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1. Author Correction: Genetic meta-analysis of diagnosed Alzheimer's disease identifies new risk loci and implicates Aβ, tau, immunity and lipid processing

Author

Kunkle, Brian W, Grenier-Boley, Benjamin, Sims, Rebecca, Bis, Joshua C, Damotte, Vincent, Naj, Adam C, Boland, Anne, Vronskaya, Maria, van der Lee, Sven J, Amlie-Wolf, Alexandre, Bellenguez, Céline, Frizatti, Aura, Chouraki, Vincent, Martin, Eden R, Sleegers, Kristel, Badarinarayan, Nandini, Jakobsdottir, Johanna, Hamilton-Nelson, Kara L, Moreno-Grau, Sonia, Olaso, Robert, Raybould, Rachel, Chen, Yuning, Kuzma, Amanda B, Hiltunen, Mikko, Morgan, Taniesha, Ahmad, Shahzad, Vardarajan, Badri N, Epelbaum, Jacques, Hoffmann, Per, Boada, Merce, Beecham, Gary W, Garnier, Jean-Guillaume, Harold, Denise, Fitzpatrick, Annette L, Valladares, Otto, Moutet, Marie-Laure, Gerrish, Amy, Smith, Albert V, Qu, Liming, Bacq, Delphine, Denning, Nicola, Jian, Xueqiu, Zhao, Yi, Del Zompo, Maria, Fox, Nick C, Choi, Seung-Hoan, Mateo, Ignacio, Hughes, Joseph T, Adams, Hieab H, Malamon, John, Sanchez-Garcia, Florentino, Patel, Yogen, Brody, Jennifer A, Dombroski, Beth A, Naranjo, Maria Candida Deniz, Daniilidou, Makrina, Eiriksdottir, Gudny, Mukherjee, Shubhabrata, Wallon, David, Uphill, James, Aspelund, Thor, Cantwell, Laura B, Garzia, Fabienne, Galimberti, Daniela, Hofer, Edith, Butkiewicz, Mariusz, Fin, Bertrand, Scarpini, Elio, Sarnowski, Chloe, Bush, Will S, Meslage, Stéphane, Kornhuber, Johannes, White, Charles C, Song, Yuenjoo, Barber, Robert C, Engelborghs, Sebastiaan, Sordon, Sabrina, Voijnovic, Dina, Adams, Perrie M, Vandenberghe, Rik, Mayhaus, Manuel, Cupples, L Adrienne, Albert, Marilyn S, De Deyn, Peter P, Gu, Wei, Himali, Jayanadra J, Beekly, Duane, Squassina, Alessio, Hartmann, Annette M, Orellana, Adelina, Blacker, Deborah, Rodriguez-Rodriguez, Eloy, Lovestone, Simon, Garcia, Melissa E, Doody, Rachelle S, Munoz-Fernadez, Carmen, Sussams, Rebecca, Lin, Honghuang, Fairchild, Thomas J, and Benito, Yolanda A

Subjects
European Alzheimer’s Disease Initiative, Cohorts for Heart and Aging Research in Genomic Epidemiology Consortium, Genetic and Environmental Risk in AD/Defining Genetic, Alzheimer Disease Genetics Consortium, Polygenic and Environmental Risk for Alzheimer’s Disease Consortium, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

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

Published
2019

2. Genetic meta-analysis of diagnosed Alzheimer's disease identifies new risk loci and implicates Aβ, tau, immunity and lipid processing

Author

Kunkle, Brian W, Grenier-Boley, Benjamin, Sims, Rebecca, Bis, Joshua C, Damotte, Vincent, Naj, Adam C, Boland, Anne, Vronskaya, Maria, van der Lee, Sven J, Amlie-Wolf, Alexandre, Bellenguez, Céline, Frizatti, Aura, Chouraki, Vincent, Martin, Eden R, Sleegers, Kristel, Badarinarayan, Nandini, Jakobsdottir, Johanna, Hamilton-Nelson, Kara L, Moreno-Grau, Sonia, Olaso, Robert, Raybould, Rachel, Chen, Yuning, Kuzma, Amanda B, Hiltunen, Mikko, Morgan, Taniesha, Ahmad, Shahzad, Vardarajan, Badri N, Epelbaum, Jacques, Hoffmann, Per, Boada, Merce, Beecham, Gary W, Garnier, Jean-Guillaume, Harold, Denise, Fitzpatrick, Annette L, Valladares, Otto, Moutet, Marie-Laure, Gerrish, Amy, Smith, Albert V, Qu, Liming, Bacq, Delphine, Denning, Nicola, Jian, Xueqiu, Zhao, Yi, Del Zompo, Maria, Fox, Nick C, Choi, Seung-Hoan, Mateo, Ignacio, Hughes, Joseph T, Adams, Hieab H, Malamon, John, Sanchez-Garcia, Florentino, Patel, Yogen, Brody, Jennifer A, Dombroski, Beth A, Naranjo, Maria Candida Deniz, Daniilidou, Makrina, Eiriksdottir, Gudny, Mukherjee, Shubhabrata, Wallon, David, Uphill, James, Aspelund, Thor, Cantwell, Laura B, Garzia, Fabienne, Galimberti, Daniela, Hofer, Edith, Butkiewicz, Mariusz, Fin, Bertrand, Scarpini, Elio, Sarnowski, Chloe, Bush, Will S, Meslage, Stéphane, Kornhuber, Johannes, White, Charles C, Song, Yuenjoo, Barber, Robert C, Engelborghs, Sebastiaan, Sordon, Sabrina, Voijnovic, Dina, Adams, Perrie M, Vandenberghe, Rik, Mayhaus, Manuel, Cupples, L Adrienne, Albert, Marilyn S, De Deyn, Peter P, Gu, Wei, Himali, Jayanadra J, Beekly, Duane, Squassina, Alessio, Hartmann, Annette M, Orellana, Adelina, Blacker, Deborah, Rodriguez-Rodriguez, Eloy, Lovestone, Simon, Garcia, Melissa E, Doody, Rachelle S, Munoz-Fernadez, Carmen, Sussams, Rebecca, Lin, Honghuang, Fairchild, Thomas J, and Benito, Yolanda A

Subjects
Cohorts for Heart and Aging Research in Genomic Epidemiology Consortium (CHARGE), Male, Genetic and Environmental Risk in AD/Defining Genetic, Aging, European Alzheimer’s Disease Initiative (EADI), tau Proteins, Neurodegenerative, Alzheimer's Disease, Medical and Health Sciences, Alzheimer Disease, Clinical Research, Polygenic and Environmental Risk for Alzheimer’s Disease Consortium (GERAD/PERADES), Acquired Cognitive Impairment, Genetics, Humans, 2.1 Biological and endogenous factors, Genetic Predisposition to Disease, Genetic Testing, Aetiology, Aged, Amyloid beta-Peptides, Prevention, Inflammatory and immune system, Human Genome, Immunity, Neurosciences, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Biological Sciences, Lipid Metabolism, Lipids, Brain Disorders, Haplotypes, Alzheimer Disease Genetics Consortium (ADGC), Genetic Loci, Case-Control Studies, Neurological, Female, Dementia, Genome-Wide Association Study, Developmental Biology
Abstract

Risk for late-onset Alzheimer's disease (LOAD), the most prevalent dementia, is partially driven by genetics. To identify LOAD risk loci, we performed a large genome-wide association meta-analysis of clinically diagnosed LOAD (94,437 individuals). We confirm 20 previous LOAD risk loci and identify five new genome-wide loci (IQCK, ACE, ADAM10, ADAMTS1, and WWOX), two of which (ADAM10, ACE) were identified in a recent genome-wide association (GWAS)-by-familial-proxy of Alzheimer's or dementia. Fine-mapping of the human leukocyte antigen (HLA) region confirms the neurological and immune-mediated disease haplotype HLA-DR15 as a risk factor for LOAD. Pathway analysis implicates immunity, lipid metabolism, tau binding proteins, and amyloid precursor protein (APP) metabolism, showing that genetic variants affecting APP and Aβ processing are associated not only with early-onset autosomal dominant Alzheimer's disease but also with LOAD. Analyses of risk genes and pathways show enrichment for rare variants (P = 1.32 × 10-7), indicating that additional rare variants remain to be identified. We also identify important genetic correlations between LOAD and traits such as family history of dementia and education.

Published
2019

3. MAPT H1 haplotype is associated with late-onset Alzheimer's disease risk in APOE ε 4 noncarriers: Results from the dementia genetics Spanish consortium

Author

Pastor, Pau, Moreno, Fermín, Antonell, Anna, Elcoroaristizabal, Xabier, Lleó, Alberto, Blesa, Rafael, Fortea, Juan, Belbin, Olivia, Alcolea, Daniel, Carmona-Iragui, María, Sánchez-Saudinós, M Belén, Sala, Isabel, Anton-Aguirre, Sofía, Coto, Eliecer, Morenas, Estrella, Ribosa, Roser, Colom-Cadena, Martí, Cervera, Laura, Muñoz, Laia, Dols-Icardo, Oriol, Clarimón, Jordi, Ortega-Cubero, Sara, Hernandez, Isabel, Tárraga, Lluís, Boada, Mercè, Kulisevsky, Jaime, Vázquez-Higuera, José Luis, Infante, Jon, Rábano, Alberto, Fernández-Blázquez, Miguel Ángel, Valentí, Meritxell, Indakoetxea, Begoña, Barandiarán, Myriam, Gorostidi, Ana, Frank-García, Ana, Sastre, Isabel, Lorenzo, Elena, Ruiz, Agustín, Pastor, María A, Lennarz, Martina, Maier, Wolfgang, Rámirez, Alfredo, Serrano-Ríos, Manuel, Lee, Suzee E, Sánchez-Juan, Pascual, Consortium, Dementia Genetic Spanish, Combarros, Onofre, Lorenzo-Betancor, Oswaldo, Pastor, Maria A, Hernández, Isabel, Lafuente, Asunción, Rosende-Roca, Maitée, Mauleón, Ana, Vargas, Liliana, Rodríguez, Octavio, Calero, Miguel, Abdelnour, Carla, Alegret, Montserrat, Espinosa, Ana, Ortega, Gemma, Sanabria, Ángela, Ibarria, Marta, Diego, Susana, Canyabate, Pilar, Moreno, Mariola, Buendía, Mar, López de Munain, Adolfo, Pancho, Ana, Palacio, María Eugenia, Ruiz, Susana, Tantinya, Natalia, Tarragona, Marina, Morera, América, Guitart, Marina, Sotolongo Grau, Oscar, Martín, Elvira, Fernández, Victòria, Bullido, Maria J, Sánchez-Valle, Raquel, Molinuevo, José Luis, Lladó, Albert, Rami, Lorena, Alvarez, Victoria, de Pancorbo, Marian M, Pozueta, Ana, González Suarez, Andrea, Carro, Eva, Rodriguez-Rodriguez, Eloy, Mateo, Ignacio, Berciano, José, Bullido, María J, Instituto de Salud Carlos III, Ministerio de Ciencia e Innovación (España), Universidad Pública de Navarra, Universidad del País Vasco, Universidad Autónoma de Madrid, Fundació ACE. Institut Català de Neurociències Aplicades, University of Bonn, University of California, Universitat de Barcelona, Universitat Autònoma de Barcelona, and Universitat Oberta de Catalunya (UOC)

Subjects
Gerontology, Male, associació genètica, genetic association, Apolipoprotein E4, A152T, enfermedad de Alzheimer, genetics [Alzheimer Disease], frontotemporal dementia, MAPT, Alzheimer, Enfermedad de, genetics [Genetic Predisposition to Disease], genetics [Frontotemporal Dementia], genetics [Apolipoprotein E4], Aged, 80 and over, General Neuroscience, General Medicine, demencia frontotemporal, Middle Aged, Alzheimer's disease, Psychiatry and Mental health, Clinical Psychology, demència frontotemporal, genetics [Polymorphism, Single Nucleotide], Christian ministry, Female, Alzheimer’s disease, Frontotemporal dementia, Late onset, MAPT protein, human, tau Proteins, Polymorphism, Single Nucleotide, asociación genética, Alzheimer Disease, malaltia d'Alzheimer, mental disorders, medicine, Dementia, Humans, Genetic Predisposition to Disease, ddc:610, Genetic association, Aged, business.industry, Haplotype, medicine.disease, nervous system diseases, H1H2, genetics [tau Proteins], Alzheimer, Malaltia d', Logistic Models, Haplotypes, Spain, Disease risk, Geriatrics and Gerontology, business
Abstract

The MAPT H1 haplotype has been linked to several disorders, but its relationship with Alzheimer's disease (AD) remains controversial. A rare variant in MAPT (p.A152T) has been linked with frontotemporal dementia (FTD) and AD. We genotyped H1/H2 and p.A152T MAPT in 11,572 subjects from Spain (4,327 AD, 563 FTD, 648 Parkinson's disease (PD), 84 progressive supranuclear palsy (PSP), and 5,950 healthy controls). Additionally, we included 101 individuals from 21 families with genetic FTD. MAPT p.A152T was borderline significantly associated with FTD [odds ratio (OR)=2.03; p=0.063], but not with AD. MAPT H1 haplotype was associated with AD risk (OR=1.12; p=0.0005). Stratification analysis showed that this association was mainly driven by APOE ε4 noncarriers (OR=1.14; p=0.0025). MAPT H1 was also associated with risk for PD (OR=1.30; p=0.0003) and PSP (OR=3.18; p=8.59 × 10-8) but not FTD. Our results suggest that the MAPT H1 haplotype increases the risk of PD, PSP, and non-APOE ε4 AD., Spanish Ministry of Science and Innovation SAF 2006-10126 (2006–2009) and SAF2010-22329-C02-01 (2011–2013) to P.P and by the UTE project FIMA to P.P. Grants from the Ministry of Science (SAF2010-15558) and CIBERNED. Agust´ın Ruiz is supported by grant PI13/02434 (Acción Estratégica en Salud. Instituto de Salud Carlos III. Ministerio de Economía y Competitividad, Spain). Grant: Consolider (CSD2010-00045).

Published
2015
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