Influence of the apolipoprotein E genotype on amyloid deposition and neurofibrillary tangle formation in Alzheimer's disease
Abstract
The effect of the apolipoprotein E genotype on the development of late onset Alzheimer's disease is still debated. Neuropathological studies of Alzheimer's disease have found a great extent of amyloid deposition in cortex and blood vessel walls in association with the apolipoprotein E epsilon 4 genotype [Rebeck G. W. et al. (1993) Neuron 11, 575-580; Schmechel et al. (1993) Proc. natn. Acad. Sci. U.S.A. 90, 9649-9653]. In contrast, the relationship of apolipoprotein E genotype to neurofibrillary pathology in Alzheimer's disease has been less clear. In this study we present evidence on the influence of the apolipoprotein E genotype on Alzheimer's disease related pathology in a series of 76 autopsy cases that had pathology that fulfilled the CERAD criteria for Alzheimer's disease. We found that the presence of the apolipoprotein E epsilon 4 allele is correlated with increased amounts of both amyloid and neuritic pathology in the neocortex as determined using an image analysis system. Comparison of plaque and tangle densities with the allele doses of epsilon 2 and epsilon 4 revealed a striking parallelism, suggesting that the alleles exert their effects very early in the pathological process before deposition of plaques and tangles. Although the apolipoprotein E epsilon 2 allele had a protective effect against both amyloid deposition and neurofibrillary tangle formation, in the presence of the epsilon 4 allele this protective effect against neuritic pathology was less marked than against amyloid deposition. This differential effect on amyloid deposition and the accumulation of neuritic pathology suggests that different molecular mechanisms are involved in the effect of apolipoprotein E on amyloid deposition and on tau phosphorylation.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
APOE2 markedly delays the age of onset of Alzheimer's disease, even in the presence of the APOE4 allele.
“and markedly delaying the age of onset, even in the presence of the APOE4 allele.12,13”
From AAVrh.10-Mediated APOE2 Central Nervous System Gene Therapy for APOE4-Associated Alzheimer's Disease (2018) · cites this paper as [13]
APOE2 is a protective allele, reducing Alzheimer's disease risk by approximately 50% (1.8-fold decreased risk).
“In contrast, APOE2 is a protective allele, reducing AD risk by approximately 50% (1.8-fold decreased risk)”
From AAVrh.10-Mediated APOE2 Central Nervous System Gene Therapy for APOE4-Associated Alzheimer's Disease (2018) · cites this paper as [13]
Compared to E4 homozygotes, APOE2/E4 heterozygotes have a markedly reduced risk of developing AD.
“APOE2 homozygotes are protected from late-onset AD and, compared to E4 homozygotes, APOE2/E4 heterozygotes have a markedly reduced risk of developing AD.6,12,13”
From AAVrh.10-Mediated APOE2 Central Nervous System Gene Therapy for APOE4-Associated Alzheimer's Disease (2018) · cites this paper as [13]
Individuals who are APOE4 homozygotes have a markedly increased risk of developing AD.
“Individuals who are APOE4 homozygotes have a markedly increased risk of developing AD.”
From AAVrh.10-Mediated APOE2 Central Nervous System Gene Therapy for APOE4-Associated Alzheimer's Disease (2018) · cites this paper as [13]
APOE2 homozygotes are protected from late-onset AD.
“APOE2 homozygotes are protected from late-onset AD and, compared to E4 homozygotes, APOE2/E4 heterozygotes have a markedly reduced risk of developing AD.6,12,13”
From AAVrh.10-Mediated APOE2 Central Nervous System Gene Therapy for APOE4-Associated Alzheimer's Disease (2018) · cites this paper as [13]
Converting an APOE4 homozygote to an E4/E2 heterozygote would markedly decrease the risk for developing early-onset AD compared with E4 homozygotes.
“From epidemiologic studies, this would markedly decrease the risk for developing early-onset AD compared to E4 homozygotes.”
From AAVrh.10-Mediated APOE2 Central Nervous System Gene Therapy for APOE4-Associated Alzheimer's Disease (2018) · cites this paper as [13]
ApoE4 is associated with aggravated Alzheimer's disease neuropathology, enhanced neuroinflammation, deregulated lipid metabolism, mitochondrial dysfunction, and impaired synaptic plasticity.
“On the molecular level, ApoE4 has been associated with aggravated AD neuropathology, enhanced neuroinflammation, deregulated lipid metabolism, mitochondrial dysfunction, and impaired synaptic plasticity (Nagy et al., 1995;Chang et al., 2005;Rapp et al., 2006;Klein et al., 2010;Rodriguez et al., 2014).”
From Human ApoE Isoforms Differentially Modulate Brain Glucose and Ketone Body Metabolism: Implications for Alzheimer's Disease Risk Reduction and Early Intervention (2018) · cites this paper as Nagy et al., 1995
ApoE2 is rare, occurring in about 5% of the population, and shows protection against Alzheimer's disease.
“ApoE2 is rare, occurring in 5% of the population, and it shows protection against AD.”
From Human ApoE Isoforms Differentially Modulate Brain Glucose and Ketone Body Metabolism: Implications for Alzheimer's Disease Risk Reduction and Early Intervention (2018) · cites this paper as Nagy et al., 1995
ApoE2 slows Alzheimer's disease progression and is positively associated with cognitive functions during aging.
“ApoE2 has been found to slow AD progression and be positively associated with cognitive functions during aging (Nagy et al., 1995;Craft et al., 1998;Martins et al., 2005;Shinohara et al., 2016).”
From Human ApoE Isoforms Differentially Modulate Brain Glucose and Ketone Body Metabolism: Implications for Alzheimer's Disease Risk Reduction and Early Intervention (2018) · cites this paper as Nagy et al., 1995
The APOE2 variant is a protective allele against Alzheimer's disease.
“while the APOE2 variant was the first identified protective allele against AD (Corder et al, 1994; Nagy et al, 1995).”
From APOE from astrocytes restores Alzheimer’s Aβ-pathology and DAM-like responses in APOE deficient microglia (2024) · cites this paper as Nagy et al, 1995
Some studies reported a positive relationship between neurofibrillary tangle density and apoE ε4 allele dosage.
“Although some studies reported a positive relationship between the neurofibrillary tangle density and apoE ε4 allele dosage (Ghebremedhin et al., 1998; Nagy et al., 1995; Ohm et al., 1995; Polvikoski et al., 1995)”
From The role of apolipoprotein E in Alzheimer's disease (2009) · cites this paper as Nagy et al., 1995
Cites
Corder, E. H., Saunders, A. M., Strittmatter, W. J., Schmechel, D. E., Gaskell, P. C., Small, G. W., Roses, A. D., Haines, J. L., & Pericak-Vance, M. A. (1993) · Science · doi:10.1126/science.8346443 · Cited by 9,429 · see citing works
Mirra, S. S., Heyman, A., McKeel, D., Sumi, S. M., Crain, B. J., Brownlee, L. M., Vogel, F. S., Hughes, J. P., Belle, G. V., Berg, L., et al. (1991) · Neurology · doi:10.1212/wnl.41.4.479 · Cited by 4,961 · see citing works
Apolipoprotein E: Cholesterol Transport Protein with Expanding Role in Cell Biology
Mahley, R. W. (1988) · Science · doi:10.1126/science.3283935 · Cited by 4,028 · see citing works
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 · see citing works
Protective effect of apolipoprotein E type 2 allele for late onset Alzheimer disease
Corder, E. H., Saunders, A. M., Risch, N. J., Strittmatter, W. J., Schmechel, D. E., Gaskell, P. C., Rimmler, J. B., Locke, P. A., Conneally, P. M., Schmader, K. E., et al. (1994) · Nature Genetics · doi:10.1038/ng0694-180 · Cited by 1,920 · see citing works
Schmechel, D. E., Saunders, A. M., Strittmatter, W. J., Crain, B. J., Hulette, C. M., Joo, S. H., Pericak-Vance, M. A., Goldgaber, D., & Roses, A. D. (1993) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.90.20.9649 · Cited by 1,525 · see citing works
Strittmatter, W. J., Weisgraber, K. H., Huang, D. Y., Dong, L. M., Salvesen, G. S., Pericak-Vance, M., Schmechel, D., Saunders, A. M., Goldgaber, D., & Roses, A. D. (1993) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.90.17.8098 · Cited by 1,363 · see citing works
Apolipoprotein E polymorphism and Alzheimer's disease
Poirier, J., Bertrand, P., Poirier, J., Kogan, S., Gauthier, S., Poirier, J., Gauthier, S., Davignon, J., Bouthillier, D., & Davignon, J. (1993) · The Lancet · doi:10.1016/0140-6736(93)91705-q · Cited by 1,108 · see citing works
Apolipoprotein E in sporadic Alzheimer's disease: Allelic variation and receptor interactions
William Rebeck, G., Reiter, J. S., Strickland, D. K., & Hyman, B. T. (1993) · Neuron · doi:10.1016/0896-6273(93)90070-8 · Cited by 1,107 · see citing works
Apolipoprotein E genotyping by one-stage PCR
Wenham, P. R., Price, W. H., & Blundell, G. (1991) · The Lancet · doi:10.1016/0140-6736(91)92823-k · Cited by 1,070 · see citing works
Differential Effects of Apolipoproteins E3 and E4 on Neuronal Growth in Vitro
Nathan, B. P., Bellosta, S., Sanan, D. A., Weisgraber, K. H., Mahley, R. W., & Pitas, R. E. (1994) · Science · doi:10.1126/science.8171342 · Cited by 795 · see citing works
APOLIPOPROTEIN E ALLELES AS RISK FACTORS IN ALZHEIMER'S DISEASE
Roses, M. D. (1996) · Annual Review of Medicine · doi:10.1146/annurev.med.47.1.387 · Cited by 707 · see citing works
Apolipoprotein E in animal models of CNS injury and in alzheimer's disease
Poirier, J. (1994) · Trends in Neurosciences · doi:10.1016/0166-2236(94)90156-2 · Cited by 637 · see citing works
Isoform-specific binding of apolipoprotein E to beta-amyloid.
LaDu, M. J., Falduto, M. T., Manelli, A. M., Reardon, C. A., Getz, G. S., & Frail, D. E. (1994) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(17)31529-6 · Cited by 540 · see citing works
Strittmatter, W. J., Saunders, A. M., Goedert, M., Weisgraber, K. H., Dong, L. M., Jakes, R., Huang, D. Y., Pericak-Vance, M., Schmechel, D., & Roses, A. D. (1994) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.91.23.11183 · Cited by 474 · see citing works
Strittmatter, W. J., Weisgraber, K. H., Goedert, M., Saunders, A. M., Huang, D., Corder, E. H., Dong, L., Jakes, R., Alberts, M. J., Gilbert, J. R., et al. (1994) · Experimental Neurology · doi:10.1006/exnr.1994.1019 · Cited by 433 · see citing works
Sanan, D. A., Weisgraber, K. H., Russell, S. J., Mahley, R. W., Huang, D., Saunders, A., Schmechel, D., Wisniewski, T., Frangione, B., & Roses, A. D. (1994) · Journal of Clinical Investigation · doi:10.1172/jci117407 · Cited by 404 · see citing works
Roses, A. D. (1994) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/00005072-199409000-00002 · Cited by 329 · see citing works
Nagy, Z., Esiri, M. M., Jobst, K. A., Morris, J. H., King, E. M.-F., McDonald, B., Litchfield, S., Smith, A. D., Barnetson, L. P. D., & Smith, A. D. (1995) · Dementia and Geriatric Cognitive Disorders · doi:10.1159/000106918 · Cited by 283 · see citing works
Self-citationApolipoprotein E: risk factor for Alzheimer disease.
Tsai, M. S., Tangalos, E. G., Petersen, R. C., Smith, G. E., Schaid, D. J., Kokmen, E., Ivnik, R. J., & Thibodeau, S. N. (1994) · PubMed Central · Cited by 265 · see citing works
Protection against Alzheimer's disease with apoE ∈2
Talbot, C., Lendon, C., Craddock, N., Shears, S., Morris, J., & Goate, A. (1994) · The Lancet · doi:10.1016/s0140-6736(94)92557-7 · Cited by 225 · see citing works
Ohm, T. G., Kirca, M., Bohl, J., Scharnagl, H., Groβ, W., & März, W. (1995) · Neuroscience · doi:10.1016/0306-4522(94)00596-w · Cited by 157 · see citing works
Nalbantoglu, J. N., Gilfix, B. M., Bertrand, P., Robitaille, Y., Gauthier, S. G., Rosenblatt, D. S., & Poirier, J. (1994) · Annals of Neurology · doi:10.1002/ana.410360614 · Cited by 137 · see citing works
Frequency of the apolipoprotein E ε2 allele is diminished in sporadic Alzheimer disease
West, H. L., William Rebeck, G., & Hyman, B. T. (1994) · Neuroscience Letters · doi:10.1016/0304-3940(94)91074-x · Cited by 125 · see citing works
Protective effect of apoE ∈2 in Alzheimer's disease
Benjamin, R., Leake, A., McArthur, F. K., Ince, P. G., Candy, J., Edwardson, J. A., Morris, C. M., & Bjertness, E. (1994) · The Lancet · doi:10.1016/s0140-6736(94)91804-x · Cited by 67 · see citing works
Czech, C., Förstl, H., Hentschel, F., Mönning, U., Besthorn, C., Geiger-Kabisch, C., Sattel, H. C., Masters, C. L., & Beyreuther, K. T. (1994) · European Archives of Psychiatry and Clinical Neuroscience · doi:10.1007/bf02191587 · Cited by 50 · see citing works
Houlden, H., Crook, R., Duff, K., et al. (1993) · UCL Discovery (University College London) · Cited by 8 · see citing works
Flagged first, then by citations
Cited by
Sorted by citations
Nelson, P. T., Alafuzoff, I., Bigio, E. H., Bouras, C., Braak, H., Cairns, N. J., Castellani, R. J., Crain, B. J., Davies, P., Tredici, K. D., et al. (2012) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/nen.0b013e31825018f7 · Cited by 2,050 · see citing works
The role of apolipoprotein E in Alzheimer's disease
Kim, J., Basak, J. M., & Holtzman, D. M. (2009) · Neuron · doi:10.1016/j.neuron.2009.06.026 · Cited by 1,661 · see citing works
Review Article: Genetics of Alzheimer Disease
Bekris, L. M., Yu, C.-E., Bird, T. D., & Tsuang, D. W. (2010) · Journal of Geriatric Psychiatry and Neurology · doi:10.1177/0891988710383571 · Cited by 1,029 · see citing works
Synapses and Alzheimer's Disease
Sheng, M., Sabatini, B. L., & Sudhof, T. C. (2012) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a005777 · Cited by 436 · see citing works
Huang, Y., Liu, X. Q., Wyss-Coray, T., Brecht, W. J., Sanan, D. A., & Mahley, R. W. (2001) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.151254698 · Cited by 392 · see citing works
Apolipoprotein E ε4 allele, AD pathology, and the clinical expression of Alzheimer’s disease
Bennett, D. A., Wilson, R. S., Schneider, J. A., Evans, D. A., Aggarwal, N. T., Arnold, S. E., Cochran, E. J., Berry-Kravis, E., & Bienias, J. L. (2003) · Neurology · doi:10.1212/01.wnl.0000042478.08543.f7 · Cited by 282 · see citing works
Human<i>APOE</i>Isoform-Dependent Effects on Brain β-Amyloid Levels in PDAPP Transgenic Mice
Bales, K. R., Liu, F., Wu, S., Lin, S., Koger, D., DeLong, C., Hansen, J. C., Sullivan, P. M., & Paul, S. M. (2009) · The Journal of Neuroscience · doi:10.1523/jneurosci.0887-09.2009 · Cited by 274 · see citing works
Effect of apolipoprotein E on biomarkers of amyloid load and neuronal pathology in Alzheimer disease
Vemuri, P., Wiste, H. J., Weigand, S. D., Knopman, D. S., Shaw, L. M., Trojanowski, J. Q., Aisen, P. S., Weiner, M., Petersen, R. C., Jack, C. R., et al. (2010) · Annals of Neurology · doi:10.1002/ana.21953 · Cited by 195 · see citing works
Wu, L., Zhang, X., & Zhao, L. (2018) · The Journal of Neuroscience · doi:10.1523/jneurosci.2262-17.2018 · Cited by 185 · see citing works
Serrano‐Pozo, A., Qian, J., Monsell, S. E., Betensky, R. A., & Hyman, B. T. (2015) · Annals of Neurology · doi:10.1002/ana.24369 · Cited by 176 · see citing works
APOE ε2 is associated with intact cognition but increased Alzheimer pathology in the oldest old
Berlau, D. J., Corrada, M. M., Head, E., & Kawas, C. H. (2009) · Neurology · doi:10.1212/01.wnl.0000343853.00346.a4 · Cited by 185 · see citing works
Suri, S., Heise, V., Trachtenberg, A. J., & Mackay, C. E. (2013) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2013.10.010 · Cited by 183 · see citing works
AAVrh.10-Mediated APOE2 Central Nervous System Gene Therapy for APOE4-Associated Alzheimer's Disease
Rosenberg, J. B., Kaplitt, M. G., De, B. P., Chen, A., Flagiello, T., Salami, C., Pey, E., Zhao, L., Ricart Arbona, R. J., Monette, S., et al. (2018) · Human Gene Therapy Clinical Development · doi:10.1089/humc.2017.231 · Cited by 169 · see citing works
APOE-ε2 and APOE-ε4 Correlate With Increased Amyloid Accumulation in Cerebral Vasculature
Nelson, P. T., Pious, N. M., Jicha, G. A., Wilcock, D. M., Fardo, D. W., Estus, S., & Rebeck, G. W. (2013) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/nen.0b013e31829a25b9 · Cited by 150 · see citing works
Arora, S., Layek, B., & Singh, J. (2021) · Molecular Pharmaceutics · doi:10.1021/acs.molpharmaceut.0c00461 · Cited by 149 · see citing works
Ghebremedhin, E., Schultz, C., Braak, E., & Braak, H. (1998) · Experimental Neurology · doi:10.1006/exnr.1998.6860 · Cited by 133 · see citing works
Neurotheranostics as Personalized Medicines
Kevadiya, B. D., Ottemann, B. M., Thomas, M. B., Mukadam, I., Nigam, S., McMillan, J., Gorantla, S., Bronich, T. K., Edagwa, B., & Gendelman, H. E. (2019) · Advanced Drug Delivery Reviews · doi:10.1016/j.addr.2018.10.011 · Cited by 124 · see citing works
Gender and age modify the association between APOE and AD-related neuropathology
Ghebremedhin, E., Schultz, C., Thal, D. R., Rüb, U., Ohm, T. G., Braak, E., & Braak, H. (2001) · Neurology · doi:10.1212/wnl.56.12.1696 · Cited by 108 · see citing works
Dore, G. A., Elias, M. F., Robbins, M. A., Elias, P. K., & Nagy, Z. (2009) · Diabetologia · doi:10.1007/s00125-009-1497-2 · Cited by 81 · see citing works
Self-citationCao, Q., Shin, W. S., Chan, H., Vuong, C. K., Dubois, B., Li, B., Murray, K. A., Sawaya, M. R., Feigon, J., Black, D. L., et al. (2018) · Nature Chemistry · doi:10.1038/s41557-018-0147-z · Cited by 75 · see citing works
Koch, G., Di Lorenzo, F., Loizzo, S., Motta, C., Travaglione, S., Baiula, M., Rimondini, R., Ponzo, V., Bonnì, S., Toniolo, S., et al. (2017) · Scientific Reports · doi:10.1038/s41598-017-14204-3 · Cited by 64 · see citing works
Hirsch-Reinshagen, V., & Wellington, C. L. (2007) · Current Opinion in Lipidology · doi:10.1097/mol.0b013e32813aeabf · Cited by 61 · see citing works
Apolipoprotein E decreases tau kinases and phospho-tau levels in primary neurons.
Hoe, H.-S., Freeman, J., & Rebeck, G. W. (2006) · Molecular Neurodegeneration · doi:10.1186/1750-1326-1-18 · Cited by 45 · see citing works
Alafuzoff, I., Overmyer, M., Helisalmi, S., & Soininen, H. (2000) · Journal of Alzheimer's Disease · doi:10.3233/jad-2000-2105 · Cited by 42 · see citing works
Tian, J. (2004) · Journal of Neurology, Neurosurgery & Psychiatry · doi:10.1136/jnnp.2003.012096 · Cited by 39 · see citing works
APOE2 mitigates disease-related phenotypes in an isogenic hiPSC-based model of Alzheimer’s disease
Brookhouser, N., Raman, S., Frisch, C., Srinivasan, G., & Brafman, D. A. (2021) · Molecular Psychiatry · doi:10.1038/s41380-021-01076-3 · Cited by 33 · see citing works
Preman, P., Moechars, D., Fertan, E., Wolfs, L., Serneels, L., Shah, D., Lamote, J., Poovathingal, S., Snellinx, A., Mancuso, R., et al. (2024) · EMBO Molecular Medicine · doi:10.1038/s44321-024-00162-7 · Cited by 32 · see citing works
Yates, S. C., Zafar, A., Rabai, E. M., Foxall, J. B., Nagy, S., Morrison, K. E., Clarke, C., Esiri, M. M., Christie, S., Smith, A. D., et al. (2015) · PLOS ONE · doi:10.1371/journal.pone.0114050 · Cited by 31 · see citing works
Self-citation
- Authors
- Nagy, Z. S., Esiri, M. M., Jobst, K. A., Johnston, C., Litchfield, S., Sim, E., & Smith, A. D.
- Affiliations
- University of Oxford (GB)
- Corresponding author
- Nagy, Z.S.
- Venue
- Neuroscience
- Publisher
- Elsevier BV
- Published
- 1995-12
- Volume
- 69
- Issue
- 3
- Pages
- 757-761
- ISSN
- 0306-4522 (ISSN-L)
- OpenAlex
- W1985137206
- Cited by
- 250
- References
- 27
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 12 · 2023: 6 · 2022: 11 · 2021: 13 · 2020: 10 · 2019: 9 · 2018: 8 · 2017: 5 · 2016: 7 · 2015: 9 · 2014: 5 · 2013: 13 · 2012: 7
- FWCI
- 5.21
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- University of Birmingham Research Portal (University of Birmingham) (publishedVersion)
- University of Birmingham Research Portal (University of Birmingham) (submittedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- apolipoprotein E, APOE ε4, Alzheimer's disease, amyloid deposition, neurofibrillary tangles, neuritic plaques, tau phosphorylation, neocortex, genetic risk
- MeSH terms
- Aged, Aged, 80 and over, Alleles, Alzheimer Disease, Amyloid, Apolipoproteins E, Female, Genotype, Humans, Male, Middle Aged, Neurites, Neurofibrillary Tangles, Apolipoprotein E3, Apolipoprotein E4, Apolipoprotein E2
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 ›
Are you an author, or do you see a problem with this page? Request a review
