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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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“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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Background
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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