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TREM2 Variants in Alzheimer's Disease
Open accessAbstract
BACKGROUND: Homozygous loss-of-function mutations in TREM2, encoding the triggering receptor expressed on myeloid cells 2 protein, have previously been associated with an autosomal recessive form of early-onset dementia. METHODS: We used genome, exome, and Sanger sequencing to analyze the genetic variability in TREM2 in a series of 1092 patients with Alzheimer's disease and 1107 controls (the discovery set). We then performed a meta-analysis on imputed data for the TREM2 variant rs75932628 (predicted to cause a R47H substitution) from three genomewide association studies of Alzheimer's disease and tested for the association of the variant with disease. We genotyped the R47H variant in an additional 1887 cases and 4061 controls. We then assayed the expression of TREM2 across different regions of the human brain and identified genes that are differentially expressed in a mouse model of Alzheimer's disease and in control mice. RESULTS: We found significantly more variants in exon 2 of TREM2 in patients with Alzheimer's disease than in controls in the discovery set (P=0.02). There were 22 variant alleles in 1092 patients with Alzheimer's disease and 5 variant alleles in 1107 controls (P<0.001). The most commonly associated variant, rs75932628 (encoding R47H), showed highly significant association with Alzheimer's disease (P<0.001). Meta-analysis of rs75932628 genotypes imputed from genomewide association studies confirmed this association (P=0.002), as did direct genotyping of an additional series of 1887 patients with Alzheimer's disease and 4061 controls (P<0.001). Trem2 expression differed between control mice and a mouse model of Alzheimer's disease. CONCLUSIONS: Heterozygous rare variants in TREM2 are associated with a significant increase in the risk of Alzheimer's disease. (Funded by Alzheimer's Research UK and others.).
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“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 [219]
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 [219]
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 [7]
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
“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 [7]
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 [2]
Experimental — accuracy not yet measured
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In the citing paper
“In TREM2 gene, several AD associated risk increasing variants have been recognized, such as R47H and R62H [1, 13–15].”
From Protective PLCG2 variants associate with a delayed onset of Alzheimer’s disease among heterozygous APOE ε4 carriers (2026) · 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
“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 [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
“AD-associated TREM2 risk variants – including p.H157Y, p.R98W, p.D87N, p.T66M, p.R62H, p.R47H, p.Y38C and p.Q33X [6, 43] – affect TREM2 function by various mechanisms”
From TREM2/PLCγ2 signalling in immune cells: function, structural insight, and potential therapeutic modulation (2021) · cites this paper as [6]
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 most characterised variant of TREM2 (p.R47H) shows defects in ligand binding [6, 37, 38, 97], which impacts the ability of TREM2 to recognise damage, and induce microglial changes, resulting in a dampened response to pathological insults such as Aβ deposition.”
From TREM2/PLCγ2 signalling in immune cells: function, structural insight, and potential therapeutic modulation (2021) · cites this paper as [6]
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
“Most of the genes associated with the ~40 loci identified by genome-wide association (GWA) analysis or by rare variant sequencing studies are expressed in glial cells (e.g., APOE, TREM2, BIN1, CD33, INPP5D, CTSB, CTSD, and PICALM).”
From The Major Risk Factors for Alzheimer’s Disease: Age, Sex, and Genes Modulate the Microglia Response to Aβ Plaques (2019) · cites this paper as Guerreiro 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
“For instance, TREM2 is one of the strongest risk factors for AD, and evidence suggests that TREM2 acts to recognize Aβ pathology and direct microglial responses toward the pathology (Guerreiro et al., 2013; Zhou et al., 2020).”
From β-amyloid accumulation enhances microtubule associated protein tau pathology in an APPNL-G-F/MAPTP301S mouse model of Alzheimer’s disease (2024) · cites this paper as Guerreiro 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
“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 [113]
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
“These studies have identified several common variants of several new genes to be associated with LOAD, but, with the exception of variants of triggering receptor expressed on myeloid cells 2, no rare variants were identified (49,50).”
From Molecular Basis for Increased Risk for Late-onset Alzheimer Disease Due to the Naturally Occurring L28P Mutation in Apolipoprotein E4 (2014) · cites this paper as [50]
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 [12]
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 [154]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
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 [16]
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 [11]
The 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 [11]
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 [11]
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 [219]
The cited source says what the claim attributes to it.
In the citing paper
“Another, more recently identified risk factor is the triggering receptor expressed on myeloid cells 2 (TREM2), where genetic variants also increase SAD risk [145].”
From Neuron Loss in Alzheimer’s Disease: Translation in Transgenic Mouse Models (2020) · cites this paper as [145]
The cited source says what the claim attributes to it.
In the citing paper
“Polymorphisms in the R47H allele of the TREM2 gene have recently been identified as a strong genetic risk factor for the development of AD,13 though the actual impact of these polymorphisms on microglial function remain unclear.”
From Markers of microglia in post-mortem brain samples from patients with Alzheimer’s disease: a systematic review (2018) · cites this paper as [13]
The cited source says what the claim attributes to it.
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 [2]
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 [22]
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 [34]
The cited source says what the claim attributes to it.
In the citing paper
“TREM2 is a transmembrane receptor expressed on the membrane of myeloid cells and an important susceptibility gene for AD [5].”
From Alzheimer’s disease phospholipase C-gamma-2 (PLCG2) protective variant is a functional hypermorph (2019) · cites this paper as [5]
The cited source says what the claim attributes to it.
In the citing paper
“Mutations in TREM2 have been associated with increased risk of AD [5, 18].”
From Alzheimer’s disease phospholipase C-gamma-2 (PLCG2) protective variant is a functional hypermorph (2019) · cites this paper as [5]
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 [15]
The cited source says what the claim attributes to it.
In the citing paper
“TREM2 R47H mutations impair ApoE binding88 and increase the risk of human AD,93”
From Cystatin C is glucocorticoid responsive, directs recruitment of Trem2+ macrophages, and predicts failure of cancer immunotherapy (2023) · cites this paper as [93]
The cited source says what the claim attributes to it.
In the citing paper
“Several variants in TREM2 have been linked to increased LOAD risk [1, 6].”
From TREM2/PLCγ2 signalling in immune cells: function, structural insight, and potential therapeutic modulation (2021) · cites this paper as [6]
The cited source says what the claim attributes to it.
In the citing paper
“The last decade has seen a plethora of studies linking immune-relate genes to AD [1, 6]”
From TREM2/PLCγ2 signalling in immune cells: function, structural insight, and potential therapeutic modulation (2021) · cites this paper as [6]
The cited source says what the claim attributes to it.
In the citing paper
“For example, TREM2 p.H157Y (rs2234255) has been detected not only in Caucasians [35] but also in Chinese [40] and Japanese [24], and the significance of this variant has been confirmed in the Chinese population (Table 4) [40].”
From Genetics of Alzheimer’s disease: An East Asian perspective (2023) · cites this paper as [35]
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 [35]
The cited source says what the claim attributes to it.
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 [39]
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 [12]
The cited source says what the claim attributes to it.
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 Guerreiro et al., 2013
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“Genes were defined without surrounding genomic sequence, as this yielded the most significant excess of enriched pathways in the common variation dataset11.”
From Rare coding variants in PLCG2, ABI3, and TREM2 implicate microglial-mediated innate immunity in Alzheimer's disease (2017) · cites this paper as [11]
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 [12]
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 [8]
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 [8]
In the citing paper
“When not considering fetal astrocytes, mature astrocytes (21%), and microglial cells (20.3%), the resident macrophage cells of the brain thought to play a key role in the pathologic immune response in LOAD8,14,60, became the highest expressed cell types in the genome-wide set of genes, with 5.3% of the 400 genes showing high microglial expression”
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 [8]
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 [107]
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 [107]
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 [120]
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 Guerreiro et al., 2013
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 Guerreiro et al., 2013
In the citing paper
“Notably, variants of TREM2, an immunoglobulin-like cell-surface receptor primarily expressed on microglia in the brain, were recently found to confer a 2 to 4-fold increased risk for AD [83].”
From Glial contributions to neurodegeneration in tauopathies (2017) · cites this paper as [83]
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 [163]
In the citing paper
“Many risk genes for the development of Alzheimer’s disease (AD) are exclusively or highly expressed in myeloid cells.”
From Sustained microglial depletion with CSF1R inhibitor impairs parenchymal plaque development in an Alzheimer’s disease model (2019) · cites this paper as [5]
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 [127]
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 Guerreiro et al., 2013
In the citing paper
“and identified that its expression was strongly increased by amyloid deposition in APP transgenic mice (Guerreiro et al., 2013; Matarin et al., 2015; Cheng-Hathaway et al., 2018; Song et al., 2018).”
From Genetic variability in response to amyloid beta deposition influences Alzheimer’s disease risk (2019) · cites this paper as Guerreiro 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 Guerreiro 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 [24]
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 [132]
In the citing paper
“The mutation in TREM2, has been associated with a three-fold higher risk to develop AD [122].”
From Role of Oxidative Damage in Alzheimer’s Disease and Neurodegeneration: From Pathogenic Mechanisms to Biomarker Discovery (2021) · cites this paper as [122]
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 [56]
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 [56]
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 [2]
In the citing paper
“This might be one of the major mechanisms underlying various neurodegenerative diseases with advanced age by suppression of WT TREM2 in many sporadic cases, considering that TREM2 variants associated with loss-of-function are extremely rare in frequency in humans (2).”
From Trem2 promotes anti-inflammatory responses in microglia and is suppressed under pro-inflammatory conditions (2020) · cites this paper as [2]
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 [32]
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Metadata
- Authors
- Guerreiro, R., Wojtas, A., Bras, J., Carrasquillo, M., Rogaeva, E., Majounie, E., Cruchaga, C., Sassi, C., Kauwe, J. S. K., Younkin, S., Hazrati, L., Collinge, J., Pocock, J., Lashley, T., Williams, J., Lambert, J.-C., Amouyel, P., Goate, A., Rademakers, R., Morgan, K., Powell, J., St. George-Hyslop, P., Singleton, A., & Hardy, J.
- Affiliations
- UCL Queen Square Institute of Neurology (GB)
- ORCID
- Venue
- New England Journal of Medicine
- Publisher
- Massachusetts Medical Society
- Published
- 2013-01-10
- Volume
- 368
- Issue
- 2
- Pages
- 117-127
- ISSN
- 0028-4793 (ISSN-L)
- 1533-4406
- PMC
- PMC3631573
- OpenAlex
- W2124490243
- Cited by
- 3,020
- References
- 33
- Citations by year
- 2026: 165 · 2025: 204 · 2024: 238 · 2023: 245 · 2022: 265 · 2021: 250 · 2020: 269 · 2019: 234 · 2018: 251 · 2017: 203 · 2016: 194 · 2015: 196 · 2014: 160 · 2013: 137
- FWCI
- 106.95
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- New England Journal of Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Digital Commons@Becker (Washington University School of Medicine) (submittedVersion)
- Research Explorer (The University of Manchester) (submittedVersion)
- Universitätsbibliographie, Universität Duisburg-Essen (submittedVersion)
- UCL Discovery (University College London) (submittedVersion)
- eScholarship@McGill (McGill) (submittedVersion)
- ORCA Online Research @Cardiff (Cardiff University) (submittedVersion)
- Research Portal (King's College London) (submittedVersion)
- Bristol Research (University of Bristol) (submittedVersion)
- Funders
- U.S. Department of Health and Human Services
- University of Dundee
- Wellcome Trust (WT089698, 089703, 081864, 089698, 095317)
- Alzheimer Society
- National Institute for Health and Care Research (NF-SI-0512-10033)
- University College London
- Fondation pour la Recherche sur Alzheimer
- National Institutes of Health (5p30ns069329-02)
- Canadian Institutes of Health Research
- Medical Research Council (MC_G1000735, MR/K013041/1)
- National Institute on Aging (R01AG042611, R01AG018023, U01AG006786, R01-AG18023, R01AG041797, P50AG008702, Z01AG000950, P50AG005681, U24AG056270, U24AG021886, P50AG016574)
- National Institute of Neurological Disorders and Stroke (P30-NS069329, 5P30 NS069329-02)
- 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 › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- TREM2, Alzheimer's disease, loss-of-function mutations, rare variants, genetic risk, mouse models of Alzheimer's disease, early-onset dementia, myeloid cells
- MeSH terms
- Aged, Alzheimer Disease, Animals, Brain, Genotype, Heterozygote, Humans, Membrane Glycoproteins, Mice, Inbred A, Mutation, Receptors, Immunologic, Risk Factors, RNA, Messenger, Genetic Variation, Sequence Analysis, DNA, Mice, Genome-Wide Association Study, Exome, Genotyping Techniques
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