GWAS of longitudinal amyloid accumulation on18F-florbetapir PET in Alzheimer’s disease implicates microglial activation gene IL1RAP

Ramanan, Vijay K; Risacher, Shannon L.; Nho, Kwangsik; Kim, Sungeun; Shen, Li; McDonald, Brenna C.; Yoder, Karmen K.; Hutchins, Gary D.; West, John D.; Tallman, Eileen F.; Gao, Sujuan; Foroud, 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.; for the Alzheimer’s Disease Neuroimaging Initiative (ADNI)

doi:10.1093/brain/awv231

Cited by 133Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

GWAS of longitudinal amyloid accumulation on18F-florbetapir PET in Alzheimer’s disease implicates microglial activation gene IL1RAP

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Ramanan, Vijay K, Risacher, Shannon L., Nho, Kwangsik, Kim, Sungeun, Shen, Li, McDonald, Brenna C., Yoder, Karmen K., Hutchins, Gary D. +16 more·2015·Brain

DOI 10.1093/brain/awv231PMC PMC4671479

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Abstract

Brain amyloid deposition is thought to be a seminal event in Alzheimer’s disease. To identify genes influencing Alzheimer’s disease pathogenesis, we performed a genome-wide association study of longitudinal change in brain amyloid burden measured by 18F-florbetapir PET. A novel association with higher rates of amyloid accumulation independent from APOE (apolipoprotein E) ε4 status was identified in IL1RAP (interleukin-1 receptor accessory protein; rs12053868-G; P = 1.38 × 10−9) and was validated by deep sequencing. IL1RAP rs12053868-G carriers were more likely to progress from mild cognitive impairment to Alzheimer’s disease and exhibited greater longitudinal temporal cortex atrophy on MRI. In independent cohorts rs12053868-G was associated with accelerated cognitive decline and lower cortical 11C-PBR28 PET signal, a marker of microglial activation. These results suggest a crucial role of activated microglia in limiting amyloid accumulation and nominate the IL-1/IL1RAP pathway as a potential target for modulating this process. In 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.

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A combined analysis of neuroimaging and genetic data found an association between a polymorphism in the IL1RAP gene and increased rate of Aβ accumulation in human brains of both AD and non-AD subjects.
“A combined analysis of neuroimaging and genetic data found an association between a polymorphism in the IL1RAP gene and increased rate of Aβ accumulation in human brains of both AD and non-AD subjects (measured by Aβ-binding positron emission tomography tracer; Ramanan et al., 2015).”
From Microglia in Alzheimer’s disease (2018) · cites this paper as Ramanan et al., 2015
Early microglial activation in response to amyloid plaques, as assessed by in vivo microglial imaging, is correlated with increased grey matter volume and reduced rate of cognitive decline.
“This is consistent with the finding that early microglial activation in response to amyloid plaques, as assessed by in vivo microglial imaging studies, is correlated with increased grey matter volume and reduced rate of cognitive decline46,47.”
From Large-scale proteomic analysis of Alzheimer’s disease brain and cerebrospinal fluid reveals early changes in energy metabolism associated with microglia and astrocyte activation (2020) · cites this paper as [47]

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Authors: Ramanan, V. K., Risacher, S. L., Nho, K., Kim, S., Shen, L., McDonald, B. C., Yoder, K. K., Hutchins, G. D., West, J. D., Tallman, E. F., Gao, S., Foroud, T. M., Farlow, M. R., De Jager, P. L., Bennett, D. A., Aisen, P. S., Petersen, R. C., Jack, C. R., Toga, A. W., Green, R. C., Jagust, W. J., Weiner, M. W., Saykin, A. J., & (ADNI), F. T. A. D. N. I.
Affiliations: Indiana University Indianapolis (US)
Rush University Medical Center (US)
University of Southern California (US)
Mayo Clinic (US)
Brigham and Women's Hospital (US)
University of California, Berkeley (US)
San Francisco VA Medical Center (US)
ORCID: Ramanan, Vijay K
Risacher, Shannon L.
Nho, Kwangsik
Kim, Sungeun
Shen, Li
McDonald, Brenna C.
Yoder, Karmen K.
Hutchins, Gary D.
West, John D.
Gao, Sujuan
Foroud, Tatiana M.
Farlow, Martin R.
Bennett, David A.
Petersen, Ronald C.
Jack, Clifford R.
Toga, Arthur W.
Green, Robert C.
Jagust, William J.
Weiner, Michael W.
Saykin, Andrew J.
Venue: Brain
Publisher: Oxford University Press (OUP)
Published: 2015-08-11
Volume: 138
Issue: 10
Pages: 3076-3088
ISSN: 0006-8950 (ISSN-L)
1460-2156
DOI: 10.1093/brain/awv231
PMC: PMC4671479
OpenAlex: W2175730819
Cited by: 133
References: 92
Citations by year: 2026: 5 · 2025: 12 · 2024: 9 · 2023: 5 · 2022: 8 · 2021: 18 · 2020: 17 · 2019: 21 · 2018: 11 · 2017: 12 · 2016: 13 · 2015: 1
FWCI: 8.99
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Brain (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
eScholarship (California Digital Library) (submittedVersion)
HighWire Press Open Archive (submittedVersion)
IUScholarWorks (Indiana University) (submittedVersion)
Purdue University Indianapolis (Indiana University) (submittedVersion)
PMC
Funders: National Science Foundation (1117335, 0521433, P30AG010129, W81XWH-12-2-0012, U01 AG024904)
U.S. Department of Defense (U01 AG024904, AG024904)
Alzheimer's Association (K01 AG030514, P30AG10161, AG010129, R01 AG15819, U01 AG024904, P30 AG010129, W81XWH-12-2-0012)
Bristol-Myers Squibb (U01 AG024904, AG024904, W81XWH-12-2-0012)
Eli Lilly and Company (U01 AG024904, AG024904, W81XWH-12-2-0012)
Pfizer (AG024904, W81XWH-12-2-0012, U01 AG024904)
Biogen (W81XWH-12-2-0012, U01 AG024904, AG024904)
University of Southern California (R01 AG15819, W81XWH-12-2-0012, P30 AG10161, U01 AG024904)
Indiana Clinical and Translational Sciences Institute (U54-RR025761, RR020128, RR027710, RR025761)
Lilly Endowment
F. Hoffmann-La Roche (W81XWH-12-2-0012, AG024904, U01 AG024904)
Medpace (U01 AG024904)
Meso Scale Diagnostics (U01 AG024904, AG024904, W81XWH-12-2-0012)
Synarc (U01 AG024904, P30 AG010129, K01 AG030514)
BioClinica (U01 AG024904, W81XWH-12-2-0012, AG024904)
Novartis Pharmaceuticals Corporation (W81XWH-12-2-0012, U01 AG024904, AG024904)
Northern California Institute for Research and Education (U01 AG024904, W81XWH-12-2-0012, K01 AG030514, P30 AG010129)
Brin Wojcicki Foundation
Eisai (W81XWH-12-2-0012, U01 AG024904, AG024904)
Servier (AG024904, W81XWH-12-2-0012, U01 AG024904)
IXICO (AG024904, W81XWH-12-2-0012, U01 AG024904)
National Institutes of Health (UL1TR001108, 1c06rr020128-01, 5u01ag024904-10, W81XWH-12-2-0012, U01-AG024904, AG09466, AG010129, AG024904, AG10161, AG15819, RR025761)
Genentech (W81XWH-12-2-0012, AG024904, U01 AG024904)
University of California, San Diego (K01 AG030514)
Canadian Institutes of Health Research (U01 AG024904, W81XWH-12-2-0012, K01 AG030514, P30 AG010129)
National Institute on Aging (U01-AG-024904, R01AG017917, P30AG010129, P30AG010133, AG34374, K01AG049050, AG-17917, K01AG030514, R01AG015819, P30AG010161, P50AG005142, P01AG009466, R01AG019771, RF1AG015819, R01AG034374, U24AG021886)
National Institute of Biomedical Imaging and Bioengineering (P41EB015922)
U.S. National Library of Medicine (R01LM011360, R00LM011384)
National Center for Research Resources (U54 RR025761, RR027710-01, S10RR027710, RR020128, UL1RR025761, C06-RR020128)
National Center for Advancing Translational Sciences
Topics: Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords: Alzheimer's disease, IL1RAP, microglial activation, 18F-florbetapir PET, APOE ε4, mild cognitive impairment, cognitive decline, amyloid clearance, prodromal Alzheimer's disease
MeSH terms: Acetamides, Aged, Aged, 80 and over, Alzheimer Disease, Amyloid, Aniline Compounds, Cerebral Cortex, Ethylene Glycols, Female, Genotype, Humans, Longitudinal Studies, Male, Pyridines, Polymorphism, Single Nucleotide, Positron-Emission Tomography, Apolipoprotein E4, Interleukin-1 Receptor Accessory Protein, Genetic Association Studies

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GWAS of longitudinal amyloid accumulation on18F-florbetapir PET in Alzheimer’s disease implicates microglial activation gene IL1RAP

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