The <i>MS4A</i> gene cluster is a key modulator of soluble TREM2 and Alzheimer’s disease risk
Yuetiva Deming(University of Wisconsin–Madison), Fabia Filipello(Washington University in St. Louis), Francesca Cignarella(Washington University in St. Louis), Claudia Cantoni(Washington University in St. Louis), Simon Hsu(Washington University in St. Louis), Robert Mikesell(Washington University in St. Louis), Zeran Li(Washington University in St. Louis), Jorge L. Del‐Aguila(Washington University in St. Louis), Umber Dube(Washington University in St. Louis), Fabiana Farias(Washington University in St. Louis), Joseph Bradley(Washington University in St. Louis), John Budde(Washington University in St. Louis), Laura Ibáñez(Washington University in St. Louis), María Victoria Fernández(Washington University in St. Louis), Kaj Blennow(Sahlgrenska University Hospital), Henrik Zetterberg(Sahlgrenska University Hospital), Amanda Heslegrave(UK Dementia Research Institute), Per Johansson(Lund University), Johan Svensson(University of Gothenburg), Bengt Nellgård(Sahlgrenska University Hospital), Alberto Lleó(Universitat Autònoma de Barcelona), Daniel Alcolea(Universitat Autònoma de Barcelona), Jordi Clarimón(Universitat Autònoma de Barcelona), Lorena Rami(Hospital Clínic de Barcelona), José Luís Molinuevo(Pasqual Maragall Foundation), Marc Suárez‐Calvet(German Center for Neurodegenerative Diseases), Estrella Morenas‐Rodríguez(Munich Cluster for Systems Neurology), Gernot Kleinberger(Bioscience Research), Michael Ewers(Ludwig-Maximilians-Universität München), Oscar Harari(Washington University in St. Louis), Christian Haass(German Center for Neurodegenerative Diseases), Tom J. Brett(Washington University in St. Louis), Bruno A. Benítez(Washington University in St. Louis), Celeste M. Karch(Washington University in St. Louis), Laura Piccio(The University of Sydney), Carlos Cruchaga(Washington University in St. Louis)
Cited by 281Open Access
Abstract
Common variants in the microglia-specific MS4A gene cluster modify risk for late-onset Alzheimer’s disease and modulate extracellular soluble TREM2.