Attenzione: i dati modificati non sono ancora stati salvati. Per confermare inserimenti o cancellazioni di voci è necessario confermare con il tasto SALVA/INSERISCI in fondo alla pagina
IRIS
Bipolar disorder is a leading contributor to the global burden of disease1. Despite high heritability (60–80%), the majority of the underlying genetic determinants remain unknown2. We analysed data from participants of European, East Asian, African American and Latino ancestries (n = 158,036 cases with bipolar disorder, 2.8 million controls), combining clinical, community and self-reported samples. We identified 298 genome-wide significant loci in the multi-ancestry meta-analysis, a fourfold increase over previous findings3, and identified an ancestry-specific association in the East Asian cohort. Integrating results from fine-mapping and other variant-to-gene mapping approaches identified 36 credible genes in the aetiology of bipolar disorder. Genes prioritized through fine-mapping were enriched for ultra-rare damaging missense and protein-truncating variations in cases with bipolar disorder4, highlighting convergence of common and rare variant signals. We report differences in the genetic architecture of bipolar disorder depending on the source of patient ascertainment and on bipolar disorder subtype (type I or type II). Several analyses implicate specific cell types in the pathophysiology of bipolar disorder, including GABAergic interneurons and medium spiny neurons. Together, these analyses provide additional insights into the genetic architecture and biological underpinnings of bipolar disorder.
Genomics yields biological and phenotypic insights into bipolar disorder
O'Connell, Kevin S;Koromina, Maria;van der Veen, Tracey;Boltz, Toni;David, Friederike S;Yang, Jessica Mei Kay;Lin, Keng-Han;Wang, Xin;Coleman, Jonathan R I;Mitchell, Brittany L;McGrouther, Caroline C;Rangan, Aaditya V;Lind, Penelope A;Koch, Elise;Harder, Arvid;Parker, Nadine;Bendl, Jaroslav;Adorjan, Kristina;Agerbo, Esben;Albani, Diego;Alemany, Silvia;Alliey-Rodriguez, Ney;Als, Thomas D;Andlauer, Till F M;Antoniou, Anastasia;Ask, Helga;Bass, Nicholas;Bauer, Michael;Beins, Eva C;Bigdeli, Tim B;Pedersen, Carsten Bøcker;Boks, Marco P;Børte, Sigrid;Bosch, Rosa;Brum, Murielle;Brumpton, Ben M;Brunkhorst-Kanaan, Nathalie;Budde, Monika;Bybjerg-Grauholm, Jonas;Byerley, William;Cabana-Domínguez, Judit;Cairns, Murray J;Carpiniello, Bernardo;Casas, Miquel;Cervantes, Pablo;Chatzinakos, Chris;Chen, Hsi-Chung;Clarence, Tereza;Clarke, Toni-Kim;Claus, Isabelle;Coombes, Brandon;Corfield, Elizabeth C;Cruceanu, Cristiana;Cuellar-Barboza, Alfredo;Czerski, Piotr M;Dafnas, Konstantinos;Dale, Anders M;Dalkner, Nina;Degenhardt, Franziska;DePaulo, J Raymond;Djurovic, Srdjan;Drange, Ole Kristian;Escott-Price, Valentina;Fanous, Ayman H;Fellendorf, Frederike T;Ferrier, I Nicol;Forty, Liz;Frank, Josef;Frei, Oleksandr;Freimer, Nelson B;Fullard, John F;Garnham, Julie;Gizer, Ian R;Gordon, Scott D;Gordon-Smith, Katherine;Greenwood, Tiffany A;Grove, Jakob;Guzman-Parra, José;Ha, Tae Hyon;Hahn, Tim;Haraldsson, Magnus;Hautzinger, Martin;Havdahl, Alexandra;Heilbronner, Urs;Hellgren, Dennis;Herms, Stefan;Hickie, Ian B;Hoffmann, Per;Holmans, Peter A;Huang, Ming-Chyi;Ikeda, Masashi;Jamain, Stéphane;Johnson, Jessica S;Jonsson, Lina;Kalman, Janos L;Kamatani, Yoichiro;Kennedy, James L;Kim, Euitae;Kim, Jaeyoung;Kittel-Schneider, Sarah;Knowles, James A;Kogevinas, Manolis;Kranz, Thorsten M;Krebs, Kristi;Kushner, Steven A;Lavebratt, Catharina;Lawrence, Jacob;Leber, Markus;Lee, Heon-Jeong;Liao, Calwing;Lucae, Susanne;Lundberg, Martin;MacIntyre, Donald J;Maier, Wolfgang;Maihofer, Adam X;Malaspina, Dolores;Manchia, Mirko;Maratou, Eirini;Martinsson, Lina;Mattheisen, Manuel;McGregor, Nathaniel W;McInnis, Melvin G;McKay, James D;Medeiros, Helena;Meyer-Lindenberg, Andreas;Millischer, Vincent;Morris, Derek W;Moutsatsou, Paraskevi;Mühleisen, Thomas W;O'Donovan, Claire;Olsen, Catherine M;Panagiotaropoulou, Georgia;Papiol, Sergi;Pardiñas, Antonio F;Park, Hye Youn;Perry, Amy;Pfennig, Andrea;Pisanu, Claudia;Potash, James B;Quested, Digby;Rapaport, Mark H;Regeer, Eline J;Rice, John P;Rivera, Margarita;Schulte, Eva C;Senner, Fanny;Shadrin, Alexey;Shilling, Paul D;Sigurdsson, Engilbert;Sindermann, Lisa;Sirignano, Lea;Siskind, Dan;Slaney, Claire;Sloofman, Laura G;Smeland, Olav B;Smith, Daniel J;Sobell, Janet L;Soler Artigas, Maria;Stein, Dan J;Stein, Frederike;Su, Mei-Hsin;Sung, Heejong;Świątkowska, Beata;Terao, Chikashi;Tesfaye, Markos;Tesli, Martin;Thorgeirsson, Thorgeir E;Thorp, Jackson G;Toma, Claudio;Tondo, Leonardo;Tooney, Paul A;Tsai, Shih-Jen;Tsermpini, Evangelia Eirini;Vawter, Marquis P;Vedder, Helmut;Vreeker, Annabel;Walters, James T R;Winsvold, Bendik S;Witt, Stephanie H;Won, Hong-Hee;Ye, Robert;Young, Allan H;Zandi, Peter P;Zillich, Lea;Adolfsson, Rolf;Alda, Martin;Alfredsson, Lars;Backlund, Lena;Baune, Bernhard T;Bellivier, Frank;Bengesser, Susanne;Berrettini, Wade H;Biernacka, Joanna M;Boehnke, Michael;Børglum, Anders D;Breen, Gerome;Carr, Vaughan J;Catts, Stanley;Cichon, Sven;Corvin, Aiden;Craddock, Nicholas;Dannlowski, Udo;Dikeos, Dimitris;Etain, Bruno;Ferentinos, Panagiotis;Frye, Mark;Fullerton, Janice M;Gawlik, Micha;Gershon, Elliot S;Goes, Fernando S;Green, Melissa J;Grigoroiu-Serbanescu, Maria;Hauser, Joanna;Henskens, Frans A;Hjerling-Leffler, Jens;Hougaard, David M;Hveem, Kristian;Iwata, Nakao;Jones, Ian;Jones, Lisa A;Kahn, René S;Kelsoe, John R;Kircher, Tilo;Kirov, George;Kuo, Po-Hsiu;Landén, Mikael;Leboyer, Marion;Li, Qingqin S;Lissowska, Jolanta;Lochner, Christine;Loughland, Carmel;Luykx, Jurjen J;Martin, Nicholas G;Mathews, Carol A;Mayoral, Fermin;McElroy, Susan L;McIntosh, Andrew M;McMahon, Francis J;Medland, Sarah E;Melle, Ingrid;Milani, Lili;Mitchell, Philip B;Morken, Gunnar;Mors, Ole;Mortensen, Preben Bo;Müller-Myhsok, Bertram;Myers, Richard M;Myung, Woojae;Neale, Benjamin M;Nievergelt, Caroline M;Nordentoft, Merete;Nöthen, Markus M;Nurnberger, John I;O'Donovan, Michael C;Oedegaard, Ketil J;Olsson, Tomas;Owen, Michael J;Paciga, Sara A;Pantelis, Christos;Pato, Carlos N;Pato, Michele T;Patrinos, George P;Pawlak, Joanna M;Ramos-Quiroga, Josep Antoni;Reif, Andreas;Reininghaus, Eva Z;Ribasés, Marta;Rietschel, Marcella;Ripke, Stephan;Rouleau, Guy A;Roussos, Panos;Saito, Takeo;Schall, Ulrich;Schalling, Martin;Schofield, Peter R;Schulze, Thomas G;Scott, Laura J;Scott, Rodney J;Serretti, Alessandro;Smoller, Jordan W;Squassina, Alessio;Stahl, Eli A;Stefansson, Hreinn;Stefansson, Kari;Stordal, Eystein;Streit, Fabian;Sullivan, Patrick F;Turecki, Gustavo;Vaaler, Arne E;Vieta, Eduard;Vincent, John B;Waldman, Irwin D;Weickert, Cynthia S;Weickert, Thomas W;Werge, Thomas;Whiteman, David C;Zwart, John-Anker;Edenberg, Howard J;McQuillin, Andrew;Forstner, Andreas J;Mullins, Niamh;Di Florio, Arianna;Ophoff, Roel A;Andreassen, Ole A
2025-01-01
Abstract
Bipolar disorder is a leading contributor to the global burden of disease1. Despite high heritability (60–80%), the majority of the underlying genetic determinants remain unknown2. We analysed data from participants of European, East Asian, African American and Latino ancestries (n = 158,036 cases with bipolar disorder, 2.8 million controls), combining clinical, community and self-reported samples. We identified 298 genome-wide significant loci in the multi-ancestry meta-analysis, a fourfold increase over previous findings3, and identified an ancestry-specific association in the East Asian cohort. Integrating results from fine-mapping and other variant-to-gene mapping approaches identified 36 credible genes in the aetiology of bipolar disorder. Genes prioritized through fine-mapping were enriched for ultra-rare damaging missense and protein-truncating variations in cases with bipolar disorder4, highlighting convergence of common and rare variant signals. We report differences in the genetic architecture of bipolar disorder depending on the source of patient ascertainment and on bipolar disorder subtype (type I or type II). Several analyses implicate specific cell types in the pathophysiology of bipolar disorder, including GABAergic interneurons and medium spiny neurons. Together, these analyses provide additional insights into the genetic architecture and biological underpinnings of bipolar disorder.
I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11387/191358
Citazioni
ND
6
ND
social impact
Conferma cancellazione
Sei sicuro che questo prodotto debba essere cancellato?
simulazione ASN
Il report seguente simula gli indicatori relativi alla propria produzione scientifica in relazione alle soglie ASN 2023-2025 del proprio SC/SSD. Si ricorda che il superamento dei valori soglia (almeno 2 su 3) è requisito necessario ma non sufficiente al conseguimento dell'abilitazione. La simulazione si basa sui dati IRIS e sugli indicatori bibliometrici alla data indicata e non tiene conto di eventuali periodi di congedo obbligatorio, che in sede di domanda ASN danno diritto a incrementi percentuali dei valori. La simulazione può differire dall'esito di un’eventuale domanda ASN sia per errori di catalogazione e/o dati mancanti in IRIS, sia per la variabilità dei dati bibliometrici nel tempo. Si consideri che Anvur calcola i valori degli indicatori all'ultima data utile per la presentazione delle domande.
La presente simulazione è stata realizzata sulla base delle specifiche raccolte sul tavolo ER del Focus Group IRIS coordinato dall’Università di Modena e Reggio Emilia e delle regole riportate nel DM 589/2018 e allegata Tabella A. Cineca, l’Università di Modena e Reggio Emilia e il Focus Group IRIS non si assumono alcuna responsabilità in merito all’uso che il diretto interessato o terzi faranno della simulazione. Si specifica inoltre che la simulazione contiene calcoli effettuati con dati e algoritmi di pubblico dominio e deve quindi essere considerata come un mero ausilio al calcolo svolgibile manualmente o con strumenti equivalenti.