New insights into the genetic etiology of Alzheimer’s disease and related dementias
Characterization of the genetic landscape of Alzheimer’s disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/‘pro...
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| Published in: | Nature genetics Vol. 54; no. 4; pp. 412 - 436 |
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| Main Authors: | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
| Published: |
New York
Nature Publishing Group US
01.04.2022
Nature Publishing Group |
| Subjects: | |
| ISSN: | 1061-4036, 1546-1718, 1546-1718 |
| Online Access: | Get full text |
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| Abstract | Characterization of the genetic landscape of Alzheimer’s disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/‘proxy’ AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the
APOE
ε4 allele.
Meta-analysis of genome-wide association studies on Alzheimer’s disease and related dementias identifies new loci and enables generation of a new genetic risk score associated with the risk of future Alzheimer’s disease and dementia. |
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| AbstractList | Characterization of the genetic landscape of Alzheimer's disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/'proxy' AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele. Characterization of the genetic landscape of Alzheimer's disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/'proxy' AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE epsilon 4 allele. Meta-analysis of genome-wide association studies on Alzheimer's disease and related dementias identifies new loci and enables generation of a new genetic risk score associated with the risk of future Alzheimer's disease and dementia. Characterization of the genetic landscape of Alzheimer’s disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/‘proxy’ AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele. Meta-analysis of genome-wide association studies on Alzheimer’s disease and related dementias identifies new loci and enables generation of a new genetic risk score associated with the risk of future Alzheimer’s disease and dementia. Characterization of the genetic landscape of Alzheimer’s disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/‘proxy’ AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele. Meta-analysis of genome-wide association studies on Alzheimer’s disease and related dementias identifies new loci and enables generation of a new genetic risk score associated with the risk of future Alzheimer’s disease and dementia. Characterization of the genetic landscape of Alzheimer's disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/'proxy' AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele.Characterization of the genetic landscape of Alzheimer's disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/'proxy' AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele. Characterization of the genetic landscape of Alzheimer’s disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/‘proxy’ AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele. |
| Author | Cuccaro, Michael L. Peloso, Gina Peters, Oliver Schmid, Matthias Fin, Bertrand Windle, Gill Montes, Angel Martín Fornage, Myriam Amin, Najaf Archetti, Silvana Song, Yeunjoo Binetti, Giuliano Medina, Miguel Galimberti, Daniela Sakka, Paraskevi Tybjærg-Hansen, Anne Kilander, Lena Pastor, Ana Belén Eiriksdottir, Gudny Bressler, Jan de Rojas, Itziar Bizarro, Alessandra Reyes-Dumeyer, Dolly Chen, Hung-Hsin Kauwe, John Masullo, Carlo Vandenberghe, Rik Wiltfang, Jens Stordal, Eystein Pineda, Juan A. Boerwinkle, Eric Moebus, Susanne Rainero, Innocenzo Lunetta, Kathryn L. Fenoglio, Chiara Hampel, Harald Sha, Jin Lopez, Oscar Padovani, Alessandro Royo, Jose Luis Hiltunen, Mikko Menéndez-González, Manuel Nordestgaard, Børge G. Lauria, Alessandra Armstrong, Nicola J. Alegret, Montserrat Boada, Mercè Scamosci, Michela Spottke, Annika Frank-García, Ana Rodriguez-Rodriguez, Eloy Damotte, Vincent Roberto, Natalia Kleineidam, Luca Holstege, Henne Pericard, Pierre Aarsland, Dag Sorbi, Sandro Nielsen, Sune Fallgaard Fongang, Bernard Ewers, Michael Barral, Sandra Ha |
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organization: German Center for Neurodegenerative Diseases (DZNE Bonn), Institute of Medical Biometry, Informatics and Epidemiology, University Hospital of Bonn – sequence: 314 givenname: Anja surname: Schneider fullname: Schneider, Anja organization: Department of Neurodegenerative Diseases and Geriatric Psychiatry, University Hospital Bonn, German Center for Neurodegenerative Diseases (DZNE Bonn) – sequence: 318 givenname: Manuel surname: Serrano fullname: Serrano, Manuel organization: Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas, CIBERDEM, Hospital Clínico San Carlos – sequence: 326 givenname: Alina surname: Solomon fullname: Solomon, Alina organization: Institute of Clinical Medicine, Neurology, University of Eastern, Division of Clinical Geriatrics, Center for Alzheimer Research, Care Sciences and Society (NVS), Karolinska Institutet – sequence: 327 givenname: Yeunjoo orcidid: 0000-0002-7452-3731 surname: Song fullname: Song, Yeunjoo 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Lluís surname: Tárraga fullname: Tárraga, Lluís organization: Research Center and Memory Clinic Fundació ACE, Institut Català de Neurociències Aplicades, Universitat Internacional de Catalunya, CIBERNED, Network Center for Biomedical Research in Neurodegenerative Diseases, National Institute of Health Carlos III – sequence: 338 givenname: Tegos surname: Thomas fullname: Thomas, Tegos organization: First Department of Neurology, Medical School, Aristotle University of Thessaloniki, Alzheimer Hellas – sequence: 339 givenname: Giuseppe orcidid: 0000-0001-7075-8245 surname: Tosto fullname: Tosto, Giuseppe organization: Taub Institute on Alzheimer’s Disease and the Aging Brain, Department of Neurology, Columbia University, Department of Neurology, Columbia University – sequence: 361 givenname: David orcidid: 0000-0002-2634-7198 surname: Wallon fullname: Wallon, David organization: Department of Neurology and CNR-MAJ, F 76000, Normandy Center for Genomic and Personalized Medicine, Normandie University, UNIROUEN, INSERM U1245, CHU Rouen – sequence: 362 givenname: Li-San surname: Wang fullname: Wang, Li-San organization: Department of Pathology and Laboratory Medicine, University of Pennsylvania Perelman School of Medicine – sequence: 364 givenname: Leonie surname: Weinhold fullname: Weinhold, Leonie organization: Institute of Medical Biometry, Informatics and Epidemiology, University Hospital of Bonn – sequence: 365 givenname: Jens orcidid: 0000-0003-1492-5330 surname: Wiltfang fullname: Wiltfang, Jens organization: Department of Psychiatry and Psychotherapy, University Medical Center Goettingen, German Center for Neurodegenerative Diseases (DZNE), Medical Science Department, iBiMED – sequence: 369 givenname: Habil orcidid: 0000-0001-5902-6238 surname: Zare fullname: Zare, Habil organization: Glenn Biggs Institute for Alzheimer’s & Neurodegenerative Diseases, University of Texas Health Sciences Center – sequence: 383 givenname: Lindsay A. orcidid: 0000-0001-5533-4225 surname: Farrer fullname: Farrer, Lindsay A. organization: Institute of Biomedicine, University of Eastern Finland, Medicine Biomedical Genetics Boston University School of Medicine, Department of Neurology, Boston University School of Medicine – sequence: 384 givenname: Bruce M. orcidid: 0000-0002-7278-2190 surname: Psaty fullname: Psaty, Bruce M. organization: Framingham Heart Study, Department of Pathology and Laboratory Medicine, University of Pennsylvania, Department of Health Service, University of Washington – sequence: 396 givenname: Julie orcidid: 0000-0002-4069-0259 surname: Williams fullname: Williams, Julie organization: MRC Centre for Neuropsychiatric Genetics and Genomics, Division of Psychological Medicine and Clinical Neuroscience, School of Medicine, Cardiff University, UKDRI@ Cardiff, School of Medicine, Cardiff University – sequence: 397 givenname: Ruth orcidid: 0000-0003-4084-5027 surname: Frikke-Schmidt fullname: Frikke-Schmidt, Ruth organization: Department of Clinical Medicine, University of Copenhagen, Department of Clinical Biochemistry, Rigshospitalet – sequence: 399 givenname: Jean-François surname: Deleuze fullname: Deleuze, Jean-François organization: CEA, Centre National de Recherche en Génomique Humaine, Université Paris-Saclay |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/35379992$$D View this record in MEDLINE/PubMed https://hal.science/hal-03668928$$DView record in HAL https://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-204358$$DView record from Swedish Publication Index (Stockholms universitet) https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-473589$$DView record from Swedish Publication Index (Uppsala universitet) http://kipublications.ki.se/Default.aspx?queryparsed=id:149225642$$DView record from Swedish Publication Index (Karolinska Institutet) |
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| Contributor | Rodrigo-Herrero, Silvia Roveta, Fausto Escuela, R Vigo-Ortega, R Shofany, Jacob Laatikainen, Tiina Rossor, Martin Zoia, Chiara Paola Labrador, Ma Periñán, Mt Gurling, Hugh Collinge, John Strandberg, Timo Matoska, Vaclav Mauleón, Ana Peltonen, Markku O'Donovan, Michael C Takalo, Mari Anastasiou, Costas Zompo, Maria Del Fox, Nick Alonso, María Dolores Benussi, Alberto Sala, Gessica Macias-García, D Mummery, Catherine Natunen, Teemu Proitsi, Petra Vacca, Alessandro Antikainen, Riitta Laske, Christoph Shaw, Christopher E Gwilliam, Rhian Vargas, Liliana Bass, Nicholas J Diego, Susana Chipi, Elena Merlín, Isabel Sastre Guitart, Marina Owen, Michael J Perneczky, Robert Aguilera, Nuria Lindström, Jaana Serpente, Maria Piras, Federica Boecker, Henning McGuinness, Bernadette Carrion-Claro, M Bastiani, Patrizia Ciullo, Valentina Lacidogna, Giordano Adarmes-Gómez, Ad Gailhajenet, Anna Jones, Lesley Passmore, Peter Powell, John F Pineda-Sánchez, R Marín, M Preckler, Silvia Ibarria, Marta Martín, Elvira Cañabate, Pilar Laczo, Jan Jesús, S Lawlor, Brian Lynch, Aoi |
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| PublicationDate | 2022-04-01 |
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| PublicationTitle | Nature genetics |
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| PublicationYear | 2022 |
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| Title | New insights into the genetic etiology of Alzheimer’s disease and related dementias |
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