Abstract

Despite a substantial genetic component, efforts to identify common genetic variation underlying depression have largely been unsuccessful. In the current study we aimed to identify rare genetic variants that might have large effects on depression in the general population. Using high-coverage exome-sequencing, we studied the exonic variants in 1265 individuals from the Rotterdam study (RS), who were assessed for depressive symptoms. We identified a missense Asn396Sermutation (rs77960347) in the endothelial lipase (LIPG) gene, occurring with an allele frequency of 1% in the general population, which was significantly associated with depressive symptoms (P-value=5.2 × 10−08, β=7.2). Replication in three independent data sets (N=3612) confirmed the association of Asn396Ser(P-value=7.1 × 10−03, β=2.55) with depressive symptoms. LIPGis predicted to have enzymatic function in steroid biosynthesis, cholesterol biosynthesis and thyroid hormone metabolic processes. The Asn396Servariant is predicted to have a damaging effect on the function of LIPG. Within the discovery population, carriers also showed an increased burden of white matter lesions (P-value=3.3 × 1−02) and a higher risk of Alzheimer’s disease (odds ration=2.01; P-value=2.8 × 10−02) compared with the non-carriers. Together, these findings implicate the Asn396Servariant of LIPGin the pathogenesis of depressive symptoms in the general population.

Published
2017
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14. Erratum: Exome-sequencing in a large population-based study reveals a rare Asn396Servariant in the LIPGgene associated with depressive symptoms

Author

Amin, N, Jovanova, O, Adams, H H H, Dehghan, A, Kavousi, M, Vernooij, M W, Peeters, R P, de Vrij, F M S, van der Lee, S J, van Rooij, J G J, van Leeuwen, E M, Chaker, L, Demirkan, A, Hofman, A, Brouwer, R W W, Kraaij, R, Willems van Dijk, K, Hankemeier, T, van Ijcken, W F J, Uitterlinden, A G, Niessen, W J, Franco, O H, Kushner, S A, Ikram, M A, Tiemeier, H, and van Duijn, C M

Abstract

Correction to: Molecular Psychiatry advance online publication, 19 July 2016; doi:10.1038/mp.2016.101 In the abstract, the P-value of the white matter lesions should have been listed as 3.3 × 10−02. Also in the abstract, the higher risk of Alzheimer’s disease should have been listed as an odds ratio, not an odds ration.

Published
2017
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15. Epigenome-wide meta-analysis of blood DNA methylation and its association with subcortical volumes: findings from the ENIGMA Epigenetics Working Group.

Author

Jia T, Chu C, Liu Y, van Dongen J, Papastergios E, Armstrong NJ, Bastin ME, Carrillo-Roa T, den Braber A, Harris M, Jansen R, Liu J, Luciano M, Ori APS, Roiz Santiañez R, Ruggeri B, Sarkisyan D, Shin J, Sungeun K, Tordesillas Gutiérrez D, Van't Ent D, Ames D, Artiges E, Bakalkin G, Banaschewski T, Bokde ALW, Brodaty H, Bromberg U, Brouwer R, Büchel C, Burke Quinlan E, Cahn W, de Zubicaray GI, Ehrlich S, Ekström TJ, Flor H, Fröhner JH, Frouin V, Garavan H, Gowland P, Heinz A, Hoare J, Ittermann B, Jahanshad N, Jiang J, Kwok JB, Martin NG, Martinot JL, Mather KA, McMahon KL, McRae AF, Nees F, Papadopoulos Orfanos D, Paus T, Poustka L, Sämann PG, Schofield PR, Smolka MN, Stein DJ, Strike LT, Teeuw J, Thalamuthu A, Trollor J, Walter H, Wardlaw JM, Wen W, Whelan R, Apostolova LG, Binder EB, Boomsma DI, Calhoun V, Crespo-Facorro B, Deary IJ, Hulshoff Pol H, Ophoff RA, Pausova Z, Sachdev PS, Saykin A, Wright MJ, Thompson PM, Schumann G, and Desrivières S

Subjects
CpG Islands, Epigenesis, Genetic genetics, Genome-Wide Association Study, Humans, DNA Methylation genetics, Epigenome
Abstract

DNA methylation, which is modulated by both genetic factors and environmental exposures, may offer a unique opportunity to discover novel biomarkers of disease-related brain phenotypes, even when measured in other tissues than brain, such as blood. A few studies of small sample sizes have revealed associations between blood DNA methylation and neuropsychopathology, however, large-scale epigenome-wide association studies (EWAS) are needed to investigate the utility of DNA methylation profiling as a peripheral marker for the brain. Here, in an analysis of eleven international cohorts, totalling 3337 individuals, we report epigenome-wide meta-analyses of blood DNA methylation with volumes of the hippocampus, thalamus and nucleus accumbens (NAcc)-three subcortical regions selected for their associations with disease and heritability and volumetric variability. Analyses of individual CpGs revealed genome-wide significant associations with hippocampal volume at two loci. No significant associations were found for analyses of thalamus and nucleus accumbens volumes. Cluster-based analyses revealed additional differentially methylated regions (DMRs) associated with hippocampal volume. DNA methylation at these loci affected expression of proximal genes involved in learning and memory, stem cell maintenance and differentiation, fatty acid metabolism and type-2 diabetes. These DNA methylation marks, their interaction with genetic variants and their impact on gene expression offer new insights into the relationship between epigenetic variation and brain structure and may provide the basis for biomarker discovery in neurodegeneration and neuropsychiatric conditions., (© 2019. The Author(s).)

Published
2021
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