Ramanan, Vijay K.Risacher, Shannon L.Nho, KwangsikKim, SungeunShen, LiMcDonald, Brenna C.Yoder, Karmen K.Hutchins, Gary D.West, John D.Tallman, Eileen F.Gao, SujuanForoud, Tatiana M.Farlow, Martin R.De Jager, Philip L.Bennett, David A.Aisen, Paul S.Petersen, Ronald C.Jack, Clifford R.Toga, Arthur W.Green, Robert C.Jagust, William J.Weiner, Michael W.Saykin, Andrew J.2016-12-152016-12-152015-10Ramanan, V. K., Risacher, S. L., Nho, K., Kim, S., Shen, L., McDonald, B. C., … Alzheimer’s Disease Neuroimaging Initiative (ADNI). (2015). GWAS of longitudinal amyloid accumulation on 18F-florbetapir PET in Alzheimer’s disease implicates microglial activation gene IL1RAP. Brain: A Journal of Neurology, 138(Pt 10), 3076–3088. http://doi.org/10.1093/brain/awv2310006-8950 1460-2156https://hdl.handle.net/1805/11625In a genome-wide study, Ramanan et al. discover an association between the microglial activation gene IL1RAP and higher rates of amyloid plaque accumulation as measured by PET in prodromal Alzheimer’s disease. Activated microglia may be crucial in amyloid clearance, and targeting the interleukin-1/IL1RAP pathway may be a potential therapeutic approach.en-USPublisher's PolicyAlzheimer’s diseaseamyloidgeneticsinterleukin-1microgliaGWAS of longitudinal amyloid accumulation on 18F-florbetapir PET in Alzheimer’s disease implicates microglial activation gene IL1RAP.Article