The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
Apolipoprotein E in sporadic Alzheimer's disease: Allelic variation and receptor interactions
Abstract
An increased prevalence of apolipoprotein E (ApoE) epsilon 4 allele exists in late onset familial Alzheimer's disease. We found, in sporadic Alzheimer's disease, that 62% of patients possessed an ApoE-epsilon 4 allele, compared with 20% of controls. ApoE-epsilon 4/4 patients had more senile plaques (SPs) than epsilon 3/3 patients. ApoE immunoreactivity of SPs was equivalent in both groups. Two receptors bind ApoE complexes, the low density lipoprotein (LDL) receptor and the LDL receptor-related protein (LRP). In normal brain, anti-LRP antibodies strongly stained neurons and lightly stained astrocytes; anti-LDL receptor antibodies stained only the neuropil and astrocytes. In Alzheimer's disease, SPs and reactive astrocytes were also strongly LRP immunoreactive. Colocalization of ApoE and LRP to SPs implies that these molecules may be involved in metabolism of components of SPs.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
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?
In the citing paper
“APOE4 is the strongest genetic determinant of late-onset AD, increasing risk in a gene dose-dependent manner, whereas APOE2 confers substantial protection 1 -5 .”
From APOE2 attenuates APOE4-associated amyloid pathology and related toxicity in a mouse model of Alzheimer’s disease (2026) · cites this paper as [2]
In the citing paper
“As APOE4 carriers make up 55–75% of AD cases17–20”
From The APOE-R136S mutation protects against APOE4-driven tau pathology, neurodegeneration, and neuroinflammation (2023) · cites this paper as [19]
In the citing paper
“Studies indicate that APOE binding is integral to some of these processes [16–20] with differences in APOE isoform-specific receptor binding affinity and lipid interactions affecting neuroinflammation, tau pathology, and amyloid plaque dynamics [21–24].”
From APOE Christchurch enhances a disease-associated microglial response to plaque but suppresses response to tau pathology (2025) · cites this paper as [24]
In the citing paper
“Collectively, these recent findings underscore the influence of APOE and APOE3Ch on both Aβ and tau pathology, either directly or through downstream effects such as neuroinflammation.”
From APOE Christchurch enhances a disease-associated microglial response to plaque but suppresses response to tau pathology (2025) · cites this paper as [24]
In the citing paper
“Initial histopathological studies investigating the relationship between amyloid plaques and apoE isoforms demonstrated a positive correlation between plaque density and apoE ε4 allele dose (Rebeck et al., 1993; Schmechel et al., 1993).”
From The role of apolipoprotein E in Alzheimer's disease (2009) · cites this paper as Rebeck et al., 1993
In the citing paper
“By immunostaining, these activated astrocytes express both the LDLR and LRP (data not shown), consistent with the previous observations summarized above that these are the two primary members of the LDLR family that are expressed by activated astrocytes (4 -7, 29 -31).”
From Apolipoprotein E Receptors Mediate the Effects of β-Amyloid on Astrocyte Cultures (2000) · cites this paper as [6]
In the citing paper
“neural cells express a variety of apoE receptors in the low density lipoprotein receptor (LDLR) family (4 -7).”
From Apolipoprotein E Receptors Mediate the Effects of β-Amyloid on Astrocyte Cultures (2000) · cites this paper as [6]
Citations
Cites
Goate, A., Chartier-Harlin, M.-C., Mullan, M., Brown, J., Crawford, F., Fidani, L., Giuffra, L., Haynes, A., Irving, N., James, L., et al. (1991) · Nature · doi:10.1038/349704a0 · Cited by 4,659
Strittmatter, W. J., Saunders, A. M., Schmechel, D., Pericak-Vance, M., Enghild, J., Salvesen, G. S., & Roses, A. D. (1993) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.90.5.1977 · Cited by 4,268
Neurofibrillary tangles but not senile plaques parallel duration and severity of Alzheimer's disease
Arriagada, P. V., Growdon, J. H., Hedley-Whyte, E. T., & Hyman, B. T. (1992) · Neurology · doi:10.1212/wnl.42.3.631 · Cited by 2,668
Self-citationAmyloid deposition as the central event in the aetiology of Alzheimer’s disease
Hardy, J., & Allsop, D. (1991) · Trends in Pharmacological Sciences · doi:10.1016/0165-6147(91)90609-v · Cited by 2,538
Apolipoprotein E polymorphism and atherosclerosis.
Davignon, J., Gregg, R. E., & Sing, C. F. (1988) · Arteriosclerosis: An Official Journal of the American Heart Association, Inc. · doi:10.1161/01.atv.8.1.1 · Cited by 1,981
Amyloid β-peptide is produced by cultured cells during normal metabolism
Haass, C., Schlossmacher, M. G., Hung, A. Y., Vigo-Pelfrey, C., Mellon, A., Ostaszewski, B. L., Lieberburg, I., Koo, E. H., Schenk, D., Teplow, D. B., et al. (1992) · Nature · doi:10.1038/359322a0 · Cited by 1,921
Production of the Alzheimer Amyloid β Protein by Normal Proteolytic Processing
Shoji, M., Golde, T. E., Ghiso, J., Cheung, T. T., Estus, S., Shaffer, L. M., Cai, X.-D., McKay, D. M., Tintner, R., Frangione, B., et al. (1992) · Science · doi:10.1126/science.1439760 · Cited by 1,447
Astrocytes synthesize apolipoprotein E and metabolize apolipoprotein E-containing lipoproteins
Pitas, R. E., Boyles, J. K., Lee, S. H., Foss, D., & Mahley, R. W. (1987) · Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism · doi:10.1016/0005-2760(87)90295-5 · Cited by 693
Research works printed but not linked: 32
- Abraham, 1988, Immunochemical identification of the serine protease inhibitor α1-antichymotrypsin in the brain amyloid deposits of Alzheimer's disease, Cell, 52, 487, 10.1016/0092-8674(88)90462-X · DOI
- Arriagada, 1992, Distribution of Alzheimer-type pathologic changes in nondemented elderly individuals matches the pattern in Alzheimer's disease, Neurology, 42, 1681, 10.1212/WNL.42.9.1681 · DOI · Paper page
- Bauer, 1991, Interleukin-6 and α-2-macroglobulin indicate an acute-phase state in Alzheimer's disease cortices, FEBS Lett., 285, 111, 10.1016/0014-5793(91)80737-N · DOI · Paper page
- Beisiegel, 1981, Monoclonal antibodies to the low density lipoprotein receptor as probes for study of receptormediated endocytosis and the genetics of familial hypercholesterolemia, J. Biol. Chem., 256, 11923, 10.1016/S0021-9258(19)68494-2 · DOI · Paper page
- Beisiegel, 1989, The LDL-receptor-related protein, LRP, is an apolipoprotein E-binding protein, Nature, 341, 162, 10.1038/341162a0 · DOI
- Borth, 1992, α2-Macroglobulin, a multifunctional binding protein with targeting characteristics, FASEB J., 6, 3345, 10.1096/fasebj.6.15.1281457 · DOI
- Diedrich, 1991, Neuropathological changes in Scrapie and Alzheimer's disease are associated with increased expression of apolipoprotein E and cathepsin D in astrocytes, J. Virol., 65, 4759, 10.1128/JVI.65.9.4759-4768.1991 · DOI
- Herz, 1990, Low density lipoprotein receptor-related protein mediates endocytosis of monoclonal antibodies in cultured cells and rabbit liver, J. Biol. Chem., 265, 21355, 10.1016/S0021-9258(17)45368-3 · DOI
- Hixson, 1990, Restriction isotyping of human apolipoprotein E by gene amplification and cleavage with Hhal, J. Lipid Res., 31, 545, 10.1016/S0022-2275(20)43176-1 · DOI · Paper page
- Hyman, 1992, Kunitz protease inhibitor-containing amyloid β protein precursor immunoreactivity in Alzheimer's disease, J. Neuropathol. Exp. Neurol., 51, 76, 10.1097/00005072-199201000-00009 · DOI
- Hyman, 1993, The lack of accumulation of senile plaques or amyloid burden in Alzheimer's disease suggests a dynamic balance between amyloid deposition and resolution, J. Neuropathol. Exp. Neurol., 10.1097/00005072-199311000-00006 · DOI
- Mahley, 1988, Apolipoprotein E: cholesterol transport protein with expanding role in cell biology, Science, 240, 622, 10.1126/science.3283935 · DOI · Paper page
- Mann, 1989, An analysis of the morphology of senile plaques in Down's syndrome patients of different ages using immunocytochemical and lectin histochemical techniques, Neuropathol. Appl. Neurobiol., 15, 317, 10.1111/j.1365-2990.1989.tb01232.x · DOI
- Mueller-Hill, 1989, Molecular biology of Alzheimer's disease, Annu. Rev. Biochem., 58, 287, 10.1146/annurev.bi.58.070189.001443 · DOI
- Mullan, 1992, A locus for familial early-onset Alzheimer's disease on the long arm of chromosome 14, proximal to the α1-anti-chymotrypsin gene, Nature Genet., 2, 340, 10.1038/ng1292-340 · DOI
- Namba, 1991, Apolipoprotein E immunoreactivity in cerebral amyloid deposits and neurofibrillary tangles in Alzheimer's disease and kuru plaque amyloid in Creutzfeldt-Jakob disease, Brain Res., 541, 163, 10.1016/0006-8993(91)91092-F · DOI · Paper page
- Pericak-Vance, 1991, Linkage studies in familial Alzheimer disease: evidence for chromosome 19 linkage, Am. J. Hum. Genet., 48, 1034
- Poirier, 1991, Astrocytic apolipoprotein E mRNA and GFAP mRNA in hippocampus after entorhinal cortex lesioning, Mol. Brain Res., 11, 97, 10.1016/0169-328X(91)90111-A · DOI
- St. George-Hyslop, 1992, Genetic evidence for a novel familial Alzheimer's disease locus on chromosome 14, Nature Genet., 2, 330, 10.1038/ng1292-330 · DOI
- Saunders, 1993, Association of apolipoprotein E allele ε4 with late-onset familial and sporadic Alzheimer's disease, Neurology, 43, 1467, 10.1212/WNL.43.8.1467 · DOI · Paper page
- Schellenberg, 1991, APP717, APP693, and PRIP gene mutations are rare in Alzheimer disease, Am. J. Hum. Genet., 49, 511
- Schellenberg, 1992, Genetic linkage evidence for a familial Alzheimer's disease locus on chromosome 14, Science, 258, 668, 10.1126/science.1411576 · DOI
- Selkoe, 1991, The molecular pathology of Alzheimer's disease, Neuron, 6, 487, 10.1016/0896-6273(91)90052-2 · DOI · Paper page
- Smith, 1993, α1-trypsin immunoreactivity in Alzheimer disease, Biophys. Biochem. Res. Commun., 193, 579, 10.1006/bbrc.1993.1663 · DOI
- Strickland, 1990, Sequence identity between the α2-macroglobulin receptor and low density lipoprotein receptor-related protein suggests that this molecule is a multifunctional receptor, J. Biol. Chem., 265, 17401, 10.1016/S0021-9258(18)38172-9 · DOI · Paper page
- Tanzi, 1992, Assessment of amyloid β protein precursor gene mutations in a large set of familial and sporadic Alzheimer disease cases, Am. J. Hum. Genet., 51, 273
- van Broeckhoven, 1992, Mapping of a gene predisposing to early-onset Alzheimer's disease to chromosome 14q24.3, Nature Genet., 2, 335, 10.1038/ng1292-335 · DOI
- van Gool, 1993, α2-Macroglobulin expression in neuritic-type plaques in patients with Alzheimer's disease, Neurobiol. Aging, 14, 233, 10.1016/0197-4580(93)90006-W · DOI
- Weisgraber, 1982, Abnormal lipoprotein receptor-binding activity of the human E apoprotein due to cysteine-arginine interchange at a single site, J. Biol. Chem., 257, 2518, 10.1016/S0021-9258(18)34954-8 · DOI · Paper page
- Williams, 1992, A novel mechanism for controlling the activity of α2-macroglobulin receptor/low density lipoprotein receptor-related protein, J. Biol. Chem., 267, 9035, 10.1016/S0021-9258(19)50384-2 · DOI · Paper page
- Wisniewski, 1992, Apolipoprotein E: a pathological chaperone protein in patients with cerebral and systemic amyloid, Neurosci. Lett., 135, 235, 10.1016/0304-3940(92)90444-C · DOI · Paper page
- Wisniewski, 1993, Apolipoprotein E: binding to soluble Alzheimer's β-amyloid, Biochem. Biophys. Res. Commun., 192, 359, 10.1006/bbrc.1993.1423 · DOI · Paper page
Cited by
Sorted by citations
Items 101–137 of 137
ApoE isoform-dependent changes in hippocampal synaptic function
Korwek, K. M., Trotter, J. H., LaDu, M. J., Sullivan, P. M., & Weeber, E. J. (2009) · Molecular Neurodegeneration · doi:10.1186/1750-1326-4-21 · Cited by 89
Apolipoprotein E and Alzheimer's disease: the protective effects of ApoE2 and E3
Rebeck, G. W., Kindy, M., & LaDu, M. J. (2002) · Journal of Alzheimer's Disease · doi:10.3233/jad-2002-4304 · Cited by 89
Self-citationToledo, J. B., Bjerke, M., Da, X., Landau, S. M., Foster, N. L., Jagust, W., Jack, C., Weiner, M., Davatzikos, C., Shaw, L. M., et al. (2015) · JAMA Neurology · doi:10.1001/jamaneurol.2014.4829 · Cited by 88
ApoE gene and exceptional longevity: Insights from three independent cohorts
Garatachea, N., Emanuele, E., Calero, M., Fuku, N., Arai, Y., Abe, Y., Murakami, H., Miyachi, M., Yvert, T., Verde, Z., et al. (2014) · Experimental Gerontology · doi:10.1016/j.exger.2014.02.004 · Cited by 84
Jackson, R. J., Keiser, M. S., Meltzer, J. C., Fykstra, D. P., Dierksmeier, S. E., Hajizadeh, S., Kreuzer, J., Morris, R., Melloni, A., Nakajima, T., et al. (2024) · Molecular Therapy · doi:10.1016/j.ymthe.2024.03.024 · Cited by 86
Self-citationJones, P. B., Adams, K. W., Rozkalne, A., Spires-Jones, T. L., Hshieh, T. T., Hashimoto, T., von Armin, C. A. F., Mielke, M., Bacskai, B. J., & Hyman, B. T. (2011) · PLoS ONE · doi:10.1371/journal.pone.0014586 · Cited by 84
Self-citationSani, S., Traul, D., Klink, A., Niaraki, N., Gonzalo-Ruiz, A., Wu, C.-K., & Geula, C. (2003) · Acta Neuropathologica · doi:10.1007/s00401-002-0626-5 · Cited by 83
ApoE isoform-specific effects on LTP: blockade by oligomeric amyloid-β1–42
Trommer, B. L., Shah, C., Yun, S. H., Gamkrelidze, G., Pasternak, E. S., Blaine Stine, W., Manelli, A., Sullivan, P., Pasternak, J. F., & LaDu, M. J. (2005) · Neurobiology of Disease · doi:10.1016/j.nbd.2004.08.011 · Cited by 82
Kida, E., Choi-Miura, N.-H., & Wisniewski, K. E. (1995) · Brain Research · doi:10.1016/0006-8993(95)00482-6 · Cited by 79
APOE and other loci affect age‐at‐onset in Alzheimer's disease families with PS2 mutation
Wijsman, E. M., Daw, E. W., Yu, X., Steinbart, E. J., Nochlin, D., Bird, T. D., & Schellenberg, G. D. (2005) · American Journal of Medical Genetics Part B: Neuropsychiatric Genetics · doi:10.1002/ajmg.b.30087 · Cited by 79
Cholinergic systems and long-term potentiation in memory-impaired apolipoprotein E-deficient mice
Krzywkowski, P., Ghribi, O., Gagné, J., Chabot, C., Kar, S., Rochford, J., Massicotte, G., & Poirier, J. (1999) · Neuroscience · doi:10.1016/s0306-4522(99)00061-5 · Cited by 74
Aβ42 neurotoxicity in primary co-cultures: effect of apoE isoform and Aβ conformation
Manelli, A. M., Bulfinch, L. C., Sullivan, P. M., & LaDu, M. J. (2007) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2006.05.024 · Cited by 72
Aβ immunotherapy for Alzheimer’s disease: effects on apoE and cerebral vasculopathy
Sakai, K., Boche, D., Carare, R., Johnston, D., Holmes, C., Love, S., & Nicoll, J. A. R. (2014) · Acta Neuropathologica · doi:10.1007/s00401-014-1340-9 · Cited by 72
Shanmugaratnam, J., Berg, E., Kimerer, L., Johnson, R. J., Amaratunga, A., Schreiber, B. M., & Fine, R. E. (1997) · Molecular Brain Research · doi:10.1016/s0169-328x(97)00176-9 · Cited by 68
Bennett, C., Crawford, F., Osborne, A., Diaz, P., Hoyne, J., Lopez, R., Roques, P., Duara, R., Rossor, M., & Mullan, M. (1995) · American Journal of Medical Genetics · doi:10.1002/ajmg.1320600102 · Cited by 67
The generation and function of soluble apoE receptors in the CNS
Rebeck, G. W., LaDu, M. J., Estus, S., Bu, G., & Weeber, E. J. (2006) · Molecular Neurodegeneration · doi:10.1186/1750-1326-1-15 · Cited by 66
Hirsch-Reinshagen, V., & Wellington, C. L. (2007) · Current Opinion in Lipidology · doi:10.1097/mol.0b013e32813aeabf · Cited by 61
Effects of APOE4 allelic dosage on lipidomic signatures in the entorhinal cortex of aged mice
Miranda, A. M., Ashok, A., Chan, R. B., Zhou, B., Xu, Y., McIntire, L. B., Area-Gomez, E., Di Paolo, G., Duff, K. E., Oliveira, T. G., et al. (2022) · Translational Psychiatry · doi:10.1038/s41398-022-01881-6 · Cited by 60
Area-Gomez, E., Larrea, D., Pera, M., Agrawal, R. R., Guilfoyle, D. N., Pirhaji, L., Shannon, K., Arain, H. A., Ashok, A., Chen, Q., et al. (2020) · Scientific Reports · doi:10.1038/s41598-020-61142-8 · Cited by 55
Differential splicing and glycosylation of Apoer2 alters synaptic plasticity and fear learning
Wasser, C. R., Masiulis, I., Durakoglugil, M. S., Lane-Donovan, C., Xian, X., Beffert, U., Agarwala, A., Hammer, R. E., & Herz, J. (2014) · Science Signaling · doi:10.1126/scisignal.2005438 · Cited by 48
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
Self-citationCholesterol Dysmetabolism in Alzheimer’s Disease: A Starring Role for Astrocytes?
Staurenghi, E., Giannelli, S., Testa, G., Sottero, B., Leonarduzzi, G., & Gamba, P. (2021) · Antioxidants · doi:10.3390/antiox10121890 · Cited by 44
Mulder, M., & Terwel, D. (1998) · Pathophysiology of Haemostasis and Thrombosis · doi:10.1159/000022429 · Cited by 40
Dickson, T. C., Saunders, H. L., & Vickers, J. C. (1997) · Neuropathology and Applied Neurobiology · doi:10.1111/j.1365-2990.1997.tb01325.x · Cited by 40
LaDu, M. J., Stine, Narita, M., Getz, G. S., Reardon, C. A., & Bu, G. (2006) · Biochemistry · doi:10.1021/bi051765s · Cited by 36
Extracellular Proteolysis of Apolipoprotein E (apoE) by Secreted Serine Neuronal Protease
Tamboli, I. Y., Heo, D., & Rebeck, G. W. (2014) · PLoS ONE · doi:10.1371/journal.pone.0093120 · Cited by 35
Self-citationTrajectories of behavioral disturbance in dementia
Chow, T. W., Fridhandler, J. D., Binns, M. A., Lee, A., Merrilees, J., Rosen, H. J., Ketelle, R., & Miller, B. L. (2012) · Journal of Alzheimer's Disease · doi:10.3233/jad-2012-111916 · Cited by 32
Human APOE genotype affects intraneuronal A 1-42 accumulation in a lentiviral gene transfer model
Zhao, W., Dumanis, S. B., Tamboli, I. Y., Rodriguez, G. A., Jo LaDu, M., Moussa, C. E. H., & William Rebeck, G. (2014) · Human Molecular Genetics · doi:10.1093/hmg/ddt525 · Cited by 32
The distribution of cerebrovascular amyloid in Alzheimer’s disease varies with ApoE genotype
Trembath, D., Ervin, J. F., Broom, L., Szymanski, M., Welsh-Bohmer, K., Pieper, C., & Hulette, C. M. (2006) · Acta Neuropathologica · doi:10.1007/s00401-006-0162-9 · Cited by 31
Tran, K. M., Kwang, N. E., Butler, C. A., Gomez-Arboledas, A., Kawauchi, S., Mar, C., Chao, D., Barahona, R. A., Da Cunha, C., Tsourmas, K. I., et al. (2025) · Molecular Neurodegeneration · doi:10.1186/s13024-024-00793-x · Cited by 28
Yamamoto, M., Ikeda, K., Ohshima, K., Tsugu, H., Kimura, H., & Tomonaga, M. (1998) · Brain Tumor Pathology · doi:10.1007/bf02482097 · Cited by 25
Use of Genetic Variation as Biomarkers for Alzheimer's Disease
Reitz, C., & Mayeux, R. (2009) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.2009.04945.x · Cited by 24
Kara, E., Marks, J. D., Roe, A. D., Commins, C., Fan, Z., Calvo-Rodriguez, M., Wegmann, S., Hudry, E., & Hyman, B. T. (2018) · Journal of Biological Chemistry · doi:10.1074/jbc.ra117.001388 · Cited by 20
Self-citationGal, J., Katsumata, Y., Zhu, H., Srinivasan, S., Chen, J., Johnson, L. A., Wang, W.-X., Golden, L. R., Wilcock, D. M., Jicha, G. A., et al. (2022) · The American Journal of Pathology · doi:10.1016/j.ajpath.2021.11.013 · Cited by 17
KAPLITT, M., GOURAS, G. K., MAKIMURA, H., JOVANOVIC, J., SWEENEY, D., GREENGARD, P., RELKIN, N. R., & GANDY, S. (1996) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.1996.tb32597.x · Cited by 12
Chen, K., Chen, Y., Ren, Y., Wang, Z., Huang, Y., Pan, M., Li, Z., Casey, M. C., Qiao, W., Shi, J., et al. (2026) · Nature Communications · doi:10.1038/s41467-026-78407-x
Jackson, R. J., Dierksmeier, S., Nishtar, M., Meltzer, J., Balduin, F., Beaumont, B., Fan, Z., Sergienko, E., Olson, S., Jackson, M. R., et al. (2026) · doi:10.64898/2026.06.09.730809
Self-citation
Metadata
- Authors
- William Rebeck, G., Reiter, J. S., Strickland, D. K., & Hyman, B. T.
- Affiliations
- Massachusetts General Hospital (US)
- American Red Cross (US)
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 1993-10
- Volume
- 11
- Issue
- 4
- Pages
- 575-580
- ISSN
- 0896-6273 (ISSN-L)
- OpenAlex
- W2091924214
- Cited by
- 1,107
- References
- 8
- Citations by year
- 2026: 16 · 2025: 14 · 2024: 27 · 2023: 24 · 2022: 25 · 2021: 20 · 2020: 25 · 2019: 16 · 2018: 18 · 2017: 34 · 2016: 25 · 2015: 25 · 2014: 31 · 2013: 24 · 2012: 27
- FWCI
- 47.97
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuron (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01gm042581-09, 1f32ag005598-01)
- National Institute on Aging (AG-08487, AG05598)
- National Institute of General Medical Sciences (GM-42581)
- 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
- apolipoprotein E, Alzheimer's disease, APOE ε4, amyloid plaques, apoE receptors, LDL receptor, LDL receptor-related protein, astrocytes
- MeSH terms
- Adult, Aged, Aged, 80 and over, Alleles, Alzheimer Disease, Apolipoproteins E, Genotype, Hippocampus, Humans, Immunohistochemistry, Middle Aged, Receptors, Immunologic, Receptors, LDL, Reference Values, Temporal Lobe, Genetic Variation, Low Density Lipoprotein Receptor-Related Protein-1
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
