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965 results on '"Dion, Patrick"'

1. An observational study of pleiotropy and penetrance of amyotrophic lateral sclerosis associated with CAG-repeat expansion of ATXN2

Author

Demaegd, Koen C., Kernan, Aoife, Cooper-Knock, Johnathan, van Vugt, Joke J. F. A., Harvey, Calum, Moll, Tobias, O’Brien, David, Gornall, Sarah, Drury, Luke, Farhan, Sali M. K., Dion, Patrick A., Rouleau, Guy A., Western, Andrea, Parsons, Paul J., Mclean, Benjamin, Benatar, Michael, van den Berg, Leonard H., Van Damme, Philip, Willem Dankbaar, Jan, Hendrikse, Jeroen, Koole, Wouter, de Bie, Charlotte, Hobson, Esther, Veldink, Jan H., van de Warrenburg, Bart, Pasterkamp, R. Jeroen, van Rheenen, Wouter, Kirby, Janine, Shaw, Pamela J., and van Es, Michael. A.

Published
2025
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3. Autism-associated CHD8 controls reactive gliosis and neuroinflammation via remodeling chromatin in astrocytes

Author

Megagiannis, Platon, Mei, Yuan, Yan, Rachel E., Yuan, Lin, Wilde, Jonathan J., Eckersberg, Hailey, Suresh, Rahul, Tan, Xinzhu, Chen, Hong, Farmer, W. Todd, Cha, Kuwook, Le, Phuong Uyen, Catoire, Helene, Rochefort, Daniel, Kwan, Tony, Yee, Brian A., Dion, Patrick, Krishnaswamy, Arjun, Cloutier, Jean-Francois, Stifani, Stefano, Petrecca, Kevin, Yeo, Gene W., Murai, Keith K., Feng, Guoping, Rouleau, Guy A., Ideker, Trey, Sanjana, Neville E., and Zhou, Yang

Published
2024
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4. Common and rare variant association analyses in amyotrophic lateral sclerosis identify 15 risk loci with distinct genetic architectures and neuron-specific biology

Author

van Rheenen, Wouter, van der Spek, Rick AA, Bakker, Mark K, van Vugt, Joke JFA, Hop, Paul J, Zwamborn, Ramona AJ, de Klein, Niek, Westra, Harm-Jan, Bakker, Olivier B, Deelen, Patrick, Shireby, Gemma, Hannon, Eilis, Moisse, Matthieu, Baird, Denis, Restuadi, Restuadi, Dolzhenko, Egor, Dekker, Annelot M, Gawor, Klara, Westeneng, Henk-Jan, Tazelaar, Gijs HP, van Eijk, Kristel R, Kooyman, Maarten, Byrne, Ross P, Doherty, Mark, Heverin, Mark, Al Khleifat, Ahmad, Iacoangeli, Alfredo, Shatunov, Aleksey, Ticozzi, Nicola, Cooper-Knock, Johnathan, Smith, Bradley N, Gromicho, Marta, Chandran, Siddharthan, Pal, Suvankar, Morrison, Karen E, Shaw, Pamela J, Hardy, John, Orrell, Richard W, Sendtner, Michael, Meyer, Thomas, Başak, Nazli, van der Kooi, Anneke J, Ratti, Antonia, Fogh, Isabella, Gellera, Cinzia, Lauria, Giuseppe, Corti, Stefania, Cereda, Cristina, Sproviero, Daisy, D’Alfonso, Sandra, Sorarù, Gianni, Siciliano, Gabriele, Filosto, Massimiliano, Padovani, Alessandro, Chiò, Adriano, Calvo, Andrea, Moglia, Cristina, Brunetti, Maura, Canosa, Antonio, Grassano, Maurizio, Beghi, Ettore, Pupillo, Elisabetta, Logroscino, Giancarlo, Nefussy, Beatrice, Osmanovic, Alma, Nordin, Angelica, Lerner, Yossef, Zabari, Michal, Gotkine, Marc, Baloh, Robert H, Bell, Shaughn, Vourc’h, Patrick, Corcia, Philippe, Couratier, Philippe, Millecamps, Stéphanie, Meininger, Vincent, Salachas, François, Mora Pardina, Jesus S, Assialioui, Abdelilah, Rojas-García, Ricardo, Dion, Patrick A, Ross, Jay P, Ludolph, Albert C, Weishaupt, Jochen H, Brenner, David, Freischmidt, Axel, Bensimon, Gilbert, Brice, Alexis, Durr, Alexandra, Payan, Christine AM, Saker-Delye, Safa, Wood, Nicholas W, Topp, Simon, Rademakers, Rosa, Tittmann, Lukas, Lieb, Wolfgang, Franke, Andre, Ripke, Stephan, Braun, Alice, and Kraft, Julia

Subjects
Human Genome, Neurodegenerative, Clinical Research, Rare Diseases, Prevention, ALS, Neurosciences, Genetics, Brain Disorders, Aetiology, 2.1 Biological and endogenous factors, Neurological, Amyotrophic Lateral Sclerosis, Brain, Cholesterol, Disease Progression, Female, Genome-Wide Association Study, Glutamine, Humans, Male, Mendelian Randomization Analysis, Microsatellite Repeats, Mutation, Neurodegenerative Diseases, Neurons, Quantitative Trait Loci, RNA-Seq, Risk Factors, SLALOM Consortium, PARALS Consortium, SLAGEN Consortium, SLAP Consortium, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease with a lifetime risk of one in 350 people and an unmet need for disease-modifying therapies. We conducted a cross-ancestry genome-wide association study (GWAS) including 29,612 patients with ALS and 122,656 controls, which identified 15 risk loci. When combined with 8,953 individuals with whole-genome sequencing (6,538 patients, 2,415 controls) and a large cortex-derived expression quantitative trait locus (eQTL) dataset (MetaBrain), analyses revealed locus-specific genetic architectures in which we prioritized genes either through rare variants, short tandem repeats or regulatory effects. ALS-associated risk loci were shared with multiple traits within the neurodegenerative spectrum but with distinct enrichment patterns across brain regions and cell types. Of the environmental and lifestyle risk factors obtained from the literature, Mendelian randomization analyses indicated a causal role for high cholesterol levels. The combination of all ALS-associated signals reveals a role for perturbations in vesicle-mediated transport and autophagy and provides evidence for cell-autonomous disease initiation in glutamatergic neurons.

Published
2021

6. Convergent coexpression of autism-associated genes suggests some novel risk genes may not be detectable in large-scale genetic studies

Author

Liao, Calwing, Moyses-Oliveira, Mariana, De Esch, Celine E.F., Bhavsar, Riya, Nuttle, Xander, Li, Aiqun, Yu, Alex, Burt, Nicholas D., Erdin, Serkan, Fu, Jack M., Wang, Minghui, Morley, Theodore, Han, Lide, Dion, Patrick A., Rouleau, Guy A., Zhang, Bin, Brennand, Kristen J., Talkowski, Michael E., and Ruderfer, Douglas M.

Published
2023
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7. Autosomal Recessive Cerebellar Ataxias

Author

Haj Salem, Ikhlass, Noreau, Anne, Bouchard, Jean-Pierre, Dion, Patrick A., Rouleau, Guy A., Dupré, Nicolas, Schmahmann, Jeremy D., Section editor, Manto, Mario U., Section editor, Manto, Mario U., editor, Gruol, Donna L., editor, Schmahmann, Jeremy D., editor, Koibuchi, Noriyuki, editor, and Sillitoe, Roy V., editor

Published
2022
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8. Copy-number variants in the contactin-5 gene are a potential risk factor for autism spectrum disorder

Author

Schmilovich, Zoe, Huguet, Guillaume, He, Qin, Musa-Johnson, Amélie, Douard, Elise, Loum, Mor Absa, Liao, Calwing, Ross, Jay P., Dionne-Laporte, Alexandre, Spiegelman, Dan, Jean-Louis, Martineau, Saci, Zohra, Hayward, Caroline, Banaschewski, Tobias, Bokde, Arun, Desrivieres, Sylvane, Lemaitre, Herve, Schumann, Gunter, Xiong, Lan, Dion, Patrick A., Jacquemont, Sébastien, Chaumette, Boris, and Rouleau, Guy A.

Published
2022
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16. Exome-wide rare variant analysis in familial essential tremor

Author

Diez-Fairen, Monica, Houle, Gabrielle, Ortega-Cubero, Sara, Bandres-Ciga, Sara, Alvarez, Ignacio, Carcel, Maria, Ibañez, Laura, Fernandez, Maria Victoria, Budde, John P., Trotta, Jean-Rémi, Tonda, Raúl, Chong, Jessica X., Bamshad, Michael J., Nickerson, Deborah A., Aguilar, Miquel, Tartari, Juan P., Gironell, Alexandre, García-Martín, Elena, Agundez, Jose AG., Alonso-Navarro, Hortensia, Jimenez-Jimenez, Felix Javier, Fernandez, Manel, Valldeoriola, Francesc, Marti, Maria Jose, Tolosa, Eduard, Coria, Francisco, Pastor, Maria A., Vilariño-Güell, Carles, Rajput, Alex, Dion, Patrick A., Cruchaga, Carlos, Rouleau, Guy A., and Pastor, Pau

Published
2021
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17. Genomic Analysis Identifies Risk Factors in Restless Legs Syndrome.

Author

Akçimen, Fulya, Chia, Ruth, Saez‐Atienzar, Sara, Ruffo, Paola, Rasheed, Memoona, Ross, Jay P., Liao, Calwing, Ray, Anindita, Dion, Patrick A., Scholz, Sonja W., Rouleau, Guy A., and Traynor, Bryan J.

Subjects
RESTLESS legs syndrome, GENETIC correlations, GENOMICS, NEUROLOGICAL disorders, REST periods
Abstract

Objective: Restless legs syndrome (RLS) is a neurological condition that causes uncomfortable sensations in the legs and an irresistible urge to move them, typically during periods of rest. The genetic basis and pathophysiology of RLS are incompletely understood. We sought to identify additional novel genetic risk factors associated with RLS susceptibility. Methods: We performed a whole‐genome sequencing and genome‐wide association meta‐analysis of RLS cases (n = 9,851) and controls (n = 38,957) in 3 population‐based biobanks (All of Us, Canadian Longitudinal Study on Aging, and CARTaGENE). Results: Genome‐wide association analysis identified 9 independent risk loci, of which 8 had been previously reported, and 1 was a novel risk locus (LMX1B, rs35196838, OR 1.14, 95% CI 1.09–1.19, p value = 2.2 × 10−9). Furthermore, a transcriptome‐wide association study also identified GLO1 and a previously unreported gene, ELFN1. A genetic correlation analysis revealed significant common variant overlaps between RLS and neuroticism (rg = 0.40, se = 0.08, p value = 5.4 × 10−7), depression (rg = 0.35, se = 0.06, p value = 2.17 × 10−8), and intelligence (rg = −0.20, se = 0.06, p value = 4.0 × 10−4). Interpretation: Our study expands the understanding of the genetic architecture of RLS, and highlights the contributions of common variants to this prevalent neurological disorder. ANN NEUROL 2024;96:994–1005 [ABSTRACT FROM AUTHOR]

Published
2024
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18. Chronic lithium treatment alters the excitatory/ inhibitory balance of synaptic networks and reduces mGluR5-PKC signalling in mouse cortical neurons

Author

Khayachi, Anouar, Ase, Ariel, Liao, Calwing, Kamesh, Anusha, Kuhlmann, Naila, Schorova, Lenka, Chaumette, Boris, Dion, Patrick, Alda, Martin, Seguela, Philippe, Rouleau, Guy, and Milnerwood, Austen

Subjects
Physiological aspects, Patient outcomes, Dosage and administration, Health aspects, Synapses -- Physiological aspects, Neural circuitry -- Physiological aspects, Cellular signal transduction -- Health aspects, Lithium drugs -- Dosage and administration -- Patient outcomes, Lithium -- Dosage and administration -- Patient outcomes
Abstract

Introduction Bipolar disorder is a major psychiatric illness that affects 1% to 3% of the population worldwide, and it is 1 of the top 10 causes of disability. (1,2) Bipolar [...], Background: Bipolar disorder is characterized by cyclical alternation between mania and depression, often comorbid with psychosis and suicide. Compared with other medications, the mood stabilizer lithium is the most effective treatment for the prevention of manic and depressive episodes. However, the pathophysiology of bipolar disorder and lithium's mode of action are yet to be fully understood. Evidence suggests a change in the balance of excitatory and inhibitory activity, favouring excitation in bipolar disorder. In the present study, we sought to establish a holistic understanding of the neuronal consequences of lithium exposure in mouse cortical neurons, and to identify underlying mechanisms of action. Methods: We used a range of technical approaches to determine the effects of acute and chronic lithium treatment on mature mouse cortical neurons. We combined RNA screening and biochemical and electrophysiological approaches with confocal immunofluorescence and live-cell calcium imaging. Results: We found that only chronic lithium treatment significantly reduced intracellular calcium flux, specifically by activating metabotropic glutamatergic receptor 5. This was associated with altered phosphorylation of protein kinase C and glycogen synthase kinase 3, reduced neuronal excitability and several alterations to synapse function. Consequently, lithium treatment shifts the excitatory-inhibitory balance toward inhibition. Limitations: The mechanisms we identified should be validated in future by similar experiments in whole animals and human neurons. Conclusion: Together, the results revealed how lithium dampens neuronal excitability and the activity of the glutamatergic network, both of which are predicted to be overactive in the manic phase of bipolar disorder. Our working model of lithium action enables the development of targeted strategies to restore the balance of overactive networks, mimicking the therapeutic benefits of lithium but with reduced toxicity.

Published
2021
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19. Evolution of a Human-Specific Tandem Repeat Associated with ALS

Author

Course, Meredith M., Gudsnuk, Kathryn, Smukowski, Samuel N., Winston, Kosuke, Desai, Nitin, Ross, Jay P., Sulovari, Arvis, Bourassa, Cynthia V., Spiegelman, Dan, Couthouis, Julien, Yu, Chang-En, Tsuang, Debby W., Jayadev, Suman, Kay, Mark A., Gitler, Aaron D., Dupre, Nicolas, Eichler, Evan E., Dion, Patrick A., Rouleau, Guy A., and Valdmanis, Paul N.

Published
2020
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22. Copy-number variants and polygenic risk for intelligence confer risk for autism spectrum disorder irrespective of their effects on cognitive ability

Author

Schmilovich, Zoe, primary, Bourque, Vincent-Raphaël, additional, Douard, Elise, additional, Huguet, Guillaume, additional, Poulain, Cécile, additional, Ross, Jay P., additional, Alipour, Paria, additional, Castonguay, Charles-Étienne, additional, Younis, Nadine, additional, Jean-Louis, Martineau, additional, Saci, Zohra, additional, Pausova, Zdenka, additional, Paus, Tomas, additional, Schuman, Gunter, additional, Porteous, David, additional, Davies, Gail, additional, Redmond, Paul, additional, Harris, Sarah E., additional, Deary, Ian J., additional, Whalley, Heather, additional, Hayward, Caroline, additional, Dion, Patrick A., additional, Jacquemont, Sébastien, additional, and Rouleau, Guy A., additional

Published
2024
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23. Autosomal Recessive Cerebellar Ataxias

Author

Haj Salem, Ikhlass, primary, Noreau, Anne, additional, Bouchard, Jean-Pierre, additional, Dion, Patrick A., additional, Rouleau, Guy A., additional, and Dupré, Nicolas, additional

Published
2021
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24. Genetic architecture and adaptations of Nunavik Inuit

Author

Zhou, Sirui, Xie (谢萍星), Pingxing, Quoibion, Amélie, Ambalavanan, Amirthagowri, Dionne-Laporte, Alexandre, Spiegelman, Dan, Bourassa, Cynthia V., Xiong, Lan, Dion, Patrick A., and Rouleau, Guy A.

Published
2019

31. Exome sequencing in amyotrophic lateral sclerosis identifies risk genes and pathways.

Author

Cirulli, Elizabeth, Lasseigne, Brittany, Petrovski, Slavé, Sapp, Peter, Dion, Patrick, Leblond, Claire, Couthouis, Julien, Lu, Yi-Fan, Wang, Quanli, Krueger, Brian, Ren, Zhong, Keebler, Jonathan, Han, Yujun, Levy, Shawn, Boone, Braden, Wimbish, Jack, Waite, Lindsay, Jones, Angela, Carulli, John, Day-Williams, Aaron, Staropoli, John, Xin, Winnie, Chesi, Alessandra, Raphael, Alya, McKenna-Yasek, Diane, Cady, Janet, Vianney de Jong, J, Kenna, Kevin, Smith, Bradley, Topp, Simon, Miller, Jack, Gkazi, Athina, Al-Chalabi, Ammar, van den Berg, Leonard, Veldink, Jan, Silani, Vincenzo, Ticozzi, Nicola, Shaw, Christopher, Baloh, Robert, Appel, Stanley, Simpson, Ericka, Lagier-Tourenne, Clotilde, Pulst, Stefan, Gibson, Summer, Trojanowski, John, Elman, Lauren, McCluskey, Leo, Grossman, Murray, Shneider, Neil, Chung, Wendy, Ravits, John, Glass, Jonathan, Sims, Katherine, Van Deerlin, Vivianna, Maniatis, Tom, Hayes, Sebastian, Ordureau, Alban, Swarup, Sharan, Landers, John, Baas, Frank, Allen, Andrew, Bedlack, Richard, Harper, J, Gitler, Aaron, Rouleau, Guy, Brown, Robert, Harms, Matthew, Cooper, Gregory, Harris, Tim, Myers, Richard, and Goldstein, David

Subjects
Adaptor Proteins, Signal Transducing, Adolescent, Adult, Aged, Aged, 80 and over, Amyotrophic Lateral Sclerosis, Autophagy, Cell Cycle Proteins, Exome, Female, Genes, Genetic Association Studies, Genetic Predisposition to Disease, Humans, Male, Membrane Transport Proteins, Middle Aged, Protein Binding, Protein Serine-Threonine Kinases, Risk, Sequence Analysis, DNA, Sequestosome-1 Protein, Transcription Factor TFIIIA, Young Adult
Abstract

Amyotrophic lateral sclerosis (ALS) is a devastating neurological disease with no effective treatment. We report the results of a moderate-scale sequencing study aimed at increasing the number of genes known to contribute to predisposition for ALS. We performed whole-exome sequencing of 2869 ALS patients and 6405 controls. Several known ALS genes were found to be associated, and TBK1 (the gene encoding TANK-binding kinase 1) was identified as an ALS gene. TBK1 is known to bind to and phosphorylate a number of proteins involved in innate immunity and autophagy, including optineurin (OPTN) and p62 (SQSTM1/sequestosome), both of which have also been implicated in ALS. These observations reveal a key role of the autophagic pathway in ALS and suggest specific targets for therapeutic intervention.

Published
2015

32. Deleterious mutations in the essential mRNA metabolism factor, hGle1, in amyotrophic lateral sclerosis

Author

Kaneb, Hannah M, Folkmann, Andrew W, Belzil, Véronique V, Jao, Li-En, Leblond, Claire S, Girard, Simon L, Daoud, Hussein, Noreau, Anne, Rochefort, Daniel, Hince, Pascale, Szuto, Anna, Levert, Annie, Vidal, Sabrina, André-Guimont, Catherine, Camu, William, Bouchard, Jean-Pierre, Dupré, Nicolas, Rouleau, Guy A, Wente, Susan R, and Dion, Patrick A

Subjects
Biochemistry and Cell Biology, Bioinformatics and Computational Biology, Genetics, Biological Sciences, Rare Diseases, Neurosciences, Brain Disorders, ALS, Neurodegenerative, Orphan Drug, 2.1 Biological and endogenous factors, Aetiology, Neurological, Amyotrophic Lateral Sclerosis, Animals, Arthrogryposis, Codon, Nonsense, DNA-Binding Proteins, Disease Models, Animal, Haploinsufficiency, HeLa Cells, Humans, Microscopy, Confocal, Motor Neurons, Mutation, Missense, Nuclear Pore, Nucleocytoplasmic Transport Proteins, Pedigree, Protein Processing, Post-Translational, RNA Splicing, RNA, Messenger, Zebrafish, Hela Cells, Medical and Health Sciences, Genetics & Heredity
Abstract

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by the selective death of motor neurons. Causative mutations in the global RNA-processing proteins TDP-43 and FUS among others, as well as their aggregation in ALS patients, have identified defects in RNA metabolism as an important feature in this disease. Lethal congenital contracture syndrome 1 and lethal arthrogryposis with anterior horn cell disease are autosomal recessive fetal motor neuron diseases that are caused by mutations in another global RNA-processing protein, hGle1. In this study, we carried out the first screening of GLE1 in ALS patients (173 familial and 760 sporadic) and identified 2 deleterious mutations (1 splice site and 1 nonsense mutation) and 1 missense mutation. Functional analysis of the deleterious mutants revealed them to be unable to rescue motor neuron pathology in zebrafish morphants lacking Gle1. Furthermore, in HeLa cells, both mutations caused a depletion of hGle1 at the nuclear pore where it carries out an essential role in nuclear export of mRNA. These results suggest a haploinsufficiency mechanism and point to a causative role for GLE1 mutations in ALS patients. This further supports the involvement of global defects in RNA metabolism in ALS.

Published
2015

35. Cognitive and Psychiatric Evaluation in SYNE1 Ataxia

Author

Gama, Maria Thereza Drumond, Braga-Neto, Pedro, Dutra, Livia Almeida, Alessi, Helena, Maria, Lilia Alves, Gadelha, Ary Araripe, Ortiz, Bruno Bertolucci, Kunii, Ilda, Correia-Silva, Silvia Regina, Dias da Silva, Magnus R., Dion, Patrick A., Rouleau, Guy A., França, Jr, Marcondes Cavalcante, Barsottini, Orlando G. P., and Pedroso, José Luiz

Published
2019
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45. Huntington's disease in an African family

Author

Kombate, Damelan, primary, Rochefort, Daniel, additional, Ephoévi-Ga, Adadé, additional, Catoire, Helene, additional, Waklatsi, Panabalo, additional, Dion, Patrick, additional, Balogou, Koffi Aa, additional, and Rouleau, Guy A., additional

Published
2023
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49. Autosomal Recessive Cerebellar Ataxias

Author

Haj Salem, Ikhlass, primary, Noreau, Anne, additional, Bouchard, Jean-Pierre, additional, Dion, Patrick A., additional, Rouleau, Guy A., additional, and Dupré, Nicolas, additional

Published
2020
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50. Author Correction: Common and rare variant association analyses in amyotrophic lateral sclerosis identify 15 risk loci with distinct genetic architectures and neuron-specific biology

Author

van Rheenen, Wouter, van der Spek, Rick A. A., Bakker, Mark K., van Vugt, Joke J. F. A., Hop, Paul J., Zwamborn, Ramona A. J., de Klein, Niek, Westra, Harm-Jan, Bakker, Olivier B., Deelen, Patrick, Shireby, Gemma, Hannon, Eilis, Moisse, Matthieu, Baird, Denis, Restuadi, Restuadi, Dolzhenko, Egor, Dekker, Annelot M., Gawor, Klara, Westeneng, Henk-Jan, Tazelaar, Gijs H. P., van Eijk, Kristel R., Kooyman, Maarten, Byrne, Ross P., Doherty, Mark, Heverin, Mark, Al Khleifat, Ahmad, Iacoangeli, Alfredo, Shatunov, Aleksey, Ticozzi, Nicola, Cooper-Knock, Johnathan, Smith, Bradley N., Gromicho, Marta, Chandran, Siddharthan, Pal, Suvankar, Morrison, Karen E., Shaw, Pamela J., Hardy, John, Orrell, Richard W., Sendtner, Michael, Meyer, Thomas, Başak, Nazli, van der Kooi, Anneke J., Ratti, Antonia, Fogh, Isabella, Gellera, Cinzia, Lauria, Giuseppe, Corti, Stefania, Cereda, Cristina, Sproviero, Daisy, D’Alfonso, Sandra, Sorarù, Gianni, Siciliano, Gabriele, Filosto, Massimiliano, Padovani, Alessandro, Chiò, Adriano, Calvo, Andrea, Moglia, Cristina, Brunetti, Maura, Canosa, Antonio, Grassano, Maurizio, Beghi, Ettore, Pupillo, Elisabetta, Logroscino, Giancarlo, Nefussy, Beatrice, Osmanovic, Alma, Nordin, Angelica, Lerner, Yossef, Zabari, Michal, Gotkine, Marc, Baloh, Robert H., Bell, Shaughn, Vourc’h, Patrick, Corcia, Philippe, Couratier, Philippe, Millecamps, Stéphanie, Meininger, Vincent, Salachas, François, Mora Pardina, Jesus S., Assialioui, Abdelilah, Rojas-García, Ricardo, Dion, Patrick A., Ross, Jay P., Ludolph, Albert C., Weishaupt, Jochen H., Brenner, David, Freischmidt, Axel, Bensimon, Gilbert, Brice, Alexis, Durr, Alexandra, Payan, Christine A. M., Saker-Delye, Safa, Wood, Nicholas W., Topp, Simon, Rademakers, Rosa, Tittmann, Lukas, Lieb, Wolfgang, Franke, Andre, Ripke, Stephan, Braun, Alice, Kraft, Julia, Whiteman, David C., Olsen, Catherine M., Uitterlinden, Andre G., Hofman, Albert, Rietschel, Marcella, Cichon, Sven, Nöthen, Markus M., Amouyel, Philippe, Traynor, Bryan J., Singleton, Andrew B., Mitne Neto, Miguel, Cauchi, Ruben J., Ophoff, Roel A., Wiedau-Pazos, Martina, Lomen-Hoerth, Catherine, van Deerlin, Vivianna M., Grosskreutz, Julian, Roediger, Annekathrin, Gaur, Nayana, Jörk, Alexander, Barthel, Tabea, Theele, Erik, Ilse, Benjamin, Stubendorff, Beatrice, Witte, Otto W., Steinbach, Robert, Hübner, Christian A., Graff, Caroline, Brylev, Lev, Fominykh, Vera, Demeshonok, Vera, Ataulina, Anastasia, Rogelj, Boris, Koritnik, Blaž, Zidar, Janez, Ravnik-Glavač, Metka, Glavač, Damjan, Stević, Zorica, Drory, Vivian, Povedano, Monica, Blair, Ian P., Kiernan, Matthew C., Benyamin, Beben, Henderson, Robert D., Furlong, Sarah, Mathers, Susan, McCombe, Pamela A., Needham, Merrilee, Ngo, Shyuan T., Nicholson, Garth A., Pamphlett, Roger, Rowe, Dominic B., Steyn, Frederik J., Williams, Kelly L., Mather, Karen A., Sachdev, Perminder S., Henders, Anjali K., Wallace, Leanne, de Carvalho, Mamede, Pinto, Susana, Petri, Susanne, Weber, Markus, Rouleau, Guy A., Silani, Vincenzo, Curtis, Charles J., Breen, Gerome, Glass, Jonathan D., Brown, Jr., Robert H., Landers, John E., Shaw, Christopher E., Andersen, Peter M., Groen, Ewout J. N., van Es, Michael A., Pasterkamp, R. Jeroen, Fan, Dongsheng, Garton, Fleur C., McRae, Allan F., Davey Smith, George, Gaunt, Tom R., Eberle, Michael A., Mill, Jonathan, McLaughlin, Russell L., Hardiman, Orla, Kenna, Kevin P., Wray, Naomi R., Tsai, Ellen, Runz, Heiko, Franke, Lude, Al-Chalabi, Ammar, Van Damme, Philip, van den Berg, Leonard H., and Veldink, Jan H.

Published
2022
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