Search

Your search keyword '"Celius, Elisabeth G."' showing total 346 results
Start Over Author "Celius, Elisabeth G."
346 results on '"Celius, Elisabeth G."'

5. Common brain disorders are associated with heritable patterns of apparent aging of the brain

Author

Kaufmann, Tobias, van der Meer, Dennis, Doan, Nhat Trung, Schwarz, Emanuel, Lund, Martina J, Agartz, Ingrid, Alnæs, Dag, Barch, Deanna M, Baur-Streubel, Ramona, Bertolino, Alessandro, Bettella, Francesco, Beyer, Mona K, Bøen, Erlend, Borgwardt, Stefan, Brandt, Christine L, Buitelaar, Jan, Celius, Elisabeth G, Cervenka, Simon, Conzelmann, Annette, Córdova-Palomera, Aldo, Dale, Anders M, de Quervain, Dominique JF, Di Carlo, Pasquale, Djurovic, Srdjan, Dørum, Erlend S, Eisenacher, Sarah, Elvsåshagen, Torbjørn, Espeseth, Thomas, Fatouros-Bergman, Helena, Flyckt, Lena, Franke, Barbara, Frei, Oleksandr, Haatveit, Beathe, Håberg, Asta K, Harbo, Hanne F, Hartman, Catharina A, Heslenfeld, Dirk, Hoekstra, Pieter J, Høgestøl, Einar A, Jernigan, Terry L, Jonassen, Rune, Jönsson, Erik G, Kirsch, Peter, Kłoszewska, Iwona, Kolskår, Knut K, Landrø, Nils Inge, Le Hellard, Stephanie, Lesch, Klaus-Peter, Lovestone, Simon, Lundervold, Arvid, Lundervold, Astri J, Maglanoc, Luigi A, Malt, Ulrik F, Mecocci, Patrizia, Melle, Ingrid, Meyer-Lindenberg, Andreas, Moberget, Torgeir, Norbom, Linn B, Nordvik, Jan Egil, Nyberg, Lars, Oosterlaan, Jaap, Papalino, Marco, Papassotiropoulos, Andreas, Pauli, Paul, Pergola, Giulio, Persson, Karin, Richard, Geneviève, Rokicki, Jaroslav, Sanders, Anne-Marthe, Selbæk, Geir, Shadrin, Alexey A, Smeland, Olav B, Soininen, Hilkka, Sowa, Piotr, Steen, Vidar M, Tsolaki, Magda, Ulrichsen, Kristine M, Vellas, Bruno, Wang, Lei, Westman, Eric, Ziegler, Georg C, Zink, Mathias, Andreassen, Ole A, and Westlye, Lars T

Subjects
Biological Psychology, Psychology, Rare Diseases, Mental Health, Neurosciences, Brain Disorders, Biomedical Imaging, Aging, Aetiology, 2.3 Psychological, social and economic factors, 1.1 Normal biological development and functioning, Underpinning research, Mental health, Neurological, Adolescent, Adult, Aged, Aged, 80 and over, Algorithms, Brain, Brain Diseases, Child, Child, Preschool, Female, Genome-Wide Association Study, Humans, Infant, Magnetic Resonance Imaging, Male, Mental Disorders, Middle Aged, Neuropsychological Tests, Schizophrenia, Sex Characteristics, Young Adult, Karolinska Schizophrenia Project, Cognitive Sciences, Neurology & Neurosurgery, Biological psychology
Abstract

Common risk factors for psychiatric and other brain disorders are likely to converge on biological pathways influencing the development and maintenance of brain structure and function across life. Using structural MRI data from 45,615 individuals aged 3-96 years, we demonstrate distinct patterns of apparent brain aging in several brain disorders and reveal genetic pleiotropy between apparent brain aging in healthy individuals and common brain disorders.

Published
2019

6. Multiple sclerosis genomic map implicates peripheral immune cells and microglia in susceptibility

Author

Patsopoulos, Nikolaos A, Baranzini, Sergio E, Santaniello, Adam, Shoostari, Parisa, Cotsapas, Chris, Wong, Garrett, Beecham, Ashley H, James, Tojo, Replogle, Joseph, Vlachos, Ioannis S, McCabe, Cristin, Pers, Tune H, Brandes, Aaron, White, Charles, Keenan, Brendan, Cimpean, Maria, Winn, Phoebe, Panteliadis, Ioannis-Pavlos, Robbins, Allison, Andlauer, Till FM, Zarzycki, Onigiusz, Dubois, Bénédicte, Goris, An, Søndergaard, Helle Bach, Sellebjerg, Finn, Sorensen, Per Soelberg, Ullum, Henrik, Thørner, Lise Wegner, Saarela, Janna, Cournu-Rebeix, Isabelle, Damotte, Vincent, Fontaine, Bertrand, Guillot-Noel, Lena, Lathrop, Mark, Vukusic, Sandra, Berthele, Achim, Pongratz, Viola, Buck, Dorothea, Gasperi, Christiane, Graetz, Christiane, Grummel, Verena, Hemmer, Bernhard, Hoshi, Muni, Knier, Benjamin, Korn, Thomas, Lill, Christina M, Luessi, Felix, Mühlau, Mark, Zipp, Frauke, Dardiotis, Efthimios, Agliardi, Cristina, Amoroso, Antonio, Barizzone, Nadia, Benedetti, Maria D, Bernardinelli, Luisa, Cavalla, Paola, Clarelli, Ferdinando, Comi, Giancarlo, Cusi, Daniele, Esposito, Federica, Ferrè, Laura, Galimberti, Daniela, Guaschino, Clara, Leone, Maurizio A, Martinelli, Vittorio, Moiola, Lucia, Salvetti, Marco, Sorosina, Melissa, Vecchio, Domizia, Zauli, Andrea, Santoro, Silvia, Mancini, Nicasio, Zuccalà, Miriam, Mescheriakova, Julia, van Duijn, Cornelia, Bos, Steffan D, Celius, Elisabeth G, Spurkland, Anne, Comabella, Manuel, Montalban, Xavier, Alfredsson, Lars, Bomfim, Izaura L, Gomez-Cabrero, David, Hillert, Jan, Jagodic, Maja, Lindén, Magdalena, Piehl, Fredrik, Jelčić, Ilijas, Martin, Roland, Sospedra, Mirela, Baker, Amie, Ban, Maria, Hawkins, Clive, Hysi, Pirro, Kalra, Seema, Karpe, Fredrik, Khadake, Jyoti, Lachance, Genevieve, Molyneux, Paul, and Neville, Matthew

Subjects
Neurosciences, Brain Disorders, Multiple Sclerosis, Human Genome, Autoimmune Disease, Clinical Research, Genetics, Neurodegenerative, Aetiology, 2.1 Biological and endogenous factors, Inflammatory and immune system, Neurological, Case-Control Studies, Cell Cycle Proteins, Chromosome Mapping, Chromosomes, Human, X, GTPase-Activating Proteins, Gene Frequency, Genetic Loci, Genome-Wide Association Study, Genomics, Humans, Inheritance Patterns, Major Histocompatibility Complex, Microglia, Polymorphism, Single Nucleotide, Quantitative Trait Loci, RNA-Seq, Transcriptome, International Multiple Sclerosis Genetics Consortium, General Science & Technology
Abstract

We analyzed genetic data of 47,429 multiple sclerosis (MS) and 68,374 control subjects and established a reference map of the genetic architecture of MS that includes 200 autosomal susceptibility variants outside the major histocompatibility complex (MHC), one chromosome X variant, and 32 variants within the extended MHC. We used an ensemble of methods to prioritize 551 putative susceptibility genes that implicate multiple innate and adaptive pathways distributed across the cellular components of the immune system. Using expression profiles from purified human microglia, we observed enrichment for MS genes in these brain-resident immune cells, suggesting that these may have a role in targeting an autoimmune process to the central nervous system, although MS is most likely initially triggered by perturbation of peripheral immune responses.

Published
2019

7. Restriction spectrum imaging of white matter and its relation to neurological disability in multiple sclerosis

Author

Sowa, Piotr, Harbo, Hanne F, White, Nathan S, Celius, Elisabeth G, Bartsch, Hauke, Berg-Hansen, Pål, Moen, Stine M, Bjørnerud, Atle, Westlye, Lars T, Andreassen, Ole A, Dale, Anders M, and Beyer, Mona K

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Clinical Research, Autoimmune Disease, Neurodegenerative, Multiple Sclerosis, Brain Disorders, Neurosciences, Clinical Trials and Supportive Activities, Neurological, Adult, Anisotropy, Brain, Diffusion Magnetic Resonance Imaging, Disability Evaluation, Female, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Nervous System Diseases, White Matter, Magnetic resonance imaging, multiple sclerosis, restriction spectrum imaging, neurite density, neurological disability, Neurology & Neurosurgery, Clinical sciences, Biological psychology
Abstract

BACKGROUND:Restriction spectrum imaging (RSI) is a recently introduced magnetic resonance imaging diffusion technique. The utility of RSI in multiple sclerosis (MS) is unknown. OBJECTIVE:To investigate the association between RSI-derived parameters and neurological disability in MS. METHODS:Seventy-seven relapsing-remitting MS patients were scanned with RSI on a 3-T scanner. RSI-derived parameters: fast and slow apparent diffusion coefficient (sADC), fractional anisotropy, restricted fractional anisotropy, neurite density (ND), cellularity, extracellular water fraction, and free water fraction, were obtained in white matter lesions (WML) and normal appearing white matter (NAWM). Patients were divided into three groups according to their expanded disability status scale (EDSS): with minimal, low, and substantial disability (3, respectively). Group comparisons and correlation analyses were performed. RESULTS:All tested RSI-derived parameters differed between WML and NAWM ( p

Published
2019

8. Author Correction: A systems biology approach uncovers cell-specific gene regulatory effects of genetic associations in multiple sclerosis

Author

Madireddy, Lohith, Patsopoulos, Nikolaos A, Cotsapas, Chris, Bos, Steffan D, Beecham, Ashley, McCauley, Jacob, Kim, Kicheol, Jia, Xiaoming, Santaniello, Adam, Caillier, Stacy J, Andlauer, Till FM, Barcellos, Lisa F, Berge, Tone, Bernardinelli, Luisa, Martinelli-Boneschi, Filippo, Booth, David R, Briggs, Farren, Celius, Elisabeth G, Comabella, Manuel, Comi, Giancarlo, Cree, Bruce AC, D'Alfonso, Sandra, Dedham, Katrina, Duquette, Pierre, Dardiotis, Efthimios, Esposito, Federica, Fontaine, Bertrand, Gasperi, Christiane, Goris, An, Dubois, Benedicte, Gourraud, Pierre-Antoine, Hadjigeorgiou, Georgios, Haines, Jonathan, Hawkins, Clive, Hemmer, Bernhard, Hintzen, Rogier, Horakova, Dana, Isobe, Noriko, Kalra, Seema, Kira, Jun-ichi, Khalil, Michael, Kockum, Ingrid, Lill, Christina M, Lincoln, Matthew R, Luessi, Felix, Martin, Roland, Oturai, Annette, Palotie, Aarno, Pericak-Vance, Margaret A, Henry, Roland, Saarela, Janna, Ivinson, Adrian, Olsson, Tomas, Taylor, Bruce V, Stewart, Graeme J, Harbo, Hanne F, Compston, Alastair, Hauser, Stephen L, Hafler, David A, Zipp, Frauke, De Jager, Philip, Sawcer, Stephen, Oksenberg, Jorge R, and Baranzini, Sergio E

Subjects
International Multiple Sclerosis Genetics Consortium
Abstract

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Published
2019

9. A systems biology approach uncovers cell-specific gene regulatory effects of genetic associations in multiple sclerosis

Author

Madireddy, Lohith, Patsopoulos, Niklaos A, Cotsapas, Chris, Bos, Steffan D, Beecham, Ashley, McCauley, Jacob, Kim, Kicheol, Jia, Xiaoming, Santaniello, Adam, Caillier, Stacy J, Andlauer, Till FM, Barcellos, Lisa F, Berge, Tone, Bernardinelli, Luisa, Martinelli-Boneschi, Filippo, Booth, David R, Briggs, Farren, Celius, Elisabeth G, Comabella, Manuel, Comi, Giancarlo, Cree, Bruce AC, D'Alfonso, Sandra, Dedham, Katrina, Duquette, Pierre, Efthimios, Dardiotis, Esposito, Federica, Fontaine, Bertrand, Gasperi, Christiane, Goris, An, Dubois, Benedicte, Gourraud, Pierre-Antoine, Hadjigeorgiou, Georgios, Haines, Jonathan, Hawkins, Clive, Hemmer, Bernhard, Hintzen, Rogier, Horakova, Dana, Isobe, Noriko, Kalra, Seema, Kira, Jun-ichi, Khalil, Michael, Kockum, Ingrid, Lill, Christina M, Lincoln, Matthew R, Luessi, Felix, Martin, Roland, Oturai, Annette, Palotie, Aarno, Pericak-Vance, Margaret A, Henry, Roland, Saarela, Janna, Ivinson, Adrian, Olsson, Tomas, Taylor, Bruce V, Stewart, Graeme J, Harbo, Hanne F, Compston, Alastair, Hauser, Stephen L, Hafler, David A, Zipp, Frauke, De Jager, Philip, Sawcer, Stephen, Oksenberg, Jorge R, and Baranzini, Sergio E

Subjects
Human Genome, Autoimmune Disease, Multiple Sclerosis, Genetics, Biotechnology, Brain Disorders, Neurodegenerative, Clinical Research, Neurosciences, 2.1 Biological and endogenous factors, Aetiology, Inflammatory and immune system, Gene Expression Regulation, Genes, Regulator, Genetic Predisposition to Disease, Genome-Wide Association Study, Genotype, Humans, Polymorphism, Single Nucleotide, Systems Biology, International Multiple Sclerosis Genetics Consortium
Abstract

Genome-wide association studies (GWAS) have identified more than 50,000 unique associations with common human traits. While this represents a substantial step forward, establishing the biology underlying these associations has proven extremely difficult. Even determining which cell types and which particular gene(s) are relevant continues to be a challenge. Here, we conduct a cell-specific pathway analysis of the latest GWAS in multiple sclerosis (MS), which had analyzed a total of 47,351 cases and 68,284 healthy controls and found more than 200 non-MHC genome-wide associations. Our analysis identifies pan immune cell as well as cell-specific susceptibility genes in T cells, B cells and monocytes. Finally, genotype-level data from 2,370 patients and 412 controls is used to compute intra-individual and cell-specific susceptibility pathways that offer a biological interpretation of the individual genetic risk to MS. This approach could be adopted in any other complex trait for which genome-wide data is available.

Published
2019

12. Pregnancy outcomes and postpartum relapse rates in women with RRMS treated with alemtuzumab in the phase 2 and 3 clinical development program over 16 years

Author

Oh, Jiwon, Achiron, Anat, Celius, Elisabeth G., Chambers, Christina, Derwenskus, Joy, Devonshire, Virginia, Hellwig, Kerstin, Hutton, George J., McCombe, Pamela, Moore, Marie, Rog, David, Schneider, Jean-Raphael, Simm, Renata Faria, Sousa, Livia, Vincent, Stephen G., Chung, Luke, Daizadeh, Nadia, Mitchell, Colin, and Compston, D. Alastair S.

Published
2020
Full Text
View/download PDF

13. Peripapillary retinal layer thickness is associated with retinal oxygen saturation in newly diagnosed patients with multiple sclerosis

Author

Nes, Dragana, primary, Berg‐Hansen, Pål, additional, de Rodez Benavent, Sigrid A., additional, Høgestøl, Einar A., additional, Beyer, Mona K., additional, Rinker, Daniel A., additional, Veiby, Nina, additional, Karabeg, Mia, additional, Petrovski, Beáta Éva, additional, Celius, Elisabeth G., additional, Harbo, Hanne F., additional, and Petrovski, Goran, additional

Published
2024
Full Text
View/download PDF

14. Multiple sclerosis risk loci and disease severity in 7,125 individuals from 10 studies.

Author

George, Michaela F, Briggs, Farren BS, Shao, Xiaorong, Gianfrancesco, Milena A, Kockum, Ingrid, Harbo, Hanne F, Celius, Elisabeth G, Bos, Steffan D, Hedström, Anna, Shen, Ling, Bernstein, Allan, Alfredsson, Lars, Hillert, Jan, Olsson, Tomas, Patsopoulos, Nikolaos A, De Jager, Philip L, Oturai, Annette B, Søndergaard, Helle B, Sellebjerg, Finn, Sorensen, Per S, Gomez, Refujia, Caillier, Stacy J, Cree, Bruce AC, Oksenberg, Jorge R, Hauser, Stephen L, D'Alfonso, Sandra, Leone, Maurizio A, Martinelli Boneschi, Filippo, Sorosina, Melissa, van der Mei, Ingrid, Taylor, Bruce V, Zhou, Yuan, Schaefer, Catherine, and Barcellos, Lisa F

Subjects
Genetics, Neurosciences
Abstract

ObjectiveWe investigated the association between 52 risk variants identified through genome-wide association studies and disease severity in multiple sclerosis (MS).MethodsTen unique MS case data sets were analyzed. The Multiple Sclerosis Severity Score (MSSS) was calculated using the Expanded Disability Status Scale at study entry and disease duration. MSSS was considered as a continuous variable and as 2 dichotomous variables (median and extreme ends; MSSS of ≤5 vs >5 and MSSS of

Published
2016

15. Quality of Life Improves with Alemtuzumab Over 6 Years in Relapsing-Remitting Multiple Sclerosis Patients with or without Autoimmune Thyroid Adverse Events: Post Hoc Analysis of the CARE-MS Studies

Author

Bertolotto, Antonio, Arroyo, Rafael, Celius, Elisabeth G., Comi, Giancarlo, Havrdova, Eva Kubala, Honeycutt, William David, Hunter, Samuel F., Izquierdo, Guillermo, Kornek, Barbara, Miller, Tamara, Mitsikostas, Dimos D., Singer, Barry A., Ziemssen, Tjalf, Chung, Luke, Daizadeh, Nadia, Afsar, Salman, Hashemi, Lobat, and Senior, Peter

Published
2020
Full Text
View/download PDF

16. Low-Frequency and Rare-Coding Variation Contributes to Multiple Sclerosis Risk

Author

Mitrovič, Mitja, Patsopoulos, Nikolaos A., Beecham, Ashley H., Dankowski, Theresa, Goris, An, Dubois, Bénédicte, D’hooghe, Marie B., Lemmens, Robin, Van Damme, Philip, Søndergaard, Helle Bach, Sellebjerg, Finn, Sorensen, Per Soelberg, Ullum, Henrik, Thørner, Lise W., Werge, Thomas, Saarela, Janna, Cournu-Rebeix, Isabelle, Damotte, Vincent, Fontaine, Bertrand, Guillot-Noel, Lena, Lathrop, Mark, Vukusik, Sandra, Gourraud, Pierre-Antoine, Andlauer, Till F.M., Pongratz, Viola, Buck, Dorothea, Gasperi, Christiane, Bayas, Antonios, Heesen, Christoph, Kümpfel, Tania, Linker, Ralf, Paul, Friedemann, Stangel, Martin, Tackenberg, Björn, Bergh, Florian Then, Warnke, Clemens, Wiendl, Heinz, Wildemann, Brigitte, Zettl, Uwe, Ziemann, Ulf, Tumani, Hayrettin, Gold, Ralf, Grummel, Verena, Hemmer, Bernhard, Knier, Benjamin, Lill, Christina M., Luessi, Felix, Dardiotis, Efthimios, Agliardi, Cristina, Barizzone, Nadia, Mascia, Elisabetta, Bernardinelli, Luisa, Comi, Giancarlo, Cusi, Daniele, Esposito, Federica, Ferrè, Laura, Comi, Cristoforo, Galimberti, Daniela, Leone, Maurizio A., Sorosina, Melissa, Mescheriakova, Julia, Hintzen, Rogier, van Duijn, Cornelia, Teunissen, Charlotte E., Bos, Steffan D., Myhr, Kjell-Morten, Celius, Elisabeth G., Lie, Benedicte A., Spurkland, Anne, Comabella, Manuel, Montalban, Xavier, Alfredsson, Lars, Stridh, Pernilla, Hillert, Jan, Jagodic, Maja, Piehl, Fredrik, Jelčić, Ilijas, Martin, Roland, Sospedra, Mireia, Ban, Maria, Hawkins, Clive, Hysi, Pirro, Kalra, Seema, Karpe, Fredrik, Khadake, Jyoti, Lachance, Genevieve, Neville, Matthew, Santaniello, Adam, Caillier, Stacy J., Calabresi, Peter A., Cree, Bruce A.C., Cross, Anne, Davis, Mary F., Haines, Jonathan L., de Bakker, Paul I.W., Delgado, Silvia, Dembele, Marieme, Edwards, Keith, Fitzgerald, Kathryn C., Hakonarson, Hakon, Konidari, Ioanna, Lathi, Ellen, Manrique, Clara P., Pericak-Vance, Margaret A., Piccio, Laura, Schaefer, Cathy, McCabe, Cristin, Weiner, Howard, Goldstein, Jacqueline, Olsson, Tomas, Hadjigeorgiou, Georgios, Taylor, Bruce, Tajouri, Lotti, Charlesworth, Jac, Booth, David R., Harbo, Hanne F., Ivinson, Adrian J., Hauser, Stephen L., Compston, Alastair, Stewart, Graeme, Zipp, Frauke, Barcellos, Lisa F., Baranzini, Sergio E., Martinelli-Boneschi, Filippo, D’Alfonso, Sandra, Ziegler, Andreas, Oturai, Annette, McCauley, Jacob L., Sawcer, Stephen J., Oksenberg, Jorge R., De Jager, Philip L., Kockum, Ingrid, Hafler, David A., and Cotsapas, Chris

Published
2018
Full Text
View/download PDF

17. Analysis of immune-related loci identifies 48 new susceptibility variants for multiple sclerosis.

Author

International Multiple Sclerosis Genetics Consortium (IMSGC), Beecham, Ashley H, Patsopoulos, Nikolaos A, Xifara, Dionysia K, Davis, Mary F, Kemppinen, Anu, Cotsapas, Chris, Shah, Tejas S, Spencer, Chris, Booth, David, Goris, An, Oturai, Annette, Saarela, Janna, Fontaine, Bertrand, Hemmer, Bernhard, Martin, Claes, Zipp, Frauke, D'Alfonso, Sandra, Martinelli-Boneschi, Filippo, Taylor, Bruce, Harbo, Hanne F, Kockum, Ingrid, Hillert, Jan, Olsson, Tomas, Ban, Maria, Oksenberg, Jorge R, Hintzen, Rogier, Barcellos, Lisa F, Wellcome Trust Case Control Consortium 2 (WTCCC2), International IBD Genetics Consortium (IIBDGC), Agliardi, Cristina, Alfredsson, Lars, Alizadeh, Mehdi, Anderson, Carl, Andrews, Robert, Søndergaard, Helle Bach, Baker, Amie, Band, Gavin, Baranzini, Sergio E, Barizzone, Nadia, Barrett, Jeffrey, Bellenguez, Céline, Bergamaschi, Laura, Bernardinelli, Luisa, Berthele, Achim, Biberacher, Viola, Binder, Thomas MC, Blackburn, Hannah, Bomfim, Izaura L, Brambilla, Paola, Broadley, Simon, Brochet, Bruno, Brundin, Lou, Buck, Dorothea, Butzkueven, Helmut, Caillier, Stacy J, Camu, William, Carpentier, Wassila, Cavalla, Paola, Celius, Elisabeth G, Coman, Irène, Comi, Giancarlo, Corrado, Lucia, Cosemans, Leentje, Cournu-Rebeix, Isabelle, Cree, Bruce AC, Cusi, Daniele, Damotte, Vincent, Defer, Gilles, Delgado, Silvia R, Deloukas, Panos, di Sapio, Alessia, Dilthey, Alexander T, Donnelly, Peter, Dubois, Bénédicte, Duddy, Martin, Edkins, Sarah, Elovaara, Irina, Esposito, Federica, Evangelou, Nikos, Fiddes, Barnaby, Field, Judith, Franke, Andre, Freeman, Colin, Frohlich, Irene Y, Galimberti, Daniela, Gieger, Christian, Gourraud, Pierre-Antoine, Graetz, Christiane, Graham, Andrew, Grummel, Verena, Guaschino, Clara, Hadjixenofontos, Athena, Hakonarson, Hakon, Halfpenny, Christopher, Hall, Gillian, Hall, Per, Hamsten, Anders, Harley, James, and Harrower, Timothy

Subjects
International Multiple Sclerosis Genetics Consortium, Wellcome Trust Case Control Consortium 2, International IBD Genetics Consortium, Humans, Multiple Sclerosis, Genetic Predisposition to Disease, Chromosome Mapping, Gene Frequency, Genotype, Polymorphism, Single Nucleotide, Genetic Variation, Genome-Wide Association Study, Genetic Loci, White People, Neurosciences, Prevention, Autoimmune Disease, Genetics, Brain Disorders, Human Genome, Neurodegenerative, Aetiology, 2.1 Biological and endogenous factors, Inflammatory and immune system, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

Using the ImmunoChip custom genotyping array, we analyzed 14,498 subjects with multiple sclerosis and 24,091 healthy controls for 161,311 autosomal variants and identified 135 potentially associated regions (P < 1.0 × 10(-4)). In a replication phase, we combined these data with previous genome-wide association study (GWAS) data from an independent 14,802 subjects with multiple sclerosis and 26,703 healthy controls. In these 80,094 individuals of European ancestry, we identified 48 new susceptibility variants (P < 5.0 × 10(-8)), 3 of which we found after conditioning on previously identified variants. Thus, there are now 110 established multiple sclerosis risk variants at 103 discrete loci outside of the major histocompatibility complex. With high-resolution Bayesian fine mapping, we identified five regions where one variant accounted for more than 50% of the posterior probability of association. This study enhances the catalog of multiple sclerosis risk variants and illustrates the value of fine mapping in the resolution of GWAS signals.

Published
2013

18. No evidence of association between mutant alleles of the CYP27B1 gene and multiple sclerosis.

Author

Ban, Maria, Caillier, Stacy, Mero, Inger-Lise, Myhr, Kjell-Morten, Celius, Elisabeth G, Aarseth, Jan, Torkildsen, Øivind, Harbo, Hanne F, Oksenberg, Jorge, Hauser, Stephen L, Sawcer, Stephen, and Compston, Alastair

Subjects
Humans, Multiple Sclerosis, 25-Hydroxyvitamin D3 1-alpha-Hydroxylase, Gene Frequency, Mutation, Norway, Female, Male, Genetic Association Studies, United Kingdom, Neurology & Neurosurgery, Clinical Sciences, Neurosciences
Abstract

An association has previously been reported between susceptibility to multiple sclerosis and the rare mutant alleles of the CYP27B1 gene responsible for autosomal recessive vitamin D-dependent rickets type 1 (VDDR1). In an attempt to replicate this finding, we screened 495 multiplex families and 2,092 single affected families, together with 4,594 cases and 3,583 controls (a total of 17,073 individuals) but were unable to find any evidence supporting this putative association. Our data do not indicate that mutations responsible for VDDR1 influence the risk of developing multiple sclerosis.

Published
2013

19. Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis.

Author

International Multiple Sclerosis Genetics Consortium, Wellcome Trust Case Control Consortium 2, Sawcer, Stephen, Hellenthal, Garrett, Pirinen, Matti, Spencer, Chris CA, Patsopoulos, Nikolaos A, Moutsianas, Loukas, Dilthey, Alexander, Su, Zhan, Freeman, Colin, Hunt, Sarah E, Edkins, Sarah, Gray, Emma, Booth, David R, Potter, Simon C, Goris, An, Band, Gavin, Oturai, Annette Bang, Strange, Amy, Saarela, Janna, Bellenguez, Céline, Fontaine, Bertrand, Gillman, Matthew, Hemmer, Bernhard, Gwilliam, Rhian, Zipp, Frauke, Jayakumar, Alagurevathi, Martin, Roland, Leslie, Stephen, Hawkins, Stanley, Giannoulatou, Eleni, D'alfonso, Sandra, Blackburn, Hannah, Martinelli Boneschi, Filippo, Liddle, Jennifer, Harbo, Hanne F, Perez, Marc L, Spurkland, Anne, Waller, Matthew J, Mycko, Marcin P, Ricketts, Michelle, Comabella, Manuel, Hammond, Naomi, Kockum, Ingrid, McCann, Owen T, Ban, Maria, Whittaker, Pamela, Kemppinen, Anu, Weston, Paul, Hawkins, Clive, Widaa, Sara, Zajicek, John, Dronov, Serge, Robertson, Neil, Bumpstead, Suzannah J, Barcellos, Lisa F, Ravindrarajah, Rathi, Abraham, Roby, Alfredsson, Lars, Ardlie, Kristin, Aubin, Cristin, Baker, Amie, Baker, Katharine, Baranzini, Sergio E, Bergamaschi, Laura, Bergamaschi, Roberto, Bernstein, Allan, Berthele, Achim, Boggild, Mike, Bradfield, Jonathan P, Brassat, David, Broadley, Simon A, Buck, Dorothea, Butzkueven, Helmut, Capra, Ruggero, Carroll, William M, Cavalla, Paola, Celius, Elisabeth G, Cepok, Sabine, Chiavacci, Rosetta, Clerget-Darpoux, Françoise, Clysters, Katleen, Comi, Giancarlo, Cossburn, Mark, Cournu-Rebeix, Isabelle, Cox, Mathew B, Cozen, Wendy, Cree, Bruce AC, Cross, Anne H, Cusi, Daniele, Daly, Mark J, Davis, Emma, de Bakker, Paul IW, Debouverie, Marc, D'hooghe, Marie Beatrice, Dixon, Katherine, Dobosi, Rita, Dubois, Bénédicte, and Ellinghaus, David

Subjects
International Multiple Sclerosis Genetics Consortium, Wellcome Trust Case Control Consortium 2, T-Lymphocytes, Helper-Inducer, Humans, Multiple Sclerosis, Genetic Predisposition to Disease, HLA-A Antigens, HLA-DR Antigens, Sample Size, Cell Differentiation, Immunity, Cellular, Major Histocompatibility Complex, Polymorphism, Single Nucleotide, Alleles, Genome, Human, Europe, Genome-Wide Association Study, HLA-DRB1 Chains, Genetics, Neurosciences, Neurodegenerative, Clinical Research, Brain Disorders, Autoimmune Disease, Human Genome, 2.1 Biological and endogenous factors, Neurological, Inflammatory and immune system, General Science & Technology
Abstract

Multiple sclerosis is a common disease of the central nervous system in which the interplay between inflammatory and neurodegenerative processes typically results in intermittent neurological disturbance followed by progressive accumulation of disability. Epidemiological studies have shown that genetic factors are primarily responsible for the substantially increased frequency of the disease seen in the relatives of affected individuals, and systematic attempts to identify linkage in multiplex families have confirmed that variation within the major histocompatibility complex (MHC) exerts the greatest individual effect on risk. Modestly powered genome-wide association studies (GWAS) have enabled more than 20 additional risk loci to be identified and have shown that multiple variants exerting modest individual effects have a key role in disease susceptibility. Most of the genetic architecture underlying susceptibility to the disease remains to be defined and is anticipated to require the analysis of sample sizes that are beyond the numbers currently available to individual research groups. In a collaborative GWAS involving 9,772 cases of European descent collected by 23 research groups working in 15 different countries, we have replicated almost all of the previously suggested associations and identified at least a further 29 novel susceptibility loci. Within the MHC we have refined the identity of the HLA-DRB1 risk alleles and confirmed that variation in the HLA-A gene underlies the independent protective effect attributable to the class I region. Immunologically relevant genes are significantly overrepresented among those mapping close to the identified loci and particularly implicate T-helper-cell differentiation in the pathogenesis of multiple sclerosis.

Published
2011

20. Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis

Author

Sawcer, Stephen, Hellenthal, Garrett, Pirinen, Matti, Spencer, Chris CA, Patsopoulos, Nikolaos A, Moutsianas, Loukas, Dilthey, Alexander, Su, Zhan, Freeman, Colin, Hunt, Sarah E, Edkins, Sarah, Gray, Emma, Booth, David R, Potter, Simon C, Goris, An, Band, Gavin, Oturai, Annette Bang, Strange, Amy, Saarela, Janna, Bellenguez, Celine, Fontaine, Bertrand, Gillman, Matthew, Hemmer, Bernhard, Gwilliam, Rhian, Zipp, Frauke, Jayakumar, Alagurevathi, Martin, Roland, Leslie, Stephen, Hawkins, Stanley, Giannoulatou, Eleni, D'alfonso, Sandra, Blackburn, Hannah, Boneschi, Filippo Martinelli, Liddle, Jennifer, Harbo, Hanne F, Perez, Marc L, Spurkland, Anne, Waller, Matthew J, Mycko, Marcin P, Ricketts, Michelle, Comabella, Manuel, Hammond, Naomi, Kockum, Ingrid, McCann, Owen T, Ban, Maria, Whittaker, Pamela, Kemppinen, Anu, Weston, Paul, Hawkins, Clive, Widaa, Sara, Zajicek, John, Dronov, Serge, Robertson, Neil, Bumpstead, Suzannah J, Barcellos, Lisa F, Ravindrarajah, Rathi, Abraham, Roby, Alfredsson, Lars, Ardlie, Kristin, Aubin, Cristin, Baker, Amie, Baker, Katharine, Baranzini, Sergio E, Bergamaschi, Laura, Bergamaschi, Roberto, Bernstein, Allan, Berthele, Achim, Boggild, Mike, Bradfield, Jonathan P, Brassat, David, Broadley, Simon A, Buck, Dorothea, Butzkueven, Helmut, Capra, Ruggero, Carroll, William M, Cavalla, Paola, Celius, Elisabeth G, Cepok, Sabine, Chiavacci, Rosetta, Clerget-Darpoux, Francoise, Clysters, Katleen, Comi, Giancarlo, Cossburn, Mark, Cournu-Rebeix, Isabelle, Cox, Mathew B, Cozen, Wendy, Cree, Bruce AC, Cross, Anne H, Cusi, Daniele, Daly, Mark J, Davis, Emma, de Bakker, Paul IW, Debouverie, Marc, D'hooghe, Marie Beatrice, Dixon, Katherine, Dobosi, Rita, Dubois, Benedicte, Ellinghaus, David, Elovaara, Irina, and Esposito, Federica

Subjects
Neurosciences, Prevention, Multiple Sclerosis, Biotechnology, Autoimmune Disease, Genetics, Brain Disorders, Human Genome, Neurodegenerative, 2.1 Biological and endogenous factors, Aetiology, Neurological, Inflammatory and immune system, Alleles, Cell Differentiation, Europe, Genetic Predisposition to Disease, Genome, Human, Genome-Wide Association Study, HLA-A Antigens, HLA-DR Antigens, HLA-DRB1 Chains, Humans, Immunity, Cellular, Major Histocompatibility Complex, Polymorphism, Single Nucleotide, Sample Size, T-Lymphocytes, Helper-Inducer, International Multiple Sclerosis Genetics Consortium, Wellcome Trust Case Control Consortium 2, General Science & Technology
Abstract

Multiple sclerosis is a common disease of the central nervous system in which the interplay between inflammatory and neurodegenerative processes typically results in intermittent neurological disturbance followed by progressive accumulation of disability. Epidemiological studies have shown that genetic factors are primarily responsible for the substantially increased frequency of the disease seen in the relatives of affected individuals, and systematic attempts to identify linkage in multiplex families have confirmed that variation within the major histocompatibility complex (MHC) exerts the greatest individual effect on risk. Modestly powered genome-wide association studies (GWAS) have enabled more than 20 additional risk loci to be identified and have shown that multiple variants exerting modest individual effects have a key role in disease susceptibility. Most of the genetic architecture underlying susceptibility to the disease remains to be defined and is anticipated to require the analysis of sample sizes that are beyond the numbers currently available to individual research groups. In a collaborative GWAS involving 9,772 cases of European descent collected by 23 research groups working in 15 different countries, we have replicated almost all of the previously suggested associations and identified at least a further 29 novel susceptibility loci. Within the MHC we have refined the identity of the HLA-DRB1 risk alleles and confirmed that variation in the HLA-A gene underlies the independent protective effect attributable to the class I region. Immunologically relevant genes are significantly overrepresented among those mapping close to the identified loci and particularly implicate T-helper-cell differentiation in the pathogenesis of multiple sclerosis.

Published
2011

21. T cell responses to SARS-CoV-2 vaccination differ by disease-modifying therapy for multiple sclerosis

Author

Wolf, Asia-Sophia, primary, Ravussin, Anthony, additional, König, Marton, additional, Øverås, Mathias H., additional, Solum, Guri, additional, Kjønstad, Ingrid Fadum, additional, Chopra, Adity, additional, Holmøy, Trygve, additional, Harbo, Hanne F., additional, Syversen, Silje Watterdal, additional, Jørgensen, Kristin Kaasen, additional, Høgestøl, Einar August, additional, Vaage, Jon Torgils, additional, Celius, Elisabeth G., additional, Lund-Johansen, Fridtjof, additional, Munthe, Ludvig A., additional, Nygaard, Gro Owren, additional, and Mjaaland, Siri, additional

Published
2023
Full Text
View/download PDF

22. Expert opinion on the long-term use of cladribine tablets for multiple sclerosis:Systematic literature review of real-world evidence

Author

Oreja-Guevara, Celia, Brownlee, Wallace, Celius, Elisabeth G., Centonze, Diego, Giovannoni, Gavin, Hodgkinson, Suzanne, Kleinschnitz, Christoph, Havrdova, Eva Kubala, Magyari, Melinda, Selchen, Daniel, Vermersch, Patrick, Wiendl, Heinz, Van Wijmeersch, Bart, Salloukh, Hashem, Yamout, Bassem, Oreja-Guevara, Celia, Brownlee, Wallace, Celius, Elisabeth G., Centonze, Diego, Giovannoni, Gavin, Hodgkinson, Suzanne, Kleinschnitz, Christoph, Havrdova, Eva Kubala, Magyari, Melinda, Selchen, Daniel, Vermersch, Patrick, Wiendl, Heinz, Van Wijmeersch, Bart, Salloukh, Hashem, and Yamout, Bassem

Abstract

Background: Treatment with cladribine tablets (CladT), an immune reconstitution therapy for relapsing multiple sclerosis (RMS), involves two short courses of treatment in Year 1 and Year 2. Most patients achieve sustained efficacy with CladT, but a small proportion may experience new disease activity (DA). Following completion of the indicated dose, physicians may have questions relating to the long-term management of these patients. Since the EU approval of CladT over 5 years ago, real-world evidence (RWE) is increasing and may provide some insights and guidance for clinical practice. We describe a systematic literature review (SLR) of RWE and provide expert opinions relating to six questions regarding the long-term use of CladT. Methods: Pertinent clinical questions were developed by a steering committee (SC) of 14 international multiple sclerosis (MS) experts regarding breakthrough DA in Year 1, new DA after 2 years or more of treatment, long-term management of stable patients, and whether additional courses of CladT may be required or safe. An SLR was performed in EMBASE and PubMed using the population, intervention, comparators, outcomes, study design (PICOS) framework to identify relevant studies within the last 15 years. Searches of key congress proceedings for the last 2–3 years were also performed. Following review of the results and RWE, the SC drafted and agreed on expert opinion statements for each question. Results: A total of 35 publications reporting RWE for CladT were included in this review. In the real world, breakthrough DA in Year 1 is of low incidence (1.1–21.9%) but can occur, particularly in patients switching from anti-lymphocyte trafficking agents. In most patients, this DA did not lead to treatment discontinuation. Reported rates of DA after the full therapeutic effect of CladT has been achieved (end of Year 2, 3 or 4) range from 12.0 to 18.7% in the few studies identified. No RWE was identified to support management decisions for stable

Published
2023

23. NR1H3 p.Arg415Gln Is Not Associated to Multiple Sclerosis Risk

Author

Antel, Jack, Ban, Maria, Baranzini, Sergio, Barcellos, Lisa, Barizzone, Nadia, Beecham, Ashley, Berge, Tone, Bernardinelli, Luisa, Booth, David, Bos, Steffan, Buck, Dorothea, Butkiewicz, Mariusz, Celius, Elisabeth G., Comabella, Manuel, Compston, Alastair, Dedham, Katrina, Cotsapas, Chris, D’ Alfonso, Sandra, De Jager, Phil, Dubois, Benedicte, Duquette, Pierre, Fontaine, Bertrand, Gasperi, Christiane, Gil, Elia, Goris, An, Gourraud, Pierre Antoine, Graetz, Christiane, Gyllenberg, Alexandra, Hadjigeorgiou, Georgios, Hafler, David, Hribko, Deanna, Haines, Jonathan, Harbo, Hanne, Hauser, Stephen, Warto, Shannon, Hawkins, Clive, Hemmer, Bernhard, Henry, Roland, Hintzen, Rogier, Horakova, Dana, Ivinson, Adrian, Howard, Melissa, Jelcic, Ilijas, Kaskow, Belinda, Kira, Jun-Ichi, Kleinova, Pavlina, Kockum, Ingrid, Kucerova, Karolina, Lill, Christina, Luessi, Felix, Malhotra, Sunny, Martin, Roland, Martinelli, Filippo, Matsushita, Takuya, McCabe, Cristin, McCauley, Jacob, Mescheriakkova, Julia, Mitrovic, Mitja, Moen, Stine-Marit, Montalban, Xavier, Muhlau, Mark, Nakmura, Yuri, Oksenberg, Jorge, Olsson, Tomas, Oturai, Annette, Palotie, Aarno, Patsopoulos, Nikolaos, Pavlicova, Jana, Pericak-Vance, Peggy, Piehl, Fredrik, Rebeix, Isabelle, Rioux, John, Saarela, Janna, Sawcer, Stephen, Sellebjerg, Finn, Sondergaard, Helle Bach, Sorensen, Per Soelberg, Sospedra, Mireia, Spurkland, Anne, Stewart, Graeme, Taylor, Bruce, Uitterlinden, Andre, Van Duijn, Cornelia, and Zipp, Frauke

Published
2016
Full Text
View/download PDF

24. Expert Opinion on Long-Term Use of Cladribine Tablets for Multiple Sclerosis: Systematic Literature Review of Real-World Evidence

Author

Oreja-Guevara, Celia, primary, Brownlee, Wallace, additional, Celius, Elisabeth G., additional, Centonze, Diego, additional, Giovannoni, Gavin, additional, Hodgkinson, Suzanne, additional, Kleinschnitz, Christoph, additional, Havrdova, Eva Kubala, additional, Magyari, Melinda, additional, Selchen, Daniel, additional, Vermersch, Patrick, additional, Wiendl, Heinz, additional, Van Wijmeersch, Bart, additional, Salloukh, Hashem, additional, and Yamout, Bassem, additional

Published
2023
Full Text
View/download PDF

26. Oligoclonal band phenotypes in MS differ in their HLA class II association, while specific KIR ligands at HLA class I show association to MS in general

Author

Gustavsen, Marte W., Viken, Marte K., Celius, Elisabeth G., Berge, Tone, Mero, Inger-Lise, Berg-Hansen, Pål, Aarseth, Jan H., Myhr, Kjell-Morten, Søndergaard, Helle B., Sellebjerg, Finn, Oturai, Annette B., Hillert, Jan, Alfredsson, Lars, Olsson, Tomas, Kockum, Ingrid, Lie, Benedicte A., and Harbo, Hanne F.

Published
2014
Full Text
View/download PDF

27. T cell responses to SARS-CoV-2 vaccination in people with multiple sclerosis differ between disease-modifying therapies

Author

Wolf, Asia-Sophia, primary, Ravussin, Anthony, additional, König, Marton, additional, Øverås, Mathias H., additional, Solum, Guri, additional, Kjønstad, Ingrid Fadum, additional, Chopra, Adity, additional, Holmøy, Trygve, additional, Harbo, Hanne F., additional, Syversen, Silje Watterdal, additional, Jørgensen, Kristin Kaasen, additional, Høgestøl, Einar August, additional, Vaage, Jon Torgils, additional, Celius, Elisabeth G., additional, Lund-Johansen, Fridtjof, additional, Munthe, Ludvig A., additional, Nygaard, Gro Owren, additional, and Mjaaland, Siri, additional

Published
2022
Full Text
View/download PDF

28. Network-Based Multiple Sclerosis Pathway Analysis with GWAS Data from 15,000 Cases and 30,000 Controls

Author

Baranzini, Sergio E., Khankhanian, Pouya, Patsopoulos, Nikolaos A., Li, Michael, Stankovich, Jim, Cotsapas, Chris, Søndergaard, Helle Bach, Ban, Maria, Barizzone, Nadia, Bergamaschi, Laura, Booth, David, Buck, Dorothea, Cavalla, Paola, Celius, Elisabeth G., Comabella, Manuel, Comi, Giancarlo, Compston, Alastair, Cournu-Rebeix, Isabelle, D’alfonso, Sandra, Damotte, Vincent, Din, Lennox, Dubois, Bénédicte, Elovaara, Irina, Esposito, Federica, Fontaine, Bertrand, Franke, Andre, Goris, An, Gourraud, Pierre-Antoine, Graetz, Christiane, Guerini, Franca R., Guillot-Noel, Léna, Hafler, David, Hakonarson, Hakon, Hall, Per, Hamsten, Anders, Harbo, Hanne F., Hemmer, Bernhard, Hillert, Jan, Kemppinen, Anu, Kockum, Ingrid, Koivisto, Keijo, Larsson, Malin, Lathrop, Mark, Leone, Maurizio, Lill, Christina M., Macciardi, Fabio, Martin, Roland, Martinelli, Vittorio, Martinelli-Boneschi, Filippo, McCauley, Jacob L., Myhr, Kjell-Morten, Naldi, Paola, Olsson, Tomas, Oturai, Annette, Pericak-Vance, Margaret A., Perla, Franco, Reunanen, Mauri, Saarela, Janna, Saker-Delye, Safa, Salvetti, Marco, Sellebjerg, Finn, Sørensen, Per Soelberg, Spurkland, Anne, Stewart, Graeme, Taylor, Bruce, Tienari, Pentti, Winkelmann, Juliane, Zipp, Frauke, Ivinson, Adrian J., Haines, Jonathan L., Sawcer, Stephen, DeJager, Philip, Hauser, Stephen L., and Oksenberg, Jorge R.

Published
2013
Full Text
View/download PDF

29. Exploring Retinal Blood Vessel Diameters as Biomarkers in Multiple Sclerosis

Author

Drobnjak Nes, Dragana, primary, Berg-Hansen, Pål, additional, de Rodez Benavent, Sigrid A., additional, Høgestøl, Einar A., additional, Beyer, Mona K., additional, Rinker, Daniel A., additional, Veiby, Nina, additional, Karabeg, Mia, additional, Petrovski, Beáta Éva, additional, Celius, Elisabeth G., additional, Harbo, Hanne F., additional, and Petrovski, Goran, additional

Published
2022
Full Text
View/download PDF

30. Association of adverse childhood experiences with the development of multiple sclerosis

Author

Eid, Karine, primary, Torkildsen, Øivind, additional, Aarseth, Jan, additional, Aalstad, Mari, additional, Bhan, Alok, additional, Celius, Elisabeth G, additional, Cortese, Marianna, additional, Daltveit, Anne Kjersti, additional, Holmøy, Trygve, additional, Myhr, Kjell-Morten, additional, Riise, Trond, additional, Schüler, Stephan, additional, Torkildsen, Cecilie F, additional, Wergeland, Stig, additional, Gilhus, Nils Erik, additional, and Bjørk, Marte-Helene, additional

Published
2022
Full Text
View/download PDF

31. Fourteen sequence variants that associate with multiple sclerosis discovered by meta-analysis informed by genetic correlations

Author

Olafsson, Sigurgeir, Stridh, Pernilla, Bos, Steffan Daniël, Ingason, Andres, Euesden, Jack, Sulem, Patrick, Thorleifsson, Gudmar, Gustafsson, Omar, Johannesson, Ari, Geirsson, Arni J., Thorsson, Arni V., Sigurgeirsson, Bardur, Ludviksson, Bjorn Runar, Olafsson, Elias, Kristjansdottir, Helga, Jonasson, Jon G., Olafsson, Jon Hjaltalin, Orvar, Kjartan B., Benediktsson, Rafn, Bjarnason, Ragnar, Kristjansdottir, Sjofn, Gislason, Thorarinn, Valdimarsson, Trausti, Mikaelsdottir, Evgenia, Sigurdsson, Snaevar, Jonsson, Stefan, Rafnar, Thorunn, Aarsland, Dag, Djurovic, Srdjan, Fladby, Tormod, Knudsen, Gun Peggy, Celius, Elisabeth G., Myhr, Kjell-Morten, Grondal, Gerdur, Steinsson, Kristjan, Valdimarsson, Helgi, Bjornsson, Sigurdur, Bjornsdottir, Unnur S., Bjornsson, Einar S, Nilsson, Bjorn, Andreassen, Ole A., Alfredsson, Lars, Hillert, Jan, Kockum, Ingrid Skelton, Masson, Gisli, Thorsteinsdottir, Unnur, Gudbjartsson, Daniel F., Stefansson, Hreinn, Hjaltason, Haukur, Harbo, Hanne F., Olsson, Tomas, Jonsdottir, Ingileif, and Stefansson, Kari

Published
2017
Full Text
View/download PDF

34. Disease Progression in Multiple Sclerosis: A Literature Review Exploring Patient Perspectives

Author

Celius,Elisabeth G, Thompson,Heidi, Pontaga,Maija, Langdon,Dawn, Laroni,Alice, Potra,Stanca, Bharadia,Trishna, Yeandle,David, Shanahan,Jane, van Galen,Pieter, Alexandri,Nektaria, and Kesselring,Jürg

Subjects
Patient Preference and Adherence
Abstract

Elisabeth G Celius,1 Heidi Thompson,2 Maija Pontaga,3 Dawn Langdon,4 Alice Laroni,5 Stanca Potra,6 Trishna Bharadia,7 David Yeandle,8 Jane Shanahan,9 Pieter van Galen,10 Nektaria Alexandri,11 Jürg Kesselring12 1Deparment of Neurology, Oslo University Hospital and University of Oslo, Oslo, Norway; 2The Neurology Centre, Craigavon Area Hospital, Portadown, UK; 3MS in the 21st Century Steering Group, Riga, Latvia; 4Department of Psychology, Royal Holloway, University of London, London, UK; 5Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genoa, Italy and IRCCS Ospedale Policlinico San Martino, Genoa, Italy; 6Patient Member of the MS in the 21st Century Steering Group, Bucharest, Romania; 7Patient Member of the MS in the 21st Century Steering Group, Buckinghamshire, UK; 8Patient Member of the MS in the 21st Century Steering Group, Southampton, UK; 9Patient Member of the MS in the 21st Century Steering Group, Ascot, UK; 10Patient Member of the MS in the 21st Century Steering Group, Overijse, Belgium; 11Global Medical Affairs, Neurology and Immunology, Merck KGaA, Darmstadt, Germany; 12Department of Neurology & Neurorehabilitation, Kliniken Valens, Valens, SwitzerlandCorrespondence: Elisabeth G CeliusDepartment of Neurology, Oslo University Hospital, Rikshospitalet, Postboks 4950 Nydalen, Oslo 0424, NorwayTel +47 91 50 27 70Email uxelgu@ous-hf.noPurpose: Multiple sclerosis (MS) prognosis is often uncertain. This literature review considers patients’ understanding of, and perspectives on, MS progression to better comprehend the unmet needs of people with MS (PwMS), in order to improve treatment adherence and quality of life (QoL).Methods: Literature searches for peer-reviewed papers concerning patient perspectives on the progression of MS and comparable conditions, published between January 2000 and January 2020, were conducted.Results: Little qualitative evidence exists that examines PwMS’ perspectives on MS progression. The understanding and meaning ascribed to terms such as “disease progression” vary. Some PwMS find disease labels stigmatizing, confusing, and disconnected from reality. The lack of a clear definition of progression and discrepancies between PwMS and healthcare professional (HCP) perspectives may contribute to misunderstanding and poor communication. Patient descriptions of progression and relapses include symptoms in addition to those evaluated by standard severity and disability measures. Compared with HCPs, PwMS are still focused on relapse prevention but place higher priority on QoL and ascribe different relative importance to the causes of poor adherence to treatment plans. PwMS want to discuss progression and likely prognosis. Such communication needs to be personalized and delivered with sensitivity, at an appropriate time. Poor treatment adherence may arise from a lack of understanding and poor communication, particularly around treatment goals. The few studies that directly considered patient perspectives on the progression of comparable conditions supported and extended the perspectives of PwMS. Lack of adequate communication by HCPs was the most common theme.Conclusion: Patient perspectives on disease progression in MS and other chronic progressive conditions are under-investigated and under-reported. The limited evidence available highlights the importance of providing adequate information and effective HCP communication. While further studies are needed, the current evidence base offers information and insights that may help HCPs to enhance patient care, well-being, and treatment adherence.Keywords: multiple sclerosis, disease progression, patient engagement, shared decision-making, communication

Published
2021

37. Publisher Correction:Common brain disorders are associated with heritable patterns of apparent aging of the brain (Nature Neuroscience, (2019), 22, 10, (1617-1623), 10.1038/s41593-019-0471-7)

Author

Kaufmann, Tobias, van der Meer, Dennis, Doan, Nhat Trung, Schwarz, Emanuel, Lund, Martina J., Agartz, Ingrid, Alnæs, Dag, Barch, Deanna M., Baur-Streubel, Ramona, Bertolino, Alessandro, Bettella, Francesco, Beyer, Mona K., Bøen, Erlend, Borgwardt, Stefan, Brandt, Christine L., Buitelaar, Jan, Celius, Elisabeth G., Cervenka, Simon, Conzelmann, Annette, Córdova-Palomera, Aldo, Dale, Anders M., de Quervain, Dominique J.F., Di Carlo, Pasquale, Djurovic, Srdjan, Dørum, Erlend S., Eisenacher, Sarah, Elvsåshagen, Torbjørn, Espeseth, Thomas, Fatouros-Bergman, Helena, Flyckt, Lena, Franke, Barbara, Frei, Oleksandr, Haatveit, Beathe, Håberg, Asta K., Harbo, Hanne F., Hartman, Catharina A., Heslenfeld, Dirk, Hoekstra, Pieter J., Høgestøl, Einar A., Jernigan, Terry L., Jonassen, Rune, Jönsson, Erik G., Farde, Lars, Engberg, Göran, Erhardt, Sophie, Schwieler, Lilly, Piehl, Fredrik, Collste, Karin, Victorsson, Pauliina, Malmqvist, Anna, Hedberg, Mikael, Orhan, Funda, Kirsch, Peter, Kłoszewska, Iwona, Kolskår, Knut K., Landrø, Nils Inge, Le Hellard, Stephanie, Lesch, Klaus Peter, Lovestone, Simon, Lundervold, Arvid, Lundervold, Astri J., Maglanoc, Luigi A., Malt, Ulrik F., Mecocci, Patrizia, Melle, Ingrid, Meyer-Lindenberg, Andreas, Moberget, Torgeir, Norbom, Linn B., Nordvik, Jan Egil, Nyberg, Lars, Oosterlaan, Jaap, Papalino, Marco, Papassotiropoulos, Andreas, Pauli, Paul, Pergola, Giulio, Persson, Karin, Richard, Geneviève, Rokicki, Jaroslav, Sanders, Anne Marthe, Selbæk, Geir, Shadrin, Alexey A., Smeland, Olav B., Soininen, Hilkka, Sowa, Piotr, Steen, Vidar M., Tsolaki, Magda, Ulrichsen, Kristine M., Vellas, Bruno, Wang, Lei, Westman, Eric, Ziegler, Georg C., Zink, Mathias, Andreassen, Ole A., and Westlye, Lars T.

Subjects
ComputingMethodologies_DOCUMENTANDTEXTPROCESSING
Abstract

In the version of this article initially published, spaces were missing in the names of Stephanie Le Hellard and Pasquale Di Carlo. The errors have been corrected in the HTML and PDF versions of the article.

Published
2020
Full Text
View/download PDF

42. Postpartum Relapse After First On-Study Pregnancy in RRMS Patients Treated With Alemtuzumab in the Phase 2 and 3 Clinical Development Program Over 8 Years (169)

Author

Celius, Elisabeth G., primary, Oh, Jiwon, additional, Achiron, Anat, additional, Compston, D Alastair S., additional, Devonshire, Virginia, additional, Hellwig, Kerstin, additional, Hutton, George J., additional, McCombe, Pamela, additional, Moore, Marie, additional, Simm, Renata Faria, additional, Sousa, Livia, additional, Vincent, Stephen G., additional, Chung, Luke, additional, Daizadeh, Nadia, additional, Mitchell, Colin, additional, and Rog, David, additional

Published
2020
Full Text
View/download PDF

43. Low-Frequency and Rare-Coding Variation Contributes to Multiple Sclerosis Risk

Author

Mitrovič, Mitja, primary, Patsopoulos, Nikolaos A., additional, Beecham, Ashley H., additional, Dankowski, Theresa, additional, Goris, An, additional, Dubois, Bénédicte, additional, D’hooghe, Marie B., additional, Lemmens, Robin, additional, Van Damme, Philip, additional, Søndergaard, Helle Bach, additional, Sellebjerg, Finn, additional, Sorensen, Per Soelberg, additional, Ullum, Henrik, additional, Thørner, Lise W., additional, Werge, Thomas, additional, Saarela, Janna, additional, Cournu-Rebeix, Isabelle, additional, Damotte, Vincent, additional, Fontaine, Bertrand, additional, Guillot-Noel, Lena, additional, Lathrop, Mark, additional, Vukusik, Sandra, additional, Gourraud, Pierre-Antoine, additional, Andlauer, Till F.M., additional, Pongratz, Viola, additional, Buck, Dorothea, additional, Gasperi, Christiane, additional, Bayas, Antonios, additional, Heesen, Christoph, additional, Kümpfel, Tania, additional, Linker, Ralf, additional, Paul, Friedemann, additional, Stangel, Martin, additional, Tackenberg, Björn, additional, Bergh, Florian Then, additional, Warnke, Clemens, additional, Wiendl, Heinz, additional, Wildemann, Brigitte, additional, Zettl, Uwe, additional, Ziemann, Ulf, additional, Tumani, Hayrettin, additional, Gold, Ralf, additional, Grummel, Verena, additional, Hemmer, Bernhard, additional, Knier, Benjamin, additional, Lill, Christina M., additional, Luessi, Felix, additional, Dardiotis, Efthimios, additional, Agliardi, Cristina, additional, Barizzone, Nadia, additional, Mascia, Elisabetta, additional, Bernardinelli, Luisa, additional, Comi, Giancarlo, additional, Cusi, Daniele, additional, Esposito, Federica, additional, Ferrè, Laura, additional, Comi, Cristoforo, additional, Galimberti, Daniela, additional, Leone, Maurizio A., additional, Sorosina, Melissa, additional, Mescheriakova, Julia, additional, Hintzen, Rogier, additional, van Duijn, Cornelia, additional, Teunissen, Charlotte E., additional, Bos, Steffan D., additional, Myhr, Kjell-Morten, additional, Celius, Elisabeth G., additional, Lie, Benedicte A., additional, Spurkland, Anne, additional, Comabella, Manuel, additional, Montalban, Xavier, additional, Alfredsson, Lars, additional, Stridh, Pernilla, additional, Hillert, Jan, additional, Jagodic, Maja, additional, Piehl, Fredrik, additional, Jelčić, Ilijas, additional, Martin, Roland, additional, Sospedra, Mireia, additional, Ban, Maria, additional, Hawkins, Clive, additional, Hysi, Pirro, additional, Kalra, Seema, additional, Karpe, Fredrik, additional, Khadake, Jyoti, additional, Lachance, Genevieve, additional, Neville, Matthew, additional, Santaniello, Adam, additional, Caillier, Stacy J., additional, Calabresi, Peter A., additional, Cree, Bruce A.C., additional, Cross, Anne, additional, Davis, Mary F., additional, Haines, Jonathan L., additional, de Bakker, Paul I.W., additional, Delgado, Silvia, additional, Dembele, Marieme, additional, Edwards, Keith, additional, Fitzgerald, Kathryn C., additional, Hakonarson, Hakon, additional, Konidari, Ioanna, additional, Lathi, Ellen, additional, Manrique, Clara P., additional, Pericak-Vance, Margaret A., additional, Piccio, Laura, additional, Schaefer, Cathy, additional, McCabe, Cristin, additional, Weiner, Howard, additional, Goldstein, Jacqueline, additional, Olsson, Tomas, additional, Hadjigeorgiou, Georgios, additional, Taylor, Bruce, additional, Tajouri, Lotti, additional, Charlesworth, Jac, additional, Booth, David R., additional, Harbo, Hanne F., additional, Ivinson, Adrian J., additional, Hauser, Stephen L., additional, Compston, Alastair, additional, Stewart, Graeme, additional, Zipp, Frauke, additional, Barcellos, Lisa F., additional, Baranzini, Sergio E., additional, Martinelli-Boneschi, Filippo, additional, D’Alfonso, Sandra, additional, Ziegler, Andreas, additional, Oturai, Annette, additional, McCauley, Jacob L., additional, Sawcer, Stephen J., additional, Oksenberg, Jorge R., additional, De Jager, Philip L., additional, Kockum, Ingrid, additional, Hafler, David A., additional, and Cotsapas, Chris, additional

Published
2020
Full Text
View/download PDF

44. No differential gene expression for CD4+ T cells of MS patients and healthy controls

Author

Brorson, Ina S, Eriksson, Anna, Leikfoss, Ingvild S, Celius, Elisabeth G, Berg-Hansen, Pål, Barcellos, Lisa F, Berge, Tone, Harbo, Hanne F, and Bos, Steffan D

Subjects
0301 basic medicine, Multiple sclerosis, Genetic variants, RNA sequencing, Biology, medicine.disease, Acquired immune system, CD4+ T cells, 03 medical and health sciences, Cellular and Molecular Neuroscience, 030104 developmental biology, 0302 clinical medicine, Gene expression, Immunology, medicine, Genetics, Neurology (clinical), Gene expressions, 030217 neurology & neurosurgery, Differential (mathematics)
Abstract

Background Multiple sclerosis-associated genetic variants indicate that the adaptive immune system plays an important role in the risk of developing multiple sclerosis. It is currently not well understood how these multiple sclerosis-associated genetic variants contribute to multiple sclerosis risk. CD4+ T cells are suggested to be involved in multiple sclerosis disease processes. Objective We aim to identify CD4+ T cell differential gene expression between multiple sclerosis patients and healthy controls in order to understand better the role of these cells in multiple sclerosis. Methods We applied RNA sequencing on CD4+ T cells from multiple sclerosis patients and healthy controls. Results We did not identify significantly differentially expressed genes in CD4+ T cells from multiple sclerosis patients. Furthermore, pathway analyses did not identify enrichment for specific pathways in multiple sclerosis. When we investigated genes near multiple sclerosis-associated genetic variants, we did not observe significant enrichment of differentially expressed genes. Conclusion We conclude that CD4+ T cells from multiple sclerosis patients do not show significant differential gene expression. Therefore, gene expression studies of all circulating CD4+ T cells may not result in viable biomarkers. Gene expression studies of more specific subsets of CD4+ T cells remain justified to understand better which CD4+ T cell subsets contribute to multiple sclerosis pathology.

Published
2019

45. Supplemental Material6 - Supplemental material for No differential gene expression for CD4+ T cells of MS patients and healthy controls

Author

Brorson, Ina S, Eriksson, Anna, Leikfoss, Ingvild S, Celius, Elisabeth G, Berg-Hansen, Pål, Barcellos, Lisa F, Berge, Tone, Harbo, Hanne F, and Bos, Steffan D

Subjects
FOS: Clinical medicine, 110904 Neurology and Neuromuscular Diseases, Neuroscience
Abstract

Supplemental material, Supplemental Material6 for No differential gene expression for CD4+ T cells of MS patients and healthy controls by Ina S Brorson, Anna Eriksson, Ingvild S Leikfoss, Elisabeth G Celius, Pål Berg-Hansen, Lisa F Barcellos, Tone Berge, Hanne F Harbo and Steffan D Bos in Multiple Sclerosis Journal – Experimental, Translational and Clinical

Published
2019
Full Text
View/download PDF

46. Best Practices for Long-Term Monitoring and Follow-Up of Alemtuzumab-Treated MS Patients in Real-World Clinical Settings

Author

Barclay, Krista, Carruthers, Robert, Traboulsee, Anthony, Bass, Ann D., LaGanke, Christopher, Bertolotto, Antonio, Boster, Aaron, Celius, Elisabeth G., de Seze, Jerome, Dela Cruz, Dionisio, Habek, Mario, Lee, Jong-Mi, Limmroth, Volker, Meuth, Sven G., Oreja-Guevara, Celia, Pagnotta, Patricia, Vos, Cindy, Ziemssen, Tjalf, Baker, Darren P., and Van Wijmeersch, Bart

Subjects
monitoring, real-world settings, autoimmune events, anti-CD52 monoclonal antibody, alemtuzumab, best practices, relapsing-remitting multiple sclerosis, disease-modifying therapy
Abstract

Multiple sclerosis (MS) is a chronic autoimmune neurological disease that typically affects young adults, causing irreversible physical disability and cognitive impairment. Alemtuzumab, administered intravenously as 2 initial courses of 12 mg/day (5 consecutive days at baseline, and 3 consecutive days 12 months later), resulted in significantly greater improvements in clinical and MRI outcomes vs. subcutaneous interferon beta-1a over 2 years in patients with active relapsing-remitting MS (RRMS) who were either treatment-naive (CARE-MS I; NCT00530348) or had an inadequate response to prior therapy (CARE-MS II; NCT00548405). Efficacy with alemtuzumab was maintained over 7 years in subsequent extension studies (NCT00930553; NCT02255656), in the absence of continuous treatment and with a consistent safety profile. There is an increased incidence of autoimmune events in patients treated with alemtuzumab (mainly thyroid events, but also immune thrombocytopenia and nephropathy), which imparts a need for mandatory safety monitoring for 4 years following the last treatment. The risk management strategy for alemtuzumab-treated patients includes laboratory monitoring and a comprehensive patient education and support program that enables early detection and effective management of autoimmune events, yielding optimal outcomes for MS patients. Here we provide an overview of tools and techniques that have been implemented in real-world clinical settings to reduce the burden of monitoring for both patients and healthcare providers, including customized educational materials, the use of social media, and interactive online databases for managing healthcare data. Many practices are also enhancing patient outreach efforts through coordination with specialized nursing services and ancillary caregivers. The best practice recommendations for safety monitoring described in this article, based on experiences in real-world clinical settings, may enable early detection and management of autoimmune events, and help with implementation of monitoring requirements while maximizing the benefits of alemtuzumab treatment for MS patients. Funding for the development of this manuscript was provided by Sanofi. This article was reviewed by Ericka M. Bueno, Ph.D., and Colin Mitchell, Ph.D., of Sanofi. Editorial support for this manuscript was provided by Jaya Kolipaka and Linda Wychowski, Ph.D., of Envision Scientific Solutions, and funded by Sanofi. The authors were responsible for all content and editorial decisions and received no honoraria related to the development of this publication.

Published
2019

48. Low-Frequency and Rare-Coding Variation Contributes to Multiple Sclerosis Risk

Author

Int Multiple Sclerosis Genetics, Mitrovic, Mitja, Patsopoulos, Nikoloas, Beecham, Ashley, Dankowski, Theresa, Goris, An, Dubois, Bénédicte, D'hooghe, Marie B, Lemmens, Robin, Van Damme, Philip, Bach Sondergaard, Helle, Sellebjerg, Finn, Soelberg Sorensen, Per, Ullum, Henrik, Thorner, Lise W, Werge, Thomas, Saarela, Janna, Cournu-Rebeix, Isabelle, Damotte, Vincent, Fontaine, Bertrand, Guillot-Noel, Lena, Lathrop, Mark, Vukusik, Sandra, Gourraud, Pierre-Antoine, Andlauer, Till FM, Pongratz, Viola, Buck, Dorothea, Gasperi, Christiane, Bayas, Antonios, Heesen, Christoph, Kümpfel, Tania, Linker, Ralf, Friedemann, Paul, Stangel, Martin, Tackenberg, Björn, Then Bergh, Florian, Warnke, Clemens, Wiendl, Heinz, Wildemann, Brigitte, Zettl, Uwe, Ziemann, Ulf, Tumani, Hayrettin, Gold, Ralf, Grummel, Verena, Hemmer, Bernhard, Knier, Benjamin, Lill, Christina, Luessi, Felix, Dardiotis, Efthimios, Agliardi, Cristina, Barizzone, Nadia, Mascia, Elisabetta, Bernardinelli, Luisa, Comi, Giancarlo, Cusi, Daniele, Esposito, Federica, Ferrè, Laura, Comi, Cristoforo, Galimberti, Daniela, Leone, Maurizio A, Sorosina, Melissa, Mescheriakova, Julia, Hintzen, Rogier, van Duijn, Cornelia, Theunissen, Charlotte E, Bos, Steffan D, Myhr, Kjell-Morten, Celius, Elisabeth G, Lie, Benedicte A, Spurkland, Anne, Comabella, Manuel, Montalban, Xavier, Alfredsson, Lars, Stridh, Pernilla, Hillert, Jan, Jagodic, Maja, Piehl, Fredrik, Jelcic, Ilijas, Martin, Roland, Sospedra, Mireia, Ban, Maria, Hawkins, Clive, Hysi, Pirro, Kalra, Seema, Karpe, Fredrik, Khadake, Jyoti, Lachance, Genevieve, Neville, Matthew, Santaniello, Adam, Caillier, Stacy J, Calavresi, Peter A, Cree, Bruce AC, Cross, Anne, Davis, Mary F, Haines, Jonathan L, de Bakker, Paul IW, Delgado, Silvia, Dembele, Marieme, Edwards, Keith, Fitzgerald, Kathryn C, Hakonarson, Hakon, Konidari, Ioanna, Lathi, Ellen, Manrique, Clara P, Pericak-Vance, Margaret A, Piccio, Laura, Schaefer, Cathy, McCabe, Cristin, Weiner, Howard, Goldstein, Jacqueline, Olsson, Tomas, Hadjigeorgiou, Georgios, Taylor, Bruce, Tajouri, Lotti, Charlesworth, Jac, Booth, David R, HArbo, Hanne F, Ivinson, Adrian J, Hauser, Stephen L, Compston, Alistair, Stewart, Graeme, Zipp, Frauke, Barcellos, Lisa F, Baranzini, Sergio E, Martinelli-Boneschi, Filippo, D'Alfonso, Sandra, Ziegler, Andreas, Oturai, Annette, McCauley, Jacob L, Sawcer, Stephen J, Oksenberg, Jorge R, De Jager, Philip L, Kockum, Ingrid, Hafler, David A, and Cotsapas, Chris

Subjects
Biochemistry & Molecular Biology, Science & Technology, REPLICATION, LINKAGE, Cell Biology, GENETIC RISK, GENOME-WIDE ASSOCIATION, VARIANTS, Life Sciences & Biomedicine, METAANALYSIS, POPULATION
Abstract

Multiple sclerosis is a complex neurological disease, with ∼20% of risk heritability attributable to common genetic variants, including >230 identified by genome-wide association studies. Multiple strands of evidence suggest that much of the remaining heritability is also due to additive effects of common variants rather than epistasis between these variants or mutations exclusive to individual families. Here, we show in 68,379 cases and controls that up to 5% of this heritability is explained by low-frequency variation in gene coding sequence. We identify four novel genes driving MS risk independently of common-variant signals, highlighting key pathogenic roles for regulatory T cell homeostasis and regulation, IFNγ biology, and NFκB signaling. As low-frequency variants do not show substantial linkage disequilibrium with other variants, and as coding variants are more interpretable and experimentally tractable than non-coding variation, our discoveries constitute a rich resource for dissecting the pathobiology of MS. ispartof: CELL vol:175 issue:6 pages:1679-1695 ispartof: location:United States status: published

Published
2018

49. MSJ765671_supplementary_material_3 – Supplemental material for Restriction spectrum imaging of white matter and its relation to neurological disability in multiple sclerosis

Author

Sowa, Piotr, Harbo, Hanne F, White, Nathan S, Celius, Elisabeth G, Bartsch, Hauke, Berg-Hansen, Pål, Moen, Stine M, Bjørnerud, Atle, Westlye, Lars T, Andreassen, Ole A, Dale, Anders M, and Beyer, Mona K

Subjects
FOS: Clinical medicine, 111702 Aged Health Care, FOS: Health sciences, 110904 Neurology and Neuromuscular Diseases
Abstract

Supplemental material, MSJ765671_supplementary_material_3 for Restriction spectrum imaging of white matter and its relation to neurological disability in multiple sclerosis by Piotr Sowa, Hanne F Harbo, Nathan S White, Elisabeth G Celius, Hauke Bartsch, Pål Berg-Hansen, Stine M Moen, Atle Bjørnerud, Lars T Westlye, Ole A Andreassen, Anders M Dale and Mona K Beyer in Multiple Sclerosis Journal

Published
2018
Full Text
View/download PDF

50. Retinal oximetry as a biomarker in multiple sclerosis

Author

Drobnjak Nes, Dragana, primary, Rodez Benavent, Sigrid A., additional, Berg‐Hansen, Pål, additional, Høgestøl, Einar A., additional, Beyer, Mona K., additional, Rinke, Dan A., additional, Veiby, Nina, additional, Addorisio, Vito, additional, Petrovski, Beata Eva, additional, Celius, Elisabeth G., additional, Harbo, Hanne F., additional, and Petrovski, Goran, additional

Published
2019
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results