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Variant of TREM2 Associated with the Risk of Alzheimer's Disease
Open accessAbstract
BACKGROUND: Sequence variants, including the ε4 allele of apolipoprotein E, have been associated with the risk of the common late-onset form of Alzheimer's disease. Few rare variants affecting the risk of late-onset Alzheimer's disease have been found. METHODS: We obtained the genome sequences of 2261 Icelanders and identified sequence variants that were likely to affect protein function. We imputed these variants into the genomes of patients with Alzheimer's disease and control participants and then tested for an association with Alzheimer's disease. We performed replication tests using case-control series from the United States, Norway, The Netherlands, and Germany. We also tested for a genetic association with cognitive function in a population of unaffected elderly persons. RESULTS: A rare missense mutation (rs75932628-T) in the gene encoding the triggering receptor expressed on myeloid cells 2 (TREM2), which was predicted to result in an R47H substitution, was found to confer a significant risk of Alzheimer's disease in Iceland (odds ratio, 2.92; 95% confidence interval [CI], 2.09 to 4.09; P=3.42×10(-10)). The mutation had a frequency of 0.46% in controls 85 years of age or older. We observed the association in additional sample sets (odds ratio, 2.90; 95% CI, 2.16 to 3.91; P=2.1×10(-12) in combined discovery and replication samples). We also found that carriers of rs75932628-T between the ages of 80 and 100 years without Alzheimer's disease had poorer cognitive function than noncarriers (P=0.003). CONCLUSIONS: Our findings strongly implicate variant TREM2 in the pathogenesis of Alzheimer's disease. Given the reported antiinflammatory role of TREM2 in the brain, the R47H substitution may lead to an increased predisposition to Alzheimer's disease through impaired containment of inflammatory processes. (Funded by the National Institute on Aging and others.).
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In the citing paper
“At the genetic level, GWAS and sequencing studies have found associations between AD and genes expressed in myeloid cells, including TREM2, ABCA7, and CD331,2,5,15–17.”
From A common haplotype lowers PU.1 expression in myeloid cells and delays onset of Alzheimer's disease (2017) · cites this paper as [15]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“TREM2 (219, 300, 543) and two novel rare coding variants, PLCG2 and ABI3 , implicate innate immunity in AD pathophysiology (543), but whether these variants can influence vascular-inflammatory cross-talk contributing to AD pathophysiology remains unclear.”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [300]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Genome-wide association studies (GWAS) identified many AD risk genes related to the immune response and microglia, including those implicated in phagocytosis, such as CD33 and TREM24,5,6,7,8.”
From Amyloid-β induces lipid droplet-mediated microglial dysfunction via the enzyme DGAT2 in Alzheimer’s disease (2025) · cites this paper as [8]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Prior studies proposed that these cells compact amyloid plaques through receptors implicated in phagocytosis such as TREM214, (expressed on myeloid cells and associated to increased AD risk)14,8, AXL, and MER79.”
From Amyloid-β induces lipid droplet-mediated microglial dysfunction via the enzyme DGAT2 in Alzheimer’s disease (2025) · cites this paper as [8]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Coding alterations in TREM2, a transmembrane glycoprotein expressed on myeloid lineage cells that modulates innate immune function [1], dramatically increase the risk of developing late-onset Alzheimer’s disease (LOAD) [2,3].”
From TREM2-Deficient Microglia Attenuate Tau Spreading In Vivo (2023) · cites this paper as [3]
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In the citing paper
“PLCG2 has also been shown to be a downstream component of TREM2 signaling, an important microglial AD risk gene. 7 , 8”
From The P522R protective variant of PLCG2 promotes the expression of antigen presentation genes by human microglia in an Alzheimer's disease mouse model (2022) · cites this paper as [8]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Moreover, the loss‐of‐function TREM2 variant R47H impairs microglial responses to Aβ and confers increased risk for AD.”
From PLCG2 modulates TREM2 expression and signaling in response to Alzheimer's disease pathology (2025) · cites this paper as [38]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“TREM2 loss‐of‐function impairs microglial protective functions and worsens neuronal dystrophy. 9 , 37 , 38 , 41 , 42 , 61”
From PLCG2 modulates TREM2 expression and signaling in response to Alzheimer's disease pathology (2025) · cites this paper as [38]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“In AD, amyloid pathology induces the expression of TREM2 in microglia. 36 , 37 , 38 , 39 , 40 , 41 , 60”
From PLCG2 modulates TREM2 expression and signaling in response to Alzheimer's disease pathology (2025) · cites this paper as [38]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Human genetic studies have linked rare coding variants in microglial genes, such as TREM2, and more recently PLCG2 to Alzheimer’s disease (AD) pathology.”
From PLCγ2 regulates TREM2 signalling and integrin-mediated adhesion and migration of human iPSC-derived macrophages (2021) · cites this paper as [3]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“The TREM2-R62H (AF = 0.0078) is more common in the Finnish population than the more widely known TREM2-R47H (AF = 0.00045) AD risk variant [15, 25].”
From Protective PLCG2 variants associate with a delayed onset of Alzheimer’s disease among heterozygous APOE ε4 carriers (2026) · cites this paper as [25]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“In the brain, PLCG2 is predominantly microglial expressed, positioning PLCγ2 within the same interaction network as TREM2—a notable AD risk gene (Andreone et al. 2020; Jonsson et al. 2013).”
From Alzheimer's Protection by PLCγ2 Compacts Plaques, Redistributes Microglia, and Protects Synapses in App NL ‐G‐F Mice (2026) · cites this paper as Jonsson et al. 2013
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“TREM2 deficiency leads to adverse phenotypes involving mostly the brain and the bones, and manifesting more severely in humans than mice [42, 105]”
From TREM2/PLCγ2 signalling in immune cells: function, structural insight, and potential therapeutic modulation (2021) · cites this paper as [42]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Third, recent genetic studies implicate inflammatory genes and pathways (CD33, TREM2, HLA-DRB5-DRB1) in late-onset disease pathology (112–115).”
From The Inflammatory Continuum of Traumatic Brain Injury and Alzheimer’s Disease (2018) · cites this paper as [114]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“the risk of dementia for carriers of rare APOE variants was also substantial, with effect sizes similar to those for ɛ4 as well as other rare variants in dementia risk genes such as TREM2. 43”
From APOE and dementia – resequencing and genotyping in 105,597 individuals (2020) · cites this paper as [43]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“A rare variant of the TREM2 gene encoding p.Arg47His causes a 3-fold increase in the risk for late-onset Alzheimer's disease (LOAD).”
From Microglia express ABI3 in the brains of Alzheimer's disease and Nasu-Hakola disease (2017) · cites this paper as [10]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“NGS allowed the identification of rare variants in TREM2 as major genetic risk factors for AD [39, 65].”
From The new genetic landscape of Alzheimer’s disease: from amyloid cascade to genetically driven synaptic failure hypothesis? (2019) · cites this paper as [65]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“The TREM2 variant R47H, for example, was discovered using a study design that preserved statistical power by focusing solely on genetic variants that were likely to affect protein function [11, 12]”
From Linkage, whole genome sequence, and biological data implicate variants in RAB10 in Alzheimer’s disease resilience (2017) · cites this paper as [11]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Loss-of-function (LOF) variants of TREM2, an immune receptor expressed in microglia, increase Alzheimer’s disease risk.”
From TREM2 regulates microglial cholesterol metabolism upon chronic phagocytic challenge (2020) · cites this paper as Jonsson et al., 2013
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Retromer has also been implicated in the trafficking of the microglia receptor Triggering receptor expressed on myeloid cells 2 (TREM2), with mutations in TREM2 associated with an increased risk for developing AD [154, 155].”
From Global identification of neuronal and astrocytic integral membrane proteins that require Retromer for their endosomal recycling (2026) · cites this paper as [155]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Recent sequencing studies identified a number of genes that have rare variants associated with AD9-11,18-24.”
From Rare coding variants in PLCG2, ABI3, and TREM2 implicate microglial-mediated innate immunity in Alzheimer's disease (2017) · cites this paper as [9]
The cited source says what the claim attributes to it.
In the citing paper
“Nearly 30 LOAD susceptibility loci2-12 are known, and risk is significantly polygenic13.”
From Rare coding variants in PLCG2, ABI3, and TREM2 implicate microglial-mediated innate immunity in Alzheimer's disease (2017) · cites this paper as [9]
The cited source says what the claim attributes to it.
In the citing paper
“We also observed evidence for the previously reported9,11 TREM2 rare variant p.R47H (Table 2).”
From Rare coding variants in PLCG2, ABI3, and TREM2 implicate microglial-mediated innate immunity in Alzheimer's disease (2017) · cites this paper as [9]
The cited source says what the claim attributes to it.
In the citing paper
“Microglial TREM2 variants (300, 344) are partial loss of function with impaired transport of APOE-containing lipoproteins (633).”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [300]
The cited source says what the claim attributes to it.
In the citing paper
“Genome-wide association studies (GWAS) have identified multiple loci associated with AD including to name a few, variants in PICALM , CLU , ATP-binding cassette transporter A7 ( ABCA7 ), sortilin related receptor-1 ( SORL1 ), complement receptor 1 ( CR1 ), triggering receptor expressed on myeloid cells 2 ( TREM2 ), and bridging integrator 1 ( BIN1 ) genes (219, 236, 254, 300, 343, 344, 528, 543).”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [300]
The cited source says what the claim attributes to it.
In the citing paper
“Some additional highly replicated risk genes include CR1 , BIN1 , and TREM2 (94, 119, 219, 300, 344, 543).”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [300]
The cited source says what the claim attributes to it.
In the citing paper
“In the brain, PLCγ2 is primarily expressed by microglia, where it serves as an important signaling node downstream of TREM2 and CD33 (19, 20), both also AD risk genes (21–23).”
From Multi-omics analyses reveal novel effects of PLCγ2 deficiency in the mouse brain (2023) · cites this paper as [21]
The cited source says what the claim attributes to it.
In the citing paper
“Within the brain, PLCγ2 is primarily but not exclusively expressed in microglia, where it serves as an important signaling node downstream of TREM2 and CD33 [31, 32], both also AD risk genes [33–35].”
From PLCγ2 deficiency compromises systemic immune tolerance and erodes myelin homeostasis while enhancing oxidative metabolism in the mouse brain (2026) · cites this paper as [33]
The cited source says what the claim attributes to it.
In the citing paper
“Importantly, TREM2 variants associate with an increased risk of AD [15, 25, 38–40].”
From Protective PLCG2 variants associate with a delayed onset of Alzheimer’s disease among heterozygous APOE ε4 carriers (2026) · cites this paper as [25]
The cited source says what the claim attributes to it.
In the citing paper
“In the brain, PLCG2 is predominantly microglial expressed, positioning PLCγ2 within the same interaction network as TREM2—a notable AD risk gene (Andreone et al. 2020; Jonsson et al. 2013).”
From Alzheimer's Protection by PLCγ2 Compacts Plaques, Redistributes Microglia, and Protects Synapses in App NL ‐G‐F Mice (2026) · cites this paper as Jonsson et al. 2013
The cited source says what the claim attributes to it.
In the citing paper
“The first well-known rare variant for AD is the p.R47H variant (rs75932628) in TREM2, which was independently identified by two research groups in 2013 [35, 36].”
From Genetics of Alzheimer’s disease: An East Asian perspective (2023) · cites this paper as [36]
The cited source says what the claim attributes to it.
In the citing paper
“Recently, several possibly functional, rare variants with large protective [9, 10] and risk effects [11–13] have been identified for AD in APP, APOE, PLD3, and TREM2 using novel study designs.”
From Linkage, whole genome sequence, and biological data implicate variants in RAB10 in Alzheimer’s disease resilience (2017) · cites this paper as [11]
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“The Alzheimer's disease protective P522R PLCG2 coding variant (rs72824905) is downstream of TREM2, but how it confers disease protection is poorly understood.”
From Alzheimer's Protection by PLCγ2 Compacts Plaques, Redistributes Microglia, and Protects Synapses in App NL ‐G‐F Mice (2026) · cites this paper as Jonsson et al. 2013
Experimental — accuracy not yet measuredIn the citing paper
“Neuroinflammation is a common feature of AD9 and GWAS have associated several immune-related genes with AD including ABCA7, CD33, CLU, CR1, MS4A10, 11 and recently TREM2.12, 13”
From Whole-genome sequencing suggests a chemokine gene cluster that modifies age at onset in familial Alzheimer's disease (2015) · cites this paper as [13]
In the citing paper
“The Stage 1 discovery meta-analysis produced 12 loci with genome-wide significance (P ≤ 5 × 10−8) (Table 1), all of which are previously described1,4–11.”
From Genetic meta-analysis of diagnosed Alzheimer’s disease identifies new risk loci and implicates Aβ, tau, immunity and lipid processing (2019) · cites this paper as [7]
In the citing paper
“Three other signals were not initially described in the initial IGAP GWAS: the rare R47H TREM2 coding variant previously reported by others7,8,14; ECHDC3 (rs7920721; NC_000010.10: g.11720308A>G), which was recently identified as a potential genome-wide-significant Alzheimer’s disease risk locus in several studies15–17, and ACE (rs138190086; NC_000017.10: g.61538148G>A)”
From Genetic meta-analysis of diagnosed Alzheimer’s disease identifies new risk loci and implicates Aβ, tau, immunity and lipid processing (2019) · cites this paper as [7]
In the citing paper
“an increased risk for developing AD is significantly associated with rare variants of innate immune receptors expressed in microglia, including TREM2 (107, 108), CD33 (109), and complement receptor 1 (CR1) (110)”
From Microglia Function in the Central Nervous System During Health and Neurodegeneration (2017) · cites this paper as [108]
In the citing paper
“A rare arginine 47 histidine (R47H) variant of TREM2 is associated with an increased risk for AD (107, 108). This variant impairs binding of TREM2 to many phospholipid ligands (114, 125).”
From Microglia Function in the Central Nervous System During Health and Neurodegeneration (2017) · cites this paper as [108]
In the citing paper
“TREM2, a pivotal risk factor for LOAD [119, 120], is associated with tau pathology.”
From Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation (2023) · cites this paper as [119]
In the citing paper
“The TREM2 mutation most clearly associated with AD (R47H, carried by <0.5% of most populations) increases the risk of AD approximately threefold (Guerreiro et al., 2013; Jonsson et al., 2013).”
From Microglia in Alzheimer’s disease (2018) · cites this paper as Jonsson et al., 2013
In the citing paper
“rare genetic variants associated with AD (found by gene sequencing or exome array) have also implicated microglia in determining the risk of AD (Guerreiro et al., 2013; Jonsson et al., 2013; Sims et al., 2017).”
From Microglia in Alzheimer’s disease (2018) · cites this paper as Jonsson et al., 2013
In the citing paper
“Mutations in triggering receptor expressed on myeloid cells 2 (Trem2) were associated with a 3.0- to 4.5-fold increased AD risk, almost as high as that associated with ApoE ε434,35.”
From Microglia in neurodegeneration (2018) · cites this paper as [35]
In the citing paper
“GWAS showed that the R47H variant of TREM2 was associated with a 2- to 4-fold increased risk for the development of AD.”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [164]
In the citing paper
“A proteomic relationship between AD and FTD is supported by the fact that mutations in the triggering receptor expressed on myeloid cells 2 (TREM2) protein cause microglial dysfunction and lead to AD39,40, whereas mutations in the progranulin (PGRN) protein also cause microglial dysfunction and lead to FTD41–43.”
In the citing paper
“Genetic studies show that a number of genes that have been linked to early-onset AD risk are expressed primarily in microglia.”
From Microglial signatures and their role in health and disease (2018) · cites this paper as [126]
In the citing paper
“Given that TREM2 mutations are associated with increased risk of AD in humans126,176,177, a protective role for this receptor appears to be the predominant biologic effect.”
From Microglial signatures and their role in health and disease (2018) · cites this paper as [126]
In the citing paper
“A rare mutation of TREM2 (R47H) is associated with a substantial increase in the risk of developing AD126.”
From Microglial signatures and their role in health and disease (2018) · cites this paper as [126]
In the citing paper
“The importance of microglia-mediated neuroinflammation in neurodegeneration has been confirmed by genetic studies that identified several immune gene polymorphisms as risk factors for AD [5–8].”
From Identification and therapeutic modulation of a pro-inflammatory subset of disease-associated-microglia in Alzheimer’s disease (2018) · cites this paper as [7]
In the citing paper
“We and others identified the microglial gene TREM2 as a potent risk gene for late-onset disease (Guerreiro et al., 2013; Jonsson et al., 2013)”
From Genetic variability in response to amyloid beta deposition influences Alzheimer’s disease risk (2019) · cites this paper as Jonsson et al., 2013
In the citing paper
“A decade of GWAS projects for Alzheimer’s disease has provided key and initially surprising insights into the progression of late-onset Alzheimer’s disease, particularly the dependence on the innate immune system, with the identification of genes such as TREM2 and SPI1/PU.1”
From Genetic variability in response to amyloid beta deposition influences Alzheimer’s disease risk (2019) · cites this paper as Jonsson et al., 2013
In the citing paper
“Rare variants in the microglia-enriched gene TREM2 confer high risk for LOAD (Guerreiro et al., 2013a; Jonsson et al., 2013; Sims et al., 2017).”
From Elevated TREM2 Gene Dosage Reprograms Microglia Responsivity and Ameliorates Pathological Phenotypes in Alzheimer’s Disease Models (2018) · cites this paper as Jonsson et al., 2013
In the citing paper
“identified variants in TREM2 (“triggering receptor expressed on myeloid cells 2”) as risk factors for LOAD [24, 25]”
From Microglial dysfunction in brain aging and Alzheimer's disease (2014) · cites this paper as [25]
In the citing paper
“Missense mutations in TREM2 lead to a significant risk of developing AD (Jonsson et al., 2013; Meyer-Luehmann and Prinz, 2015).”
From The role of microglia in retinal neurodegeneration: Alzheimer’s disease, parkinson, and glaucoma. (2017) · cites this paper as Jonsson et al., 2013
In the citing paper
“One of the most well-studied rare variants that confers elevated risk for AD is the R47H variant in TREM2 [131, 132].”
From Genetic architecture of Alzheimer's disease (2020) · cites this paper as [131]
In the citing paper
“In addition, two groups of investigators independently identified variants of the microglial TREM2 gene that increase susceptibility to LOAD with an odds ratio similar to that of APOEε4 [56–58].”
From Systems-based proteomics to resolve the biology of Alzheimer’s disease beyond amyloid and tau (2021) · cites this paper as [57]
In the citing paper
“Variants of the microglial TREM2 gene have been found to increase the risk of sporadic AD by approximately 3- to 5-fold [56, 57].”
From Systems-based proteomics to resolve the biology of Alzheimer’s disease beyond amyloid and tau (2021) · cites this paper as [57]
In the citing paper
“The risk from this variant has a comparable effect size with the APOEε4 allele (around 3-fold increased AD risk; 4,19–22).”
From Trem2 promotes anti-inflammatory responses in microglia and is suppressed under pro-inflammatory conditions (2020) · cites this paper as [4]
In the citing paper
“Genome-wide association studies have reported that, amongst other microglial genes, variants in TREM2 can profoundly increase the incidence of developing Alzheimer’s disease (AD).”
From Trem2 promotes anti-inflammatory responses in microglia and is suppressed under pro-inflammatory conditions (2020) · cites this paper as [4]
In the citing paper
“Data from human genetics, particularly with respect to the hypomorphic R47H allele of TREM2 that strongly increases risk for AD (32, 33, 102), provide strong evidence for a protective role for microglia.”
From The Transcriptional Landscape of Microglial Genes in Aging and Neurodegenerative Disease (2019) · cites this paper as [33]
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Cites
McKhann, G., Drachman, D., Folstein, M., Katzman, R., Price, D., & Stadlan, E. M. (1984) · Neurology · doi:10.1212/wnl.34.7.939 · Cited by 27,915
Inflammation and Alzheimer’s disease
Akiyama, H. (2000) · Neurobiology of Aging · doi:10.1016/s0197-4580(00)00124-x · Cited by 4,514
Strittmatter, W. J., Saunders, A. M., Schmechel, D., Pericak-Vance, M., Enghild, J., Salvesen, G. S., & Roses, A. D. (1993) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.90.5.1977 · Cited by 4,268
Association of apolipoprotein E allele ϵ4 with late‐onset familial and sporadic Alzheimer's disease
Saunders, A. M., Strittmatter, W. J., Schmechel, D., St. George-Hyslop, P. H., Pericak-Vance, M. A., Joo, S. H., Rosi, B. L., Gusella, J. F., Crapper-MacLachlan, D. R., Alberts, M. J., et al. (1993) · Neurology · doi:10.1212/wnl.43.8.1467 · Cited by 3,786
Harold, D., Abraham, R., Hollingworth, P., Sims, R., Gerrish, A., Hamshere, M. L., Pahwa, J. S., Moskvina, V., Dowzell, K., Williams, A., et al. (2009) · Nature Genetics · doi:10.1038/ng.440 · Cited by 3,326
Self-citationGenome-wide association study identifies variants at CLU and CR1 associated with Alzheimer's disease
the European Alzheimer's Disease Initiative Investigators, Lambert, J.-C., Heath, S., Even, G., Campion, D., Sleegers, K., Hiltunen, M., Combarros, O., Zelenika, D., Bullido, M. J., et al. (2009) · Nature Genetics · doi:10.1038/ng.439 · Cited by 2,234
Initiative, T. A. D. N., Hollingworth, P., CHARGE consortium, EADI1 consortium, Harold, D., Sims, R., Gerrish, A., Lambert, J.-C., Carrasquillo, M. M., Abraham, R., et al. (2011) · Nature Genetics · doi:10.1038/ng.803 · Cited by 1,997
Self-citationMDS Cognitive Performance Scale(C)
Morris, J. N., Fries, B. E., Mehr, D. R., Hawes, C., Phillips, C., Mor, V., & Lipsitz, L. A. (1994) · Journal of Gerontology · doi:10.1093/geronj/49.4.m174 · Cited by 1,852
Brain interleukin 1 and S-100 immunoreactivity are elevated in Down syndrome and Alzheimer disease.
Griffin, W. S., Stanley, L. C., Ling, C., White, L., MacLeod, V, Perrot, L. J., White, C. L., & Araoz, C. (1989) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.86.19.7611 · Cited by 1,777
A mutation in APP protects against Alzheimer’s disease and age-related cognitive decline
Jonsson, T., Atwal, J. K., Steinberg, S., Snaedal, J., Jonsson, P. V., Bjornsson, S., Stefansson, H., Sulem, P., Gudbjartsson, D., Maloney, J., et al. (2012) · Nature · doi:10.1038/nature11283 · Cited by 1,738
Self-citation
Flagged first, then by citations
Research works printed but not linked: 3
- Hakola HP, 1972, Acta Psychiatr Scand Suppl, 232, 1
- Nasu T, 1973, Acta Pathol Jpn, 23, 539
- Montalbetti L, 2005, Funct Neurol, 20, 71
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Items 501–600 of 1,054
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Ennerfelt, H. E., & Lukens, J. R. (2020) · Immunological Reviews · doi:10.1111/imr.12896 · Cited by 124
Cheng, Y., Song, Y., Chen, H., Li, Q., Gao, Y. Z., Lu, G., & Luo, C. (2021) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2021/5005136 · Cited by 124
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Lee, S., Xu, G., Jay, T. R., Bhatta, S., Kim, K.-W., Jung, S., Landreth, G. E., Ransohoff, R. M., & Lamb, B. T. (2014) · The Journal of Neuroscience · doi:10.1523/jneurosci.0853-14.2014 · Cited by 123
Baligács, N., Albertini, G., Borrie, S. C., Serneels, L., Pridans, C., Balusu, S., & De Strooper, B. (2024) · Nature Communications · doi:10.1038/s41467-024-54779-w · Cited by 123
Aguzzi, A., & Zhu, C. (2017) · Journal of Clinical Investigation · doi:10.1172/jci90605 · Cited by 122
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Li, J.-W., Zong, Y., Cao, X.-P., Tan, L., & Tan, L. (2018) · Annals of Translational Medicine · doi:10.21037/atm.2018.04.22 · Cited by 122
Cano, A., Turowski, P., Ettcheto, M., Duskey, J. T., Tosi, G., Sánchez-López, E., García, M. L., Camins, A., Souto, E. B., Ruiz, A., et al. (2021) · Journal of Nanobiotechnology · doi:10.1186/s12951-021-00864-x · Cited by 122
Jiang, T., Yu, J., Zhu, X., & Tan, L. (2013) · Molecular Neurobiology · doi:10.1007/s12035-013-8424-8 · Cited by 122
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Boche, D., & Gordon, M. N. (2021) · Alzheimer s & Dementia · doi:10.1002/alz.12389 · Cited by 122
Schlepckow, K., Morenas‐Rodríguez, E., Hong, S. Y., & Haass, C. (2023) · The Lancet Neurology · doi:10.1016/s1474-4422(23)00247-8 · Cited by 122
Modulation of inflammation in transgenic models of Alzheimer’s disease
Birch, A. M., Katsouri, L., & Sastre, M. (2014) · Journal of Neuroinflammation · doi:10.1186/1742-2094-11-25 · Cited by 121
Leveraging preclinical models for the development of Alzheimer disease therapeutics
Scearce-Levie, K. A., Sanchez, P. E., & Lewcock, J. W. (2020) · Nature Reviews Drug Discovery · doi:10.1038/s41573-020-0065-9 · Cited by 121
Inhomogeneous distribution of Iba‐1 characterizes microglial pathology in Alzheimer's disease
Tischer, J., Krueger, M., Mueller, W. C., Staszewski, O., Prinz, M., Streit, W. J., & Bechmann, I. (2016) · Glia · doi:10.1002/glia.23024 · Cited by 121
DESGESCO (Dementia Genetics Spanish Consortium), E. (. D. E. D. B., van der Lee, S. J., biobank), E. (. D. E. D., IFGC (International FTD-Genomics Consortium), I. (. I. P. D. G. C., IPDGC (The International Parkinson Disease Genomics Consortium), Dementia), R.-F. (. A. M. F. I. F.-T., (NBB), N. B. B., The GIFT (Genetic Investigation in Frontotemporal Dementia and Alzheimer’s Disease) Study Group, Conway, O. J., Jansen, I., et al. (2019) · Acta Neuropathologica · doi:10.1007/s00401-019-02026-8 · Cited by 120
Genetics of neurodegenerative diseases: an overview
Pihlstrøm, L., Wiethoff, S., & Houlden, H. (2017) · Handbook of clinical neurology · doi:10.1016/b978-0-12-802395-2.00022-5 · Cited by 120
Mitochondrial Regulation of Microglial Immunometabolism in Alzheimer’s Disease
Fairley, L. H., Wong, J. H., & Barron, A. M. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.624538 · Cited by 120
Cai, Y., Zhang, Y., Leng, S., Ma, Y., Jiang, Q., Wen, Q., Ju, S., & Hu, J. (2024) · Neurobiology of Disease · doi:10.1016/j.nbd.2024.106426 · Cited by 120
Whole-genome analyses of whole-brain data: working within an expanded search space
Medland, S. E., Jahanshad, N., Neale, B. M., & Thompson, P. M. (2014) · Nature Neuroscience · doi:10.1038/nn.3718 · Cited by 119
Tayeb, H. O., Murray, E. D., Price, B. H., & Tarazi, F. I. (2013) · Expert Opinion on Biological Therapy · doi:10.1517/14712598.2013.789856 · Cited by 119
Prokop, S., Miller, K. R., Labra, S. R., Pitkin, R. M., Hoxha, K., Narasimhan, S., Changolkar, L., Rosenbloom, A., Lee, V. M.-Y., & Trojanowski, J. Q. (2019) · Acta Neuropathologica · doi:10.1007/s00401-019-02048-2 · Cited by 119
Ultrastructural evidence of microglial heterogeneity in Alzheimer’s disease amyloid pathology
El Hajj, H., Savage, J. C., Bisht, K., Parent, M., Vallières, L., Rivest, S., & Tremblay, M.-È. (2019) · Journal of Neuroinflammation · doi:10.1186/s12974-019-1473-9 · Cited by 119
Slattery, C. F., Beck, J. A., Harper, L., Adamson, G., Abdi, Z., Uphill, J., Campbell, T., Druyeh, R., Mahoney, C. J., Rohrer, J. D., et al. (2014) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2014.05.1751 · Cited by 119
Cellular Regulation of Amyloid Formation in Aging and Disease
Stroo, E., Koopman, M., Nollen, E. A. A., & Mata‐Cabana, A. (2017) · Frontiers in Neuroscience · doi:10.3389/fnins.2017.00064 · Cited by 119
Systems-based proteomics to resolve the biology of Alzheimer’s disease beyond amyloid and tau
Rayaprolu, S., Higginbotham, L., Bagchi, P., Watson, C. M., Zhang, T., Levey, A. I., Rangaraju, S., & Seyfried, N. T. (2021) · Neuropsychopharmacology · doi:10.1038/s41386-020-00840-3 · Cited by 118
Self-citationRuiz, A., Dols-Icardo, O., Bullido, M. J., Pastor, P., Rodríguez-Rodríguez, E., López de Munain, A., de Pancorbo, M. M., Pérez-Tur, J., Álvarez, V., Antonell, A., et al. (2014) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2013.08.011 · Cited by 118
Götzl, J. K., Brendel, M., Werner, G., Parhizkar, S., Sebastian Monasor, L., Kleinberger, G., Colombo, A., Deussing, M., Wagner, M., Winkelmann, J., et al. (2019) · EMBO Molecular Medicine · doi:10.15252/emmm.201809711 · Cited by 118
Do Microglial Sex Differences Contribute to Sex Differences in Neurodegenerative Diseases?
Kodama, L., & Gan, L. (2019) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2019.05.001 · Cited by 118
Antignano, I., Liu, Y., Offermann, N., & Capasso, M. (2023) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-023-04775-y · Cited by 117
Infection, systemic inflammation, and Alzheimer's disease
Lim, S., Rodríguez‐Ortiz, C. J., & Kitazawa, M. (2015) · Microbes and Infection · doi:10.1016/j.micinf.2015.04.004 · Cited by 117
Chen, J., Chen, Z., Won, H., Huang, A., Lowe, J. K., Wojta, K. J., Yokoyama, J. S., Bensimon, G., Leigh, P. N., Payan, C., et al. (2018) · Molecular Neurodegeneration · doi:10.1186/s13024-018-0270-8 · Cited by 117
Dhiman, K., Blennow, K., Zetterberg, H., Martins, R. N., & Gupta, V. B. (2019) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-019-03040-5 · Cited by 117
Tzioras, M., Daniels, M. J. D., Davies, C., Baxter, P. S., King, D., McKay, S., Varga, B. V., Popovic, K., Hernandez, M., Stevenson, A. J., et al. (2023) · Cell Reports Medicine · doi:10.1016/j.xcrm.2023.101175 · Cited by 117
Impact of peripheral myeloid cells on amyloid-β pathology in Alzheimer’s disease–like mice
Prokop, S., Miller, K. R., Drost, N., Handrick, S., Mathur, V., Luo, J., Wegner, A., Wyss-Coray, T., & Heppner, F. L. (2015) · Journal of Experimental Medicine · doi:10.1084/jem.20150479 · Cited by 116
Alzheimer's Disease Mechanisms and Emerging Roads to Novel Therapeutics
Sala Frigerio, C., & De Strooper, B. (2016) · Annual Review of Neuroscience · doi:10.1146/annurev-neuro-070815-014015 · Cited by 116
The therapeutics of Alzheimer's disease: Where we stand and where we are heading
Selkoe, D. J. (2013) · Annals of Neurology · doi:10.1002/ana.24001 · Cited by 116
Phagocyte dysfunction, tissue aging and degeneration
Li, W. (2013) · Ageing Research Reviews · doi:10.1016/j.arr.2013.05.006 · Cited by 116
Gispert, J. D., Suárez‐Calvet, M., Monté, G. C., Tucholka, A., Falcón, C., Rojas, S., Rami, L., Sánchez‐Valle, R., Lladó, A., Kleinberger, G., et al. (2016) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2016.06.005 · Cited by 116
Relative risk for Alzheimer disease based on complete family history
Cannon‐Albright, L., Foster, N. L., Schliep, K. C., Farnham, J. M., Teerlink, C. C., Kaddas, H. K., Tschanz, J. T., Corcoran, C., & Kauwe, J. S. K. (2019) · Neurology · doi:10.1212/wnl.0000000000007231 · Cited by 116
Elevating microglia TREM2 reduces amyloid seeding and suppresses disease-associated microglia
Zhao, N., Qiao, W., Li, F., Ren, Y., Zheng, J., Martens, Y. A., Wang, X., Li, L., Liu, C., Chen, K., et al. (2022) · The Journal of Experimental Medicine · doi:10.1084/jem.20212479 · Cited by 116
Aminophospholipids are signal-transducing TREM2 ligands on apoptotic cells
Shirotani, K., Hori, Y., Yoshizaki, R., Higuchi, E., Colonna, M., Saito, T., Hashimoto, S., Saito, T., Saido, T. C., & Iwata, N. (2019) · Scientific Reports · doi:10.1038/s41598-019-43535-6 · Cited by 116
APOE genotype and sex affect microglial interactions with plaques in Alzheimer’s disease mice
Stephen, T. L., Cacciottolo, M., Balu, D., Morgan, T. E., LaDu, M. J., Finch, C. E., & Pike, C. J. (2019) · Acta Neuropathologica Communications · doi:10.1186/s40478-019-0729-z · Cited by 115
Microglial microRNAs mediate sex-specific responses to tau pathology
Kodama, L., Guzman, E., Etchegaray, J. I., Li, Y., Sayed, F. A., Zhou, L., Zhou, Y., Zhan, L., Le, D., Udeochu, J. C., et al. (2020) · Nature Neuroscience · doi:10.1038/s41593-019-0560-7 · Cited by 115
Jansen, I. E., Ye, H., Heetveld, S., Lechler, M. C., Michels, H., Seinstra, R. I., Lubbe, S. J., Drouet, V., Lesage, S., Majounie, E., et al. (2017) · Genome biology · doi:10.1186/s13059-017-1147-9 · Cited by 115
Microglial Corpse Clearance: Lessons From Macrophages
Márquez-Ropero, M., Benito, E., Plaza‐Zabala, A., & Sierra, A. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.00506 · Cited by 115
The neuritic plaque facilitates pathological conversion of tau in an Alzheimer’s disease mouse model
Li, T., Braunstein, K. E., Zhang, J., Lau, A., Sibener, L., Deeble, C., & Wong, P. C. (2016) · Nature Communications · doi:10.1038/ncomms12082 · Cited by 114
Precision pharmacology for Alzheimer’s disease
Hampel, H. J., Vergallo, A., Aguilar, L. F., Benda, N., Broich, K., Cuello, A. C., Cummings, J. L., Dubois, B., Federoff, H. J., Fiandaca, M. S., et al. (2018) · Pharmacological Research · doi:10.1016/j.phrs.2018.02.014 · Cited by 114
Self-citationTREM2 ectodomain and its soluble form in Alzheimer’s disease
Yang, J., Fu, Z., Zhang, X., Xiong, M., Meng, L., & Zhang, Z. (2020) · Journal of Neuroinflammation · doi:10.1186/s12974-020-01878-2 · Cited by 113
Graham, L. C., Harder, J. M., Soto, I., de Vries, W. N., John, S. W. M., & Howell, G. R. (2016) · Scientific Reports · doi:10.1038/srep21568 · Cited by 113
Alzheimer's disease in the omics era
Sancesario, G. M., & Bernardini, S. (2018) · Clinical Biochemistry · doi:10.1016/j.clinbiochem.2018.06.011 · Cited by 113
HDAC 3 negatively regulates spatial memory in a mouse model of Alzheimer's disease
Zhu, X., Wang, S., Yu, L., Jin, J., Ye, X., Liu, Y., & Xu, Y. (2017) · Aging Cell · doi:10.1111/acel.12642 · Cited by 112
Conway, O. J., Carrasquillo, M. M., Wang, X., Bredenberg, J. M., Reddy, J. S., Strickland, S. L., Younkin, C. S., Burgess, J. D., Allen, M., Lincoln, S. J., et al. (2018) · Molecular Neurodegeneration · doi:10.1186/s13024-018-0289-x · Cited by 112
Alzheimer’s Disease: Biomarkers in the Genome, Blood, and Cerebrospinal Fluid
Huynh, R. A., & Mohan, C. (2017) · Frontiers in Neurology · doi:10.3389/fneur.2017.00102 · Cited by 112
Fassler, M., Rappaport, M., Benaim, C., & George, J. (2021) · Journal of Neuroinflammation · doi:10.1186/s12974-020-01980-5 · Cited by 112
Jiang, T., Tan, L., Zhu, X.-C., Zhou, J.-S., Cao, L., Tan, M.-S., Wang, H.-F., Chen, Q., Zhang, Y.-D., & Yu, J.-T. (2015) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2015.08.019 · Cited by 111
Mietelska‐Porowska, A., & Wojda, U. (2017) · Journal of Immunology Research · doi:10.1155/2017/4626540 · Cited by 111
Microglia Polarization in Alzheimer’s Disease: Mechanisms and a Potential Therapeutic Target
Wang, Q., Yao, H., Liu, W., Ya, B., Cheng, H., Xing, Z., & Wu, Y. (2021) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2021.772717 · Cited by 111
Genetic variability in response to amyloid beta deposition influences Alzheimer’s disease risk
Salih, D. A., Bayram, S., Guelfi, S., Reynolds, R. H., Shoai, M., Ryten, M., Brenton, J. W., Zhang, D., Matarin, M., Botia, J. A., et al. (2019) · Brain Communications · doi:10.1093/braincomms/fcz022 · Cited by 110
Zheng, H., Liu, C.-C., Atagi, Y., Chen, X.-F., Jia, L., Yang, L., He, W., Zhang, X., Kang, S. S., Rosenberry, T. L., et al. (2016) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2016.03.004 · Cited by 110
A rare coding variant in TREM2 increases risk for Alzheimer's disease in Han Chinese
Jiang, T., Tan, L., Chen, Q., Tan, M.-S., Zhou, J.-S., Zhu, X.-C., Lu, H., Wang, H.-F., Zhang, Y.-D., & Yu, J.-T. (2016) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2016.02.023 · Cited by 110
Distinct Signaling Pathways Regulate TREM2 Phagocytic and NFκB Antagonistic Activities
Yao, H., Coppola, K., Schweig, J. E., Crawford, F., Mullan, M., & Paris, D. (2019) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2019.00457 · Cited by 110
Alzheimer’s Disease: Mechanism and Approach to Cell Therapy
Amemori, T., Jendelová, P., Růžička, J., Urdzíková, L. M., & Syková, E. (2015) · International Journal of Molecular Sciences · doi:10.3390/ijms161125961 · Cited by 110
A cell therapy approach to restore microglial Trem2 function in a mouse model of Alzheimer’s disease
Yoo, Y., Neumayer, G., Shibuya, Y., Mader, M. M.-D., & Wernig, M. (2023) · Cell Stem Cell · doi:10.1016/j.stem.2023.07.006 · Cited by 109
Neurodegeneration: From cellular concepts to clinical applications
Katsnelson, A., Strooper, B. D., & Zoghbi, H. Y. (2016) · Science Translational Medicine · doi:10.1126/scitranslmed.aal2074 · Cited by 109
Hoogmartens, J., Cacace, R., & Broeckhoven, C. V. (2021) · Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring · doi:10.1002/dad2.12155 · Cited by 109
Drug repositioning for Alzheimer’s disease based on systematic “omics” data mining
Zhang, M., Schmitt-Ulms, G., Sato, C., Xi, Z., Zhang, Y., Zhou, Y., St George-Hyslop, P., & Rogaeva, E. (2016) · PLOS ONE · doi:10.1371/journal.pone.0168812 · Cited by 108
Zádori, D., Veres, G., Szalárdy, L., Klivènyi, P., & Vécsei, L. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-170929 · Cited by 108
Increased Expression of TREM2 in Peripheral Blood of Alzheimer's Disease Patients
Hu, N., Tan, M., Yu, J., Sun, L., Tan, L., Wang, Y.-L., Jiang, T., & Tan, L. (2013) · Journal of Alzheimer s Disease · doi:10.3233/jad-130854 · Cited by 108
Impairment of in vivo calcium signaling in amyloid plaque-associated microglia
Brawek, B., Schwendele, B., Riester, K., Kohsaka, S., Lerdkrai, C., Liang, Y., & Garaschuk, O. (2014) · Acta Neuropathologica · doi:10.1007/s00401-013-1242-2 · Cited by 108
Mullins, A. E., Kam, K., Parekh, A., Bubu, O. M., Osorio, R. S., & Varga, A. W. (2020) · Neurobiology of Disease · doi:10.1016/j.nbd.2020.105054 · Cited by 107
Triggering receptor expressed on myeloid cells-1 (TREM-1): a new player in antiviral immunity?
Roe, K., Gibot, S., & Verma, S. (2014) · Frontiers in Microbiology · doi:10.3389/fmicb.2014.00627 · Cited by 107
Microglial large extracellular vesicles propagate early synaptic dysfunction in Alzheimer’s disease
Gabrielli, M., Prada, I., Joshi, P., Falcicchia, C., D’Arrigo, G., Rutigliano, G., Battocchio, E., Zenatelli, R., Tozzi, F., Radeghieri, A., et al. (2022) · Brain · doi:10.1093/brain/awac083 · Cited by 106
Rovelet-Lecrux, A., Charbonnier, C., Wallon, D., Nicolas, G., Seaman, M. N. J., Pottier, C., Breusegem, S. Y., Mathur, P. P., Jenardhanan, P., Le Guennec, K., et al. (2015) · Molecular Psychiatry · doi:10.1038/mp.2015.100 · Cited by 106
Biomarkers in Sporadic and Familial Alzheimer’s Disease
Lista, S., O’Bryant, S. E., Blennow, K., Dubois, B., Hugon, J., Zetterberg, H., & Hampel, H. (2015) · Journal of Alzheimer's Disease · doi:10.3233/jad-143006 · Cited by 106
Self-citationSleegers, K., Bettens, K., De Roeck, A., Van Cauwenberghe, C., Cuyvers, E., Verheijen, J., Struyfs, H., Van Dongen, J., Vermeulen, S., Engelborghs, S., et al. (2015) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2015.02.013 · Cited by 106
Wes, P. D., Easton, A. E., Corradi, J., Barten, D. M., Devidze, N., DeCarr, L. B., Truong, A. B., He, A., Barrezueta, N. X., Polson, C. T., et al. (2014) · PLoS ONE · doi:10.1371/journal.pone.0106050 · Cited by 106
Microglia in Alzheimer’s disease: A target for immunotherapy
Wang, S., & Colonna, M. (2019) · Journal of Leukocyte Biology · doi:10.1002/jlb.mr0818-319r · Cited by 106
TREM2 brain transcript-specific studies in AD and TREM2 mutation carriers
Del‐Aguila, J. L., Benítez, B. A., Li, Z., Dube, U., Mihindukulasuriya, K. A., Budde, J., Farias, F., Fernández, M. V., Ibáñez, L., Jiang, S., et al. (2019) · Molecular Neurodegeneration · doi:10.1186/s13024-019-0319-3 · Cited by 106
Jia, Y., Cao, N., Zhai, J., Zeng, Q., Zheng, P. Z., Su, R., Liao, T., Liu, J., Pei, H., Fan, Z., et al. (2020) · Advanced Science · doi:10.1002/advs.201903809 · Cited by 106
Prokopenko, D., Morgan, S. L., Mullin, K., Hofmann, O., Chapman, B., Kirchner, R., (ADNI), A. D. N. I., Amberkar, S., Wohlers, I., Lange, C., et al. (2021) · Alzheimer's & Dementia · doi:10.1002/alz.12319 · Cited by 105
The role of the immune system in neurodegenerative disorders: Adaptive or maladaptive?
Doty, K. R., Guillot-Sestier, M.-V., & Town, T. (2015) · Brain Research · doi:10.1016/j.brainres.2014.09.008 · Cited by 104
TREM2 triggers microglial density and age-related neuronal loss
Linnartz‐Gerlach, B., Bodea, L., Klaus, C., Ginolhac, A., Halder, R., Sinkkonen, L., Walter, J., Colonna, M., & Neumann, H. (2019) · Glia · doi:10.1002/glia.23563 · Cited by 104
Prakash, P., Manchanda, P., Paouri, E., Bisht, K., Sharma, K., Rajpoot, J., Wendt, V., Hossain, A., Wijewardhane, P. R., Randolph, C. E., et al. (2025) · Immunity · doi:10.1016/j.immuni.2025.04.029 · Cited by 104
Moving beyond amyloid and tau to capture the biological heterogeneity of Alzheimer’s disease
Young‐Pearse, T. L., Lee, H., Hsieh, Y., Chou, V., & Selkoe, D. J. (2023) · Trends in Neurosciences · doi:10.1016/j.tins.2023.03.005 · Cited by 104
Genetics of Alzheimer’s Disease
Ridge, P. G., Ebbert, M., & Kauwe, J. S. K. (2013) · BioMed Research International · doi:10.1155/2013/254954 · Cited by 104
Roussos, P., Katsel, P., Fam, P., Tan, W., Purohit, D. P., & Haroutunian, V. (2015) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2014.10.013 · Cited by 103
Möhle, L., Israël, N., Paarmann, K., Krohn, M., Pietkiewicz, S., Müller, A. J., Lavrik, I. N., Buguliskis, J. S., Schott, B. H., Schlüter, D., et al. (2016) · Acta Neuropathologica Communications · doi:10.1186/s40478-016-0293-8 · Cited by 103
Corlier, F. W., Hafzalla, G. W., Faskowitz, J., Kuller, L. H., Becker, J. T., López, O. L., Thompson, P. M., & Braskie, M. N. (2018) · NeuroImage · doi:10.1016/j.neuroimage.2017.12.027 · Cited by 103
Celarain, N., de Gordoa, J. S., Zelaya, M. V., Roldán, M., Larumbe, R., Pulido, L., Echávarri, C., & Mendióroz, M. (2016) · Clinical Epigenetics · doi:10.1186/s13148-016-0202-9 · Cited by 103
17q21.31 duplication causes prominent tau-related dementia with increased MAPT expression
Guennec, K. L., Quenez, O., Nicolas, G., Wallon, D., Rousseau, S., Richard, A.-C., Alexander, J., Paschou, P., Charbonnier, C., Bellenguez, C., et al. (2016) · Molecular Psychiatry · doi:10.1038/mp.2016.226 · Cited by 102
Barák, M., Fedorová, V., Pospíšilová, V., Raška, J., Vochyánová, S., Sedmík, J., Hříbková, H., Klímová, H., Váňová, T., & Bohačiaková, D. (2022) · Stem Cell Reviews and Reports · doi:10.1007/s12015-021-10254-3 · Cited by 102
Tesco, G., & Lomoio, S. (2022) · Seminars in Immunology · doi:10.1016/j.smim.2022.101628 · Cited by 102
Lacour, A., Espinosa, A., Louwersheimer, E., Heilmann, S., Hernández, I., Wolfsgruber, S., Fernández, V, Wagner, H., Rosende-Roca, M., Mauleón, A., et al. (2017) · Molecular Psychiatry · doi:10.1038/mp.2016.18 · Cited by 101
ABCA7 expression is associated with Alzheimer's disease polymorphism and disease status
Vasquez, J. B., Fardo, D. W., & Estus, S. (2013) · Neuroscience Letters · doi:10.1016/j.neulet.2013.09.058 · Cited by 101
López González, I., Garcia-Esparcia, P., Llorens, F., & Ferrer, I. (2016) · International Journal of Molecular Sciences · doi:10.3390/ijms17020206 · Cited by 101
Guo, Y., Wei, X., Yan, H., Qin, Y., Yan, S., Liu, J., Zhao, Y., Jiang, F., & Lou, H. (2019) · The FASEB Journal · doi:10.1096/fj.201900992r · Cited by 101
Öhrfelt, A., Axelsson, M., Malmeström, C., Novakova, L., Heslegrave, A., Blennow, K., Lycke, J., & Zetterberg, H. (2016) · Multiple Sclerosis Journal · doi:10.1177/1352458515624558 · Cited by 101
Soluble TREM2 and biomarkers of central and peripheral inflammation in neurodegenerative disease
Bekris, L. M., Khrestian, M., Dyne, E. D., Shao, Y. Y., Pillai, J. A., Rao, S. M., Bemiller, S. M., Lamb, B. T., Fernandez, H. H., & Leverenz, J. B. (2018) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2018.03.003 · Cited by 101
Plaque-associated local toxicity increases over the clinical course of Alzheimer disease
Serrano-Pozo, A., Betensky, R. A., Frosch, M. P., & Hyman, B. T. (2016) · The American Journal of Pathology · doi:10.1016/j.ajpath.2015.10.010 · Cited by 100
Toward precision medicine in Alzheimer’s disease
Reitz, C. (2016) · Annals of Translational Medicine · doi:10.21037/atm.2016.03.05 · Cited by 100
The A1 astrocyte paradigm: New avenues for pharmacological intervention in neurodegeneration
Hinkle, J. T., Dawson, V. L., & Dawson, T. M. (2019) · Movement Disorders · doi:10.1002/mds.27718 · Cited by 100
Metadata
- Authors
- Jonsson, T., Stefansson, H., Steinberg, S., Jonsdottir, I., Jonsson, P. V., Snaedal, J., Bjornsson, S., Huttenlocher, J., Levey, A. I., Lah, J. J., Rujescu, D., Hampel, H., Giegling, I., Andreassen, O. A., Engedal, K., Ulstein, I., Djurovic, S., Ibrahim-Verbaas, C., Hofman, A., Ikram, M. A., van Duijn, C. M., Thorsteinsdottir, U., Kong, A., & Stefansson, K.
- Affiliations
- deCODE Genetics (Iceland) (IS)
- University of Tübingen (DE)
- Emory University (US)
- Martin Luther University Halle-Wittenberg (DE)
- Goethe University Frankfurt (DE)
- Oslo University Hospital (NO)
- Norwegian National Centre for Ageing and Health (NO)
- Erasmus MC (NL)
- ORCID
- Venue
- New England Journal of Medicine
- Publisher
- Massachusetts Medical Society
- Published
- 2013-01-10
- Volume
- 368
- Issue
- 2
- Pages
- 107-116
- ISSN
- 0028-4793 (ISSN-L)
- 1533-4406
- PMC
- PMC3677583
- OpenAlex
- W2128613449
- Cited by
- 2,558
- References
- 51
- Citations by year
- 2026: 133 · 2025: 160 · 2024: 201 · 2023: 202 · 2022: 211 · 2021: 233 · 2020: 232 · 2019: 192 · 2018: 220 · 2017: 168 · 2016: 151 · 2015: 167 · 2014: 150 · 2013: 129
- FWCI
- 96.88
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- New England Journal of Medicine (publishedVersion)
- PubMed (publishedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (submittedVersion)
- RePub (Erasmus University Rotterdam) (submittedVersion, other-oa)
- Hirsla (Landspítali University Hospital) (submittedVersion, other-oa)
- Funders
- National Institute on Aging (U01AG006781, P50AG025688, U24AG021886)
- National Human Genome Research Institute (U01HG004438, U01HG004610, U01HG006375, U01HG004603)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › 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
- TREM2, Alzheimer's disease, late-onset Alzheimer's disease, genetic risk, rare variants, cognitive function, neuroinflammation, Icelandic population, replication
- MeSH terms
- Aged, 80 and over, Alzheimer Disease, Cognition, Heterozygote, Humans, Iceland, Membrane Glycoproteins, Receptors, Immunologic, Risk Factors, Genetic Variation, Case-Control Studies, Sequence Analysis, DNA, Mutation, Missense, Polymorphism, Single Nucleotide, Apolipoprotein E4, Genotyping Techniques
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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