A genome-wide association study with 1,126,563 individuals identifies new risk loci for Alzheimer’s disease
Open accessAbstract
Late-onset Alzheimer’s disease is a prevalent age-related polygenic disease that accounts for 50–70% of dementia cases. Currently, only a fraction of the genetic variants underlying Alzheimer’s disease have been identified. Here we show that increased sample sizes allowed identification of seven previously unidentified genetic loci contributing to Alzheimer’s disease. This study highlights microglia, immune cells and protein catabolism as relevant to late-onset Alzheimer’s disease, while identifying and prioritizing previously unidentified genes of potential interest. We anticipate that these results can be included in larger meta-analyses of Alzheimer’s disease to identify further genetic variants that contribute to Alzheimer’s pathology. A genome-wide association study performed in 1,126,563 individuals identifies seven new loci associated with Alzheimer’s disease and implicates microglia and immune cells in late-onset disease.
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More than 90 genetic loci are associated with Alzheimer's disease and related dementia (ADRD).
“More than 90 genetic loci are associated with Alzheimer’s disease and related dementia (ADRD).”
From Consensus meta-analysis of genome-wide association studies for Alzheimer’s disease and related dementias (2026) · cites this paper as [5]
The Genome-wide inferences section reports 38 independent loci associated with late-onset Alzheimer’s disease, not more than 90. The paper does not report a count of more than 90 loci for Alzheimer’s disease and related dementia. (LLM, conf=0.88)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredNine loci (APP, CCDC6, GRN, LILRB2, NCK2, TNIP1, TMEM106B, TSPAN14 and SHARPIN) were recently reported in three articles using part of the GWAS data included in the study.
“Nine of these loci (APP, CCDC6, GRN, LILRB2, NCK2, TNIP1, TMEM106B, TSPAN14 and SHARPIN) were recently reported in three articles using part of the GWAS data included in our study11–13.”
From New insights into the genetic etiology of Alzheimer’s disease and related dementias (2022) · cites this paper as [13]
Table 1 (Functional enrichment of significantly associated regions; page unavailable) lists eight of the nine named loci as GWAS risk loci. It does not list TSPAN14, and this source alone does not establish that the three cited articles collectively reported all nine loci or used part of the citing study’s data. (LLM, conf=0.84)
Experimental — accuracy not yet measuredIndependent association signals detected in the CD33, HLA, PICALM and RHOH loci are new compared to refs. 4-6,9.
“Compared to refs. 4–6,9, the independent association signals detected in the CD33, HLA, PICALM and RHOH loci are new”
From Consensus meta-analysis of genome-wide association studies for Alzheimer’s disease and related dementias (2026) · cites this paper as [5]
Table 1 and the Genome-wide inferences section (page unavailable) report associations at CD33, HLA-DRB1 and PICALM among 38 independent loci. They do not establish that signals at those loci are new relative to refs. 4–6,9, and the passages found do not identify a RHOH signal. (LLM, conf=0.79)
Experimental — accuracy not yet measuredRecent GWAS have identified several genes associated with AD that are predominantly or exclusively expressed in myeloid cells, including INPP5D.
“Recent genome-wide association studies (GWAS) have identified several genes associated with AD that are predominantly or exclusively expressed in myeloid cells, including INPP5D (inositol polyphosphate 5-phosphatase 1), which encodes SHIP17–10.”
From INPP5D/SHIP1 regulates endo-lysosomal function and cargo-selective phagocytosis in human microglia (2025) · cites this paper as [10]
The Tissue type, cell type and gene-set enrichment section (page unavailable) reports that Alzheimer’s-associated genes are enriched in microglia, supporting the broad link between GWAS findings and immune-related cells. The passages do not identify INPP5D as an associated gene or establish that it is predominantly or exclusively expressed in myeloid cells; searches for INPP5D and myeloid-cell expression found no such passage. (LLM, conf=0.82)
Experimental — accuracy not yet measuredLarge-scale GWAS meta-analyses have highlighted immune and myeloid cell pathways as major contributors to Alzheimer's disease risk and progression, even when individual genes do not reach genome-wide significance thresholds.
“Large-scale GWAS meta-analyses have highlighted immune and myeloid cell pathways as major contributors to Alzheimer’s disease risk and progression, even when individual genes do not reach genome-wide significance thresholds [97].”
From Genetic drivers of progression in Alzheimer’s disease are distinct from disease risk (2026) · cites this paper as [97]
The Tissue type, cell type and gene-set enrichment section (page unavailable) reports significant immune-cell recruitment gene sets and microglial enrichment, supporting a role in late-onset Alzheimer’s disease risk. It does not establish an effect on disease progression or say that these pathway findings persist when individual genes fail to reach genome-wide significance. (LLM, conf=0.86)
Experimental — accuracy not yet measured
Over 70 loci are associated with conferring risk for late-onset Alzheimer's disease.
“In recent years, genome wide association studies (GWASs) and analyses of rare-coding variants have identified over 70 loci associated with conferring risk for late-onset AD (LOAD).”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [8]
The Genome-wide inferences section reports 38 independent LOAD-associated loci, including seven not previously associated with LOAD in GWAS. It supports the existence of multiple risk loci, but does not substantiate the citing sentence’s count of over 70 across GWAS and rare-coding-variant analyses. No page number is available in our copy. (LLM, conf=0.84)
Experimental — accuracy not yet measuredGWASs have identified three single nucleotide polymorphisms, rs35349669, rs10933431, and rs7597763, at the INPP5D locus that are associated with risk for AD.
“GWASs have identified three single nucleotide polymorphisms (SNPs), rs35349669, rs10933431, and rs7597763, at the INPP5D locus that are associated risk for AD [8–10].”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [8]
Table 1 (Functional enrichment of significantly associated regions; page unavailable) reports rs7597763 as the lead variant at an Alzheimer’s disease risk locus, although our copy labels the gene “INPPD5.” Searches of the paper’s text for rs35349669 and rs10933431 found no passages identifying either variant, so this source supports only one of the three SNPs named. (LLM, conf=0.87)
Experimental — accuracy not yet measuredINPP5D/SHIP1 is a myeloid-expressed gene genetically associated with Alzheimer's disease.
“Inositol polyphosphate-5-phosphatase D (INPP5D/SHIP1) is a myeloid-expressed gene genetically-associated with AD.”
From INPP5D regulates inflammasome activation in human microglia (2023) · cites this paper as [19]
The risk-loci table (Functional enrichment of significantly associated regions; page unavailable) reports a significant Alzheimer’s disease association at a locus labeled “INPPD5,” apparently a transposition of INPP5D. The cell-type enrichment section reports microglial enrichment for associated genes collectively, but does not establish that INPP5D/SHIP1 specifically is myeloid-expressed. (LLM, conf=0.78)
Experimental — accuracy not yet measuredNine AD-GWAS associated genes in addition to CD33 were differentially expressed at the protein level: EIF4G3, TMEM106B, CTSH, SORL1, GRN, FDFT1, IL34, PTK2B, and CD2AP.
“Examination of AD-GWAS associated genes revealed nine genes in addition to CD33 which were differentially expressed at the protein level: EIF4G3, TMEM106B, CTSH, SORL1, GRN, FDFT1, IL34, PTK2B, CD2AP (Fig. 3d, e).”
From INPP5D regulates inflammasome activation in human microglia (2023) · cites this paper as [19]
The ‘Functional enrichment of significantly associated regions’ table lists several named genes, including CD33, CD2AP, TMEM106B, SORL1 and GRN, at Alzheimer’s disease GWAS loci (page not provided). The cited paper does not establish that the nine listed genes were differentially expressed at the protein level; the citing sentence points to its own Fig. 3d,e for that finding. (LLM, conf=0.86)
Experimental — accuracy not yet measuredThe induction of MGnD genes in microglia with deletions in Itgb8, Tgfbr2, Nrros or Smad2/Smad3 is associated with the suppression of AD risk factor genes, including Bin1, Havcr2 and Inpp5d.
“The induction of MGnD genes in microglia with deletions in Itgb8 , Tgfbr2 , Nrros or Smad2 / Smad3 (Extended Data Fig. 9e-h) is associated with the suppression of AD risk factor genes, including Bin1 , Havcr2 and Inpp5d 1,2 (Fig. 8j, Extended Data Fig. 9i-l and Supplementary Table 8).”
From APOE4 impairs the microglial response in Alzheimer’s disease by inducing TGFβ-mediated checkpoints (2023) · cites this paper as [2]
Table 1 (Functional enrichment of significantly associated regions; page unavailable) lists BIN1 and HAVCR2 as Alzheimer’s disease risk loci, and Gene prioritization discusses HAVCR2. The table prints “INPPD5,” not INPP5D, so our copy does not clearly establish the third named gene. The microglial-deletion and gene-suppression findings are presented with the citing authors’ own figure and table references, not attributed to this GWAS. (LLM, conf=0.82)
Experimental — accuracy not yet measuredLarge meta-analyses of genome-wide association studies have uncovered more than 80 other risk and protective loci that could potentially augment or attenuate the APOE-linked Alzheimer disease risk.
“Large meta-analyses of genome-wide association studies (GWAS) have uncovered more than 80 other risk and protective loci19,20 that could potentially augment or attenuate the APOE-linked AD risk.”
From Multifaceted roles of APOE in Alzheimer disease (2024) · cites this paper as [19]
The Genome-wide inferences section (page unavailable) reports that this GWAS meta-analysis identified 38 independent Alzheimer’s disease loci, supporting the general point that GWAS have found loci beyond APOE. It does not substantiate the claim of more than 80 other loci or show that those loci augment or attenuate APOE-linked risk. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThe S209F ABI3 variant has been validated in a secondary study.
“and has been validated in a secondary study [8].”
From Deletion of Abi3/Gngt2 influences age-progressive amyloid β and tau pathologies in distinctive ways (2022) · cites this paper as [8]
The Functional enrichment table lists a significant Alzheimer’s disease association at the ABI3 locus (lead variant rs28394864), and Genome-wide inferences says the study replicated many previously identified loci. Our copy does not identify the S209F variant or establish that this specific variant was validated in the secondary study. (LLM, conf=0.85)
Experimental — accuracy not yet measuredThe S209F variant of ABI3 (rs616338:p.Ser209Phe) increases risk of Alzheimer's disease (OR = 1.43, p = 4.5 × 10−10, MAF = 0.008).
“The S209F variant of Abelson Interactor Protein 3 (ABI3) increases risk for Alzheimer’s disease (AD)”
From Deletion of Abi3/Gngt2 influences age-progressive amyloid β and tau pathologies in distinctive ways (2022) · cites this paper as [8]
Table 1 (Functional enrichment of significantly associated regions; page unavailable) identifies ABI3 as an Alzheimer’s disease risk locus. It lists a different lead variant, rs28394864, and does not establish that S209F (rs616338) increases risk or support the quoted OR, P value, or MAF. (LLM, conf=0.86)
Experimental — accuracy not yet measuredRecent Alzheimer's disease genome-wide association studies identified new risk loci whose candidate genes are involved in innate immune functions.
“recent AD genome-wide association studies (GWASs) have identified several new genetic risk loci for AD3,4, with candidate risk genes at these loci being involved in innate immune functions4,5”
From Deletion of SPI1 in microglia exacerbates amyloid pathology by impairing microglial response in Alzheimer’s disease models (2026) · cites this paper as [4]
Experimental — accuracy not yet measuredFour loci identified in the two previous largest ADRD GWAS meta-analyses (HAVCR2, SLC2A4RG/LIME1, FOXF1 and NTN5) were not GWS in the EADB-IGAP-PGC meta-analysis.
“four loci identified in the two previous largest ADRD GWAS meta-analyses on European-ancestry samples5,6 (HAVCR2, SLC2A4RG/LIME1, FOXF1 and NTN5) were not GWS in the EADB–IGAP–PGC meta-analysis”
From Consensus meta-analysis of genome-wide association studies for Alzheimer’s disease and related dementias (2026) · cites this paper as [5]
Loci associated with Alzheimer's disease risk are enriched in genes expressed in microglia.
“Recent genetic studies on Alzheimer’s disease (AD) have brought microglia under the spotlight, as loci associated with AD risk are enriched in genes expressed in microglia.”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [8]
Microglia gene expression patterns are strongly correlated with late-onset Alzheimer's disease.
“Genome -wide association meta -analysis studies (GWASs) 1,2 and interactome investigation 3 identified microglia gene expression patterns as strongly correlated with late-onset Alzheimer's disease (AD).”
From APOE4 impairs the microglial response in Alzheimer’s disease by inducing TGFβ-mediated checkpoints (2023) · cites this paper as [2]
HAVCR2 encodes the checkpoint molecule TIM3, a promising therapeutic approach in cancer, and was recently described in a GWAS as an AD risk gene.
“the latter of which encodes the checkpoint molecule TIM3, one of the most promising new therapeutic approaches in cancer 32 that was recently described in a GWAS as an AD risk gene 2 .”
From APOE4 impairs the microglial response in Alzheimer’s disease by inducing TGFβ-mediated checkpoints (2023) · cites this paper as [2]
The most recent genome-wide association study for Alzheimer's disease in a European population included 1,126,563 individuals and identified 38 susceptibility loci.
“The most recent GWAS for AD was performed in a European population, including 1,126,563 individuals and identified 38 susceptibility loci [7].”
From Genetics of Alzheimer’s disease: An East Asian perspective (2023) · cites this paper as [7]
SNPs in SORL1 have also been identified as susceptibility loci in European populations and in a transethnic meta-analysis including South Korean and Caucasian cohorts.
“Importantly, SNPs in SORL1 have also been identified as susceptibility loci in European populations [7, 25], and in a transethnic meta-analysis that included South Korean and Caucasian cohorts.”
From Genetics of Alzheimer’s disease: An East Asian perspective (2023) · cites this paper as [7]
GWASs have provided accumulating evidence that gene polymorphisms increase the risk of the more common late-onset AD (LOAD).
“genome‐wide association studies (GWASs) have provided accumulating evidence that gene polymorphisms increase the risk of the more common late‐onset AD (LOAD). 6 , 7”
From Aberrant phase separation from a rare <i>ABI3</i> mutation drives microglial dysfunction and Alzheimer's risk (2026) · cites this paper as [7]
ABI3 is an AD risk gene.
“Recent reports have confirmed ABI3 as an AD risk gene [6–8].”
From Deletion of Abi3/Gngt2 influences age-progressive amyloid β and tau pathologies in distinctive ways (2022) · cites this paper as [8]
In the GWAS, both the minor alleles of the sentinel SNP (T) and rs6024870 (A) are protective against LOAD.
“In the GWAS, both the minor alleles of the sentinel SNP (T) and rs6024870 (A) are protective against LOAD.”
From Variant-to-function mapping of late-onset Alzheimer’s disease GWAS signals in human microglial cell models implicates <i>RTFDC1</i> at the <i>CASS4</i> locus (2024) · cites this paper as [31]
The Discussion reports a GWAS of late-onset Alzheimer’s disease, and Table 1 lists lead variants and tested alleles. Our copy does not identify rs6024870 or establish that its A allele and the unspecified sentinel SNP’s T allele are protective (searched: rs6024870, protective alleles, sentinel variant). (LLM, conf=0.74)
Experimental — accuracy not yet measuredLinked peaks identified in microglia were significantly enriched for heritability of AD across five different studies.
“Consistent with previous studies,55,56 linked peaks identified in microglia were significantly enriched for heritability of AD across five different studies2,3,4,5,6”
From Single nucleus multiomics identifies ZEB1 and MAFB as candidate regulators of Alzheimer’s disease-specific cis-regulatory elements (2023) · cites this paper as [5]
Several genome-wide association studies (GWAS) have implicated microglia as the primary cell type expressing AD genes.
“Several genome-wide association studies (GWAS) have also implicated microglia as the primary cell type expressing AD genes.82–85”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [84]
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References 95 · Cited by 1,011
Research works printed but not linked: 2
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- © The Author(s), under exclusive licence to Springer Nature America, Inc. 2021, corrected publication 2021
- Authors
- Wightman, D. P., Jansen, I. E., Savage, J. E., Shadrin, A. A., Bahrami, S., Holland, D., Rongve, A., Børte, S., Winsvold, B. S., Drange, O. K., Martinsen, A. E., Skogholt, A. H., Willer, C., Bråthen, G., Bosnes, I., Nielsen, J. B., Fritsche, L. G., Thomas, L. F., Pedersen, L. M., Gabrielsen, M. E., Johnsen, M. B., Meisingset, T. W., Zhou, W., Proitsi, P., Hodges, A., Dobson, R., Velayudhan, L., Heilbron, K., Auton, A., 23andMe Research Team, Agee, M., Aslibekyan, S., Babalola, E., Bell, R. K., Bielenberg, J., Bryc, K., Bullis, E., Cameron, B., Coker, D., Partida, G. C., Dhamija, D., Das, S., Elson, S. L., Filshtein, T., Fletez-Brant, K., Fontanillas, P., Freyman, W., Gandhi, P. M., Hicks, B., Hinds, D. A., Huber, K. E., Jewett, E. M., Jiang, Y., Kleinman, A., Kukar, K., Lane, V., Lin, K.-H., Lowe, M., Luff, M. K., McCreight, J. C., McIntyre, M. H., McManus, K. F., Micheletti, S. J., Moreno, M. E., Mountain, J. L., Mozaffari, S. V., Nandakumar, P., Noblin, E. S., O’Connell, J., Petrakovitz, A. A., Poznik, G. D., Schumacher, M., Shastri, A. J., Shelton, J. F., Shi, J., Shringarpure, S., Tian, C., Tran, V., Tung, J. Y., Wang, X., Wang, W., Weldon, C. H., Wilton, P., Sealock, J. M., Davis, L. K., Pedersen, N. L., Reynolds, C. A., Karlsson, I. K., Magnusson, S., Stefansson, H., Thordardottir, S., Jonsson, P. V., Snaedal, J., Zettergren, A., Skoog, I., Kern, S., Waern, M., Zetterberg, H., Blennow, K., Stordal, E., Hveem, K., Zwart, J.-A., Athanasiu, L., Selnes, P., Saltvedt, I., Sando, S. B., Ulstein, I., Djurovic, S., Fladby, T., Aarsland, D., Selbæk, G., Ripke, S., Stefansson, K., Andreassen, O. A., & Posthuma, D.
- Affiliations
- Amsterdam Neuroscience (NL)
- University of Oslo (NO)
- Oslo University Hospital (NO)
- University of California San Diego (US)
- Fonna Hospital Trust (NO)
- Norwegian University of Science and Technology (NO)
- University of Michigan (US)
- Statens Serum Institut (DK)
- King's College London (GB)
- University of London (GB)
- 23andMe (United States) (US)
- Vanderbilt University Medical Center (US)
- Karolinska Institutet (SE)
- University of California, Riverside (US)
- University of Gothenburg (SE)
- Sahlgrenska University Hospital (SE)
- Akershus University Hospital (NO)
- Broad Institute (US)
- ORCID
- Wightman, Douglas P.
- Jansen, Iris E.
- Savage, Jeanne E.
- Shadrin, Alexey A.
- Bahrami, Shahram
- Holland, Dominic
- Rongve, Arvid
- Børte, Sigrid
- Winsvold, Bendik S.
- Drange, Ole Kristian
- Martinsen, Amy E.
- Skogholt, Anne Heidi
- Willer, Cristen
- Bråthen, Geir
- Bosnes, Ingunn
- Nielsen, Jonas Bille
- Fritsche, Lars G.
- Thomas, Laurent F.
- Pedersen, Linda M.
- Gabrielsen, Maiken E.
- Johnsen, Marianne Bakke
- Meisingset, Tore Wergeland
- Zhou, Wei
- Proitsi, Petroula
- Hodges, Angela
- Dobson, Richard
- Velayudhan, Latha
- Heilbron, Karl
- Auton, Adam
- Aslibekyan, Stella
- Bielenberg, Jessica
- Bryc, Katarzyna
- Coker, Daniella
- Das, Sayantan
- Elson, Sarah L.
- Filshtein, Teresa
- Fontanillas, Pierre
- Freyman, Will
- Gandhi, Pooja M.
- Hinds, David A.
- Jewett, Ethan M.
- Jiang, Yunxuan
- Luff, Marie K.
- McIntyre, Matthew H.
- McManus, Kimberly F.
- Micheletti, Steven J.
- Mountain, Joanna L.
- Mozaffari, Sahar V.
- Nandakumar, Priyanka
- Poznik, G. David
- Shi, Jingchunzi
- Shringarpure, Suyash
- Tian, Chao
- Tran, Vinh
- Tung, Joyce Y.
- Wang, Xin
- Wilton, Peter
- Sealock, Julia M.
- Davis, Lea K.
- Pedersen, Nancy L.
- Reynolds, Chandra A.
- Karlsson, Ida K.
- Magnusson, Sigurdur
- Stefansson, Hreinn
- Zettergren, Anna
- Skoog, Ingmar
- Kern, Silke
- Zetterberg, Henrik
- Blennow, Kaj
- Stordal, Eystein
- Hveem, Kristian
- Zwart, John-Anker
- Athanasiu, Lavinia
- Selnes, Per
- Saltvedt, Ingvild
- Sando, Sigrid B.
- Djurovic, Srdjan
- Fladby, Tormod
- Aarsland, Dag
- Selbæk, Geir
- Ripke, Stephan
- Stefansson, Kari
- Andreassen, Ole A.
- Posthuma, Danielle
- Venue
- Nature Genetics
- Published
- 2021-09
- Volume
- 53
- Issue
- 9
- Pages
- 1276-1282
- ISSN
- 1061-4036 (ISSN-L)
- 1546-1718
- PMC
- PMC10243600
- OpenAlex
- W3197290161
- Cited by
- 1,011
- References
- 95
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- 2026: 144 · 2025: 232 · 2024: 284 · 2023: 192 · 2022: 147 · 2021: 12
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- Funders
- Alzheimer's Association (U01 AG016976, U01 AG032984, R01 AG08724, ADGC-10–196728, U24AG021886, AG033193)
- Amgen
- Eli Lilly and Company
- Massachusetts General Hospital
- Biogen
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- Norges Teknisk-Naturvitenskapelige Universitet
- South London and Maudsley NHS Foundation Trust
- Sunovion
- Regeneron Pharmaceuticals
- Wellcome Trust (082604/2/07/Z, 082604)
- Vanderbilt University Medical Center
- Broad Institute
- EU Joint Programme – Neurodegenerative Disease Research (311993)
- Development of Innovative Strategies for a Transdisciplinary approach to ALZheimer's disease
- Université de Lille
- King's College London
- University College London
- Institut National de la Santé et de la Recherche Médicale
- Bundesministerium für Bildung und Forschung (01GI0102, 01GI0711, 01GI0420)
- Erasmus Medisch Centrum
- Karolinska Institutet
- Landspítali Háskólasjúkrahús
- Universitetet i Bergen
- Universitetet i Oslo
- Háskóli Íslands
- Norges Forskningsråd (#248980, 223273, 248778, 311993)
- Sahlgrenska Universitetssjukhuset
- Göteborgs Universitet
- University College London Hospitals NHS Foundation Trust
- Siemens Healthineers
- St. Olavs Hospital Universitetssykehuset i Trondheim
- Akershus Universitetssykehus
- Hjartavernd (N01-AG-1-2100)
- Nasjonalforeningen for Folkehelsen (22731)
- H. Lundbeck A/S
- Centre hospitalier régional universitaire de Lille
- Julius Clinical
- UK Dementia Research Institute
- Amsterdam Neuroscience
- Sykehuset i Vestfold
- National Institutes of Health (223273, N01-AG-1-2100, NIA AG081220, AG016976, AG 08724, AG021886, R01 AG08724)
- University of California, San Diego
- Stanley Center for Psychiatric Research, Broad Institute
- Institute of Psychiatry, Psychology and Neuroscience, King’s College London
- Medical Research Council (503480, MC_PC_17214)
- Sahlgrenska Akademin
- Statens Serum Institut
- Faculty of Medicine and Health, University of Sydney
- National Institute on Aging (AG 016976, R01-AG08724, N01-AG12100, R01AG060470, AG17561, AG081220, U01AG016976, NIA AG081220, AG 08724, U01AG052409, AG028555, R01AG028555, AG060470, R01-AG17561, R01AG054076, U01AG032984, AG033193, AG032984, R01AG017561, R01AG008724, R01AG033193, AG021886, U24AG072122, U24AG021886, P30AG066546)
- National Heart, Lung, and Blood Institute (HL-105756, R01HL105756, AG033193)
- National Institute of Neurological Disorders and Stroke (R01NS017950)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (P50HD103537)
- H2020 European Research Council (834057)
- Health Data Research UK
- 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 › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Keywords
- late-onset Alzheimer's disease, genetic susceptibility loci, polygenic disease, microglia, immune cells, protein degradation, genetic variants, dementia genetics
- MeSH terms
- Alzheimer Disease, Humans, Proteins, Microglia, Sample Size, Genetic Predisposition to Disease, Multifactorial Inheritance, Polymorphism, Single Nucleotide, Genome-Wide Association Study, Proteolysis
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