The DOI matches its Crossref record; 20 of the 20 references it cites were found in a registry or an index.
Full-length amyloid precursor protein regulates lipoprotein metabolism and amyloid-β clearance in human astrocytes
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
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?
Simvastatin reduced pThr231Tau/tTau the same in a previously generated isogenic set of NDC (APPwt) and APPnull neurons.
“Similarly, simvastatin reduced pThr231Tau/tTau the same in a previously generated isogenic set of NDC (APPwt) and APPnull neurons (CV line 151 and IB6) (Fong et al., 2018) (Figure 3H).”
From Cholesterol Metabolism Is a Druggable Axis that Independently Regulates Tau and Amyloid-β in iPSC-Derived Alzheimer’s Disease Neurons (2019) · cites this paper as Fong et al., 2018
Inhibition of β-secretase reversed these effects in astrocytes.
“the inhibition of β-secretase reversed these effects”
From Emerging Alternative Proteinases in APP Metabolism and Alzheimer’s Disease Pathogenesis: A Focus on MT1-MMP and MT5-MMP (2019) · cites this paper as Fong et al., 2018
Human iPS-derived astrocytes deficient for APP exhibit reduced intracellular cholesterol levels.
“human astrocytes derived from induced pluripotent stem cells (iPS) deficient for APP exhibited reduced levels of intracellular cholesterol”
From Emerging Alternative Proteinases in APP Metabolism and Alzheimer’s Disease Pathogenesis: A Focus on MT1-MMP and MT5-MMP (2019) · cites this paper as Fong et al., 2018
Human iPS-derived astrocytes deficient for APP have a reduced ability to endocytose apolipoprotein E (APOE) and Aβ.
“as well as a reduced ability to endocyte apolipoprotein E (APOE) and Aβ”
From Emerging Alternative Proteinases in APP Metabolism and Alzheimer’s Disease Pathogenesis: A Focus on MT1-MMP and MT5-MMP (2019) · cites this paper as Fong et al., 2018
The Swedish APP mutation is characterized by reduced canonical APP levels due to exacerbated cleavage of APP by β-secretase.
“characterized by reduced canonical levels of APP due to exacerbated cleavage of APP by β-secretase.”
From Emerging Alternative Proteinases in APP Metabolism and Alzheimer’s Disease Pathogenesis: A Focus on MT1-MMP and MT5-MMP (2019) · cites this paper as Fong et al., 2018
Astrocytes expressing APP harboring the Swedish familial mutation show similar deficits.
“Similar deficits have been observed in astrocytes expressing APP harboring the Swedish familial mutation”
From Emerging Alternative Proteinases in APP Metabolism and Alzheimer’s Disease Pathogenesis: A Focus on MT1-MMP and MT5-MMP (2019) · cites this paper as Fong et al., 2018
Inhibiting β-secretase may benefit astrocytes.
“highlighting the potential benefits of such inhibition specifically in astrocytes (Fong et al., 2018).”
From Emerging Alternative Proteinases in APP Metabolism and Alzheimer’s Disease Pathogenesis: A Focus on MT1-MMP and MT5-MMP (2019) · cites this paper as Fong et al., 2018
Full-length APP can function as a receptor regulating cholesterol/lipoprotein metabolism and Aβ clearance.
“Another work highlights the potential of full length APP as functional receptor for the regulation of cholesterol/lipoprotein metabolism and Aβ clearance (Fong et al., 2018).”
From Emerging Alternative Proteinases in APP Metabolism and Alzheimer’s Disease Pathogenesis: A Focus on MT1-MMP and MT5-MMP (2019) · cites this paper as Fong et al., 2018
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein
Games, D., Adams, D., Alessandrini, R., Barbour, R., Borthelette, P., Blackwell, C., Carr, T., Clemens, J., Donaldson, T., Gillespie, F., et al. (1995) · Nature · doi:10.1038/373523a0 · Cited by 2,516
Decreased Clearance of CNS β-Amyloid in Alzheimer’s Disease
Mawuenyega, K. G., Sigurdson, W., Ovod, V., Munsell, L., Kasten, T., Morris, J. C., Yarasheski, K. E., & Bateman, R. J. (2010) · Science · doi:10.1126/science.1197623 · Cited by 2,078
Systematic meta-analyses of Alzheimer disease genetic association studies: the AlzGene database
Bertram, L., McQueen, M. B., Mullin, K., Blacker, D., & Tanzi, R. E. (2007) · Nature Genetics · doi:10.1038/ng1934 · Cited by 1,857
The Diploid Genome Sequence of an Individual Human
Levy, S., Sutton, G., Ng, P. C., Feuk, L., Halpern, A. L., Walenz, B. P., Axelrod, N., Huang, J., Kirkness, E. F., Denisov, G., et al. (2007) · PLoS Biology · doi:10.1371/journal.pbio.0050254 · Cited by 1,778
Citron, M., Oltersdorf, T., Haass, C., McConlogue, L., Hung, A. Y., Seubert, P., Vigo-Pelfrey, C., Lieberburg, I., & Selkoe, D. J. (1992) · Nature · doi:10.1038/360672a0 · Cited by 1,757
Alzheimer’s Disease: The Challenge of the Second Century
Holtzman, D. M., Morris, J. C., & Goate, A. M. (2011) · Science Translational Medicine · doi:10.1126/scitranslmed.3002369 · Cited by 1,424
Kong, W., Wei, J., Abidi, P., Lin, M., Inaba, S., Li, C., Wang, Y., Wang, Z., Si, S., Pan, H., et al. (2004) · Nature Medicine · doi:10.1038/nm1135 · Cited by 1,391
Lipidomics reveals a remarkable diversity of lipids in human plasma
Quehenberger, O., Armando, A. M., Brown, A. H., Milne, S. B., Myers, D. S., Merrill, A. H., Bandyopadhyay, S., Jones, K. N., Kelly, S., Shaner, R. L., et al. (2010) · Journal of Lipid Research · doi:10.1194/jlr.m009449 · Cited by 1,341
Somatic coding mutations in human induced pluripotent stem cells
Gore, A., Li, Z., Fung, H.-L., Young, J. E., Agarwal, S., Antosiewicz-Bourget, J., Canto, I., Giorgetti, A., Israel, M. A., Kiskinis, E., et al. (2011) · Nature · doi:10.1038/nature09805 · Cited by 1,273
Self-citationProbing sporadic and familial Alzheimer’s disease using induced pluripotent stem cells
Israel, M. A., Yuan, S. H., Bardy, C., Reyna, S. M., Mu, Y., Herrera, C., Hefferan, M. P., Van Gorp, S., Nazor, K. L., Boscolo, F. S., et al. (2012) · Nature · doi:10.1038/nature10821 · Cited by 1,253
Self-citationRelease of Excess Amyloid β Protein from a Mutant Amyloid β Protein Precursor
Cai, X.-D., Golde, T. E., & Younkin, S. G. (1993) · Science · doi:10.1126/science.8424174 · Cited by 913
Haass, C., Lemere, C. A., Capell, A., Citron, M., Seubert, P., Schenk, D., Lannfelt, L., & Selkoe, D. J. (1995) · Nature Medicine · doi:10.1038/nm1295-1291 · Cited by 592
Kamal, A., Almenar-Queralt, A., LeBlanc, J. F., Roberts, E. A., & Goldstein, L. S. B. (2001) · Nature · doi:10.1038/414643a · Cited by 583
Self-citationCholesterol metabolism in neurons and astrocytes
Pfrieger, F. W., & Ungerer, N. (2011) · Progress in Lipid Research · doi:10.1016/j.plipres.2011.06.002 · Cited by 500
Young-Pearse, T. L., Bai, J., Chang, R., Zheng, J. B., LoTurco, J. J., & Selkoe, D. J. (2007) · The Journal of Neuroscience · doi:10.1523/jneurosci.4701-07.2007 · Cited by 369
Kang, D. E., Pietrzik, C. U., Baum, L., Chevallier, N., Merriam, D. E., Kounnas, M. Z., Wagner, S. L., Troncoso, J. C., Kawas, C. H., Katzman, R., et al. (2000) · Journal of Clinical Investigation · doi:10.1172/jci11013 · Cited by 354
Kim, J., Castellano, J. M., Jiang, H., Basak, J. M., Parsadanian, M., Pham, V., Mason, S. M., Paul, S. M., & Holtzman, D. M. (2009) · Neuron · doi:10.1016/j.neuron.2009.11.013 · Cited by 274
Astrocytic LRP1 Mediates Brain Aβ Clearance and Impacts Amyloid Deposition
Liu, C.-C., Hu, J., Zhao, N., Wang, J., Wang, N., Cirrito, J. R., Kanekiyo, T., Holtzman, D. M., & Bu, G. (2017) · The Journal of Neuroscience · doi:10.1523/jneurosci.3442-16.2017 · Cited by 267
Pietrzik, C. U., Busse, T., Merriam, D. E., Weggen, S., & Koo, E. H. (2002) · The EMBO Journal · doi:10.1093/emboj/cdf568 · Cited by 198
Zerbinatti, C. V., Wahrle, S. E., Kim, H., Cam, J. A., Bales, K., Paul, S. M., Holtzman, D. M., & Bu, G. (2006) · Journal of Biological Chemistry · doi:10.1074/jbc.m604436200 · Cited by 129
Flagged first, then by citations
Research works printed but not linked: 58
- Hardy, 1997, Amyloid, the presenilins and Alzheimer's disease, Trends Neurosci, 20, 154, 10.1016/S0166-2236(96)01030-2 · DOI · Paper page
- Hardy, 2002, The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics, Science, 297, 353, 10.1126/science.1072994 · DOI · Paper page
- Corder, 1993, Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer's disease in late onset families, Science, 261, 921, 10.1126/science.8346443 · DOI · Paper page
- Liu, 2013, Apolipoprotein E and Alzheimer disease: risk, mechanisms and therapy, Nat. Rev. Neurol, 9, 106, 10.1038/nrneurol.2012.263 · DOI · Paper page
- Jick, 2000, Statins and the risk of dementia, Lancet, 356, 1627, 10.1016/S0140-6736(00)03155-X · DOI
- Yaffe, 2002, Serum lipoprotein levels, statin use, and cognitive function in older women, Arch. Neurol, 59, 378, 10.1001/archneur.59.3.378 · DOI
- Rockwood, 2002, Use of lipid-lowering agents, indication bias, and the risk of dementia in community-dwelling elderly people, Arch. Neurol, 59, 223, 10.1001/archneur.59.2.223 · DOI
- van der Kant, 2015, Cellular functions of the amyloid precursor protein from development to dementia, Dev. Cell, 32, 502, 10.1016/j.devcel.2015.01.022 · DOI
- Grimm, 2005, Regulation of cholesterol and sphingomyelin metabolism by amyloid-β and presenilin, Nat. Cell Biol, 7, 1118, 10.1038/ncb1313 · DOI
- Liu, 2007, Amyloid precursor protein regulates brain apolipoprotein E and cholesterol metabolism through lipoprotein receptor LRP1, Neuron, 56, 66, 10.1016/j.neuron.2007.08.008 · DOI · Paper page
- Tamboli, 2008, Loss of γ-secretase function impairs endocytosis of lipoprotein particles and membrane cholesterol homeostasis, J. Neurosci, 28, 12097, 10.1523/JNEUROSCI.2635-08.2008 · DOI · Paper page
- Pierrot, 2013, Amyloid precursor protein controls cholesterol turnover needed for neuronal activity, EMBO Mol. Med, 5, 608, 10.1002/emmm.201202215 · DOI
- Wang, 2014, Amyloid precursor protein α- and β-cleaved ectodomains exert opposing control of cholesterol homeostasis via SREBP2, FASEB J, 28, 849, 10.1096/fj.13-239301 · DOI
- Goldstein, 2006, Protein sensors for membrane sterols, Cell, 124, 35, 10.1016/j.cell.2005.12.022 · DOI · Paper page
- Deane, 2004, LRP/amyloid β-peptide interaction mediates differential brain efflux of Aβ isoforms, Neuron, 43, 333, 10.1016/j.neuron.2004.07.017 · DOI · Paper page
- Basak, 2012, Low-density lipoprotein receptor represents an apolipoprotein E-independent pathway of Aβ uptake and degradation by astrocytes, J. Biol. Chem, 287, 13959, 10.1074/jbc.M111.288746 · DOI · Paper page
- Nicolas, 2014, Amyloid precursor protein and neural development, Development, 141, 2543, 10.1242/dev.108712 · DOI
- Yuan, 2011, Cell-surface marker signatures for the isolation of neural stem cells, glia and neurons derived from human pluripotent stem cells, PLoS ONE, 6, e17540, 10.1371/journal.pone.0017540 · DOI
- Björkhem, 2004, Brain cholesterol: long secret life behind a barrier, Arterioscler. Thromb. Vasc. Biol, 24, 806, 10.1161/01.ATV.0000120374.59826.1b · DOI · Paper page
- Nieweg, 2009, Marked differences in cholesterol synthesis between neurons and glial cells from postnatal rats, J. Neurochem, 109, 125, 10.1111/j.1471-4159.2009.05917.x · DOI · Paper page
- Brown, 1997, The SREBP pathway: regulation of cholesterol metabolism by proteolysis of a membrane-bound transcription factor, Cell, 89, 331, 10.1016/S0092-8674(00)80213-5 · DOI · Paper page
- Yang, 2006, Sterol intermediates from cholesterol biosynthetic pathway as liver X receptor ligands, J. Biol. Chem, 281, 27816, 10.1074/jbc.M603781200 · DOI
- Zhang, 2016, Purification and characterization of progenitor and mature human astrocytes reveals transcriptional and functional differences with mouse, Neuron, 89, 37, 10.1016/j.neuron.2015.11.013 · DOI · Paper page
- Llorente-Cortés, 2006, Sterol regulatory element-binding protein-2 negatively regulates low density lipoprotein receptor-related protein transcription, J. Mol. Biol, 359, 950, 10.1016/j.jmb.2006.04.008 · DOI
- van Dam, 2002, Endocytosed transferrin receptors recycle via distinct dynamin and phosphatidylinositol 3-kinase-dependent pathways, J. Biol. Chem, 277, 48876, 10.1074/jbc.M206271200 · DOI
- Woodruff, 2016, Defective transcytosis of APP and lipoproteins in human iPSC-derived neurons with familial Alzheimer's disease mutations, Cell Rep, 17, 759, 10.1016/j.celrep.2016.09.034 · DOI · Paper page
- Tamaoka, 1994, APP717 missense mutation affects the ratio of amyloid β protein species (Aβ 1–42/43 and Aβ 1–40) in familial Alzheimer's disease brain, J. Biol. Chem, 269, 32721, 10.1016/S0021-9258(20)30050-8 · DOI
- Suzuki, 1994, An increased percentage of long amyloid β protein secreted by familial amyloid β protein precursor (β APP717) mutants, Science, 264, 1336, 10.1126/science.8191290 · DOI · Paper page
- Chen, 2008, Assessing the sensitivity of commercially available fluorophores to the intracellular environment, Anal. Chem, 80, 7437, 10.1021/ac8011347 · DOI
- Vassar, 1999, β-Secretase cleavage of Alzheimer's amyloid precursor protein by the transmembrane aspartic protease BACE, Science, 286, 735, 10.1126/science.286.5440.735 · DOI · Paper page
- Choy, 2012, Amyloid precursor protein (APP) traffics from the cell surface via endosomes for amyloid β (Aβ) production in the trans-Golgi network, Proc. Natl. Acad. Sci. U.S.A, 109, E2077, 10.1073/pnas.1208635109 · DOI
- Yamakawa, 2010, β-Secretase inhibitor potency is decreased by aberrant β-cleavage location of the “Swedish Mutant” amyloid precursor protein, J. Biol. Chem, 285, 1634, 10.1074/jbc.M109.066753 · DOI
- Kounnas, 1995, LDL receptor-related protein, a multifunctional apoE receptor, binds secreted β-amyloid precursor protein and mediates its degradation, Cell, 82, 331, 10.1016/0092-8674(95)90320-8 · DOI · Paper page
- Knauer, 1996, Cell surface APP751 forms complexes with protease nexin 2 ligands is internalized via the low density lipoprotein receptor-related protein (LRP), Brain Res, 740, 6, 10.1016/S0006-8993(96)00711-1 · DOI
- Pietrzik, 2004, FE65 constitutes the functional link between the low-density lipoprotein receptor-related protein and the amyloid precursor protein, J. Neurosci, 24, 4259, 10.1523/JNEUROSCI.5451-03.2004 · DOI · Paper page
- Trommsdorff, 1998, Interaction of cytosolic adaptor proteins with neuronal apolipoprotein E receptors and the amyloid precursor protein, J. Biol. Chem, 273, 33556, 10.1074/jbc.273.50.33556 · DOI · Paper page
- Bu, 2006, LRP in amyloid-β production and metabolism, Ann. N.Y. Acad. Sci, 1086, 35, 10.1196/annals.1377.005 · DOI
- Hass, 1998, Physical interaction of ApoE with amyloid precursor protein independent of the amyloid Aβ region in vitro, J. Biol. Chem, 273, 13892, 10.1016/S0021-9258(19)57838-3 · DOI
- Kamal, 2000, Axonal transport of amyloid precursor protein is mediated by direct binding to the Kinesin light chain subunit of kinesin-I, Neuron, 28, 449, 10.1016/S0896-6273(00)00124-0 · DOI · Paper page
- Schmidt, 2007, SorLA/LR11 regulates processing of amyloid precursor protein via interaction with adaptors GGA and PACS-1, J. Biol. Chem, 282, 32956, 10.1074/jbc.M705073200 · DOI · Paper page
- Barrett, 2012, The amyloid precursor protein has a flexible transmembrane domain and binds cholesterol, Science, 336, 1168, 10.1126/science.1219988 · DOI · Paper page
- McDonald, 2012, A comprehensive method for extraction and quantitative analysis of sterols and secosteroids from human plasma, J. Lipid Res, 53, 1399, 10.1194/jlr.D022285 · DOI
- Mauch, 2001, CNS synaptogenesis promoted by glia-derived cholesterol, Science, 294, 1354, 10.1126/science.294.5545.1354 · DOI · Paper page
- Karch, 2014, Alzheimer's disease genetics: from the bench to the clinic, Neuron, 83, 11, 10.1016/j.neuron.2014.05.041 · DOI · Paper page
- Ryan, 2016, Clinical phenotype and genetic associations in autosomal dominant familial Alzheimer's disease: a case series, Lancet Neurol, 15, 1326, 10.1016/S1474-4422(16)30193-4 · DOI
- Hsiao, 1996, Correlative memory deficits, Aβ elevation, and amyloid plaques in transgenic mice, Science, 274, 99, 10.1126/science.274.5284.99 · DOI · Paper page
- Mucke, 2000, High-level neuronal expression of Aβ1–42 in wild-type human amyloid protein precursor transgenic mice: synaptotoxicity without plaque formation, J. Neurosci, 20, 4050, 10.1523/JNEUROSCI.20-11-04050.2000 · DOI · Paper page
- Oddo, 2003, Triple-transgenic model of Alzheimer's disease with plaques and tangles: intracellular Aβ and synaptic dysfunction, Neuron, 39, 409, 10.1016/S0896-6273(03)00434-3 · DOI · Paper page
- Siman, 1989, Expression of β-amyloid precursor protein in reactive astrocytes following neuronal damage, Neuron, 3, 275, 10.1016/0896-6273(89)90252-3 · DOI
- Töpper, 1995, Rapid appearance of β-amyloid precursor protein immunoreactivity in glial cells following excitotoxic brain injury, Acta Neuropathol, 89, 23, 10.1007/BF00294255 · DOI
- Almenar-Queralt, 2014, UV irradiation accelerates amyloid precursor protein (APP) processing and disrupts APP axonal transport, J. Neurosci, 34, 3320, 10.1523/JNEUROSCI.1503-13.2014 · DOI
- Ulery, 2000, Modulation of β-amyloid precursor protein processing by the low density lipoprotein receptor-related protein (LRP). Evidence that LRP contributes to the pathogenesis of Alzheimer's disease, J. Biol. Chem, 275, 7410, 10.1074/jbc.275.10.7410 · DOI · Paper page
- Marzolo, 2009, Lipoprotein receptors and cholesterol in APP trafficking and proteolytic processing, implications for Alzheimer's disease, Semin. Cell Dev. Biol, 20, 191, 10.1016/j.semcdb.2008.10.005 · DOI · Paper page
- Woodruff, 2013, The presenilin-1 dE9 mutation results in reduced γ-secretase activity, but not total loss of PS1 function, in isogenic human stem cells, Cell Rep, 5, 974, 10.1016/j.celrep.2013.10.018 · DOI · Paper page
- Young, 2015, Elucidating molecular phenotypes caused by the SORL1 Alzheimer's disease genetic risk factor using human induced pluripotent stem cells, Cell Stem Cell, 16, 373, 10.1016/j.stem.2015.02.004 · DOI
- Mali, 2013, RNA-guided human genome engineering via Cas9, Science, 339, 823, 10.1126/science.1232033 · DOI · Paper page
- Ran, 2013, Genome engineering using the CRISPR-Cas9 system, Nat. Protoc, 8, 2281, 10.1038/nprot.2013.143 · DOI · Paper page
- D'Antonio, 2017, High-throughput and cost-effective characterization of induced pluripotent stem cells, Stem Cell Reports, 8, 1101, 10.1016/j.stemcr.2017.03.011 · DOI
Cited by
Sorted by citations
Amyloid-β-independent regulators of tau pathology in Alzheimer disease
van der Kant, R., Goldstein, L. S. B., & Ossenkoppele, R. (2020) · Nature reviews. Neuroscience · doi:10.1038/s41583-019-0240-3 · Cited by 580
Self-citationvan der Kant, R., Langness, V. F., Herrera, C. M., Williams, D. A., Fong, L. K., Leestemaker, Y., Steenvoorden, E., Rynearson, K. D., Brouwers, J. F., Helms, J. B., et al. (2019) · Cell Stem Cell · doi:10.1016/j.stem.2018.12.013 · Cited by 350
Self-citationCholesterol and Alzheimer’s Disease; From Risk Genes to Pathological Effects
Feringa, F. M., & van der Kant, R. (2021) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2021.690372 · Cited by 226
Poudel, P., & Park, S. (2022) · Pharmaceutics · doi:10.3390/pharmaceutics14040835 · Cited by 124
García-González, L., Pilat, D., Baranger, K., & Rivera, S. (2019) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2019.00244 · Cited by 88
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
Chebli, J., Rahmati, M., Lashley, T., Edeman, B., Oldfors, A., Zetterberg, H., & Abramsson, A. (2021) · Scientific Reports · doi:10.1038/s41598-021-98487-7 · Cited by 17
Metadata
- Authors
- Fong, L. K., Yang, M. M., dos Santos Chaves, R., Reyna, S. M., Langness, V. F., Woodruff, G., Roberts, E. A., Young, J. E., & Goldstein, L. S. B.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2018-07
- Volume
- 293
- Issue
- 29
- Pages
- 11341-11357
- ISSN
- 0021-9258
- Cited by
- 72
- References
- 20
- Language
- en
- Funders
- HHS National Institutes of Health (NIH) (T32 GM008666)
- HHS NIH National Institute on Aging (NIA) (RF1 AG048083–01, 2P50 AG005131–31)
- Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) (2013/18028–9)
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