Association of apolipoprotein E allele ϵ4 with late‐onset familial and sporadic Alzheimer's disease
Open accessAbstract
Apolipoprotein E, type epsilon 4 allele (APOE epsilon 4), is associated with late-onset familial Alzheimer's disease (AD). There is high avidity and specific binding of amyloid beta-peptide with the protein ApoE. To test the hypothesis that late-onset familial AD may represent the clustering of sporadic AD in families large enough to be studied, we extended the analyses of APOE alleles to several series of sporadic AD patients. APOE epsilon 4 is significantly associated with a series of probable sporadic AD patients (0.36 +/- 0.042, AD, versus 0.16 +/- 0.027, controls [allele frequency estimate +/- standard error], p = 0.00031). Spouse controls did not differ from CEPH grandparent controls from the Centre d'Etude du Polymorphisme Humain (CEPH) or from literature controls. A large combined series of autopsy-documented sporadic AD patients also demonstrated highly significant association with the APOE epsilon 4 allele (0.40 +/- 0.026, p < or = 0.00001). These data support the involvement of ApoE epsilon 4 in the pathogenesis of late-onset familial and sporadic AD. ApoE isoforms may play an important role in the metabolism of beta-peptide, and APOE epsilon 4 may operate as a susceptibility gene (risk factor) for the clinical expression of AD.
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The greatest risk factors for late-onset Alzheimer's are older age, genetics (especially the e4 form of the APOE gene), and having a family history of Alzheimer's.
“The greatest risk factors for late-onset Alzheimer's are older age, 62,63 genetics 64,65 -especially the e4 form of the apolipoprotein E (APOE) gene -and having a family history of Alzheimer's.[66][67][68][69]”
From 2023 Alzheimer's disease facts and figures (2023) · cites this paper as [64]
The Abstract and Statistical analysis section identify APOE ε4 as a susceptibility factor for late-onset familial and sporadic Alzheimer’s disease and discuss clustering in families. They do not establish that having a family history is itself one of the greatest risk factors; the paper also does not rank these factors against older age. (LLM, conf=0.81)
Experimental — accuracy not yet measuredBetween 45% and 50% of Alzheimer's disease patients carry at least one APOE4 allele compared to only 15% of age-matched healthy controls.
“Between 45% and 50% of AD patients carry at least one APOE4 allele compared to only 15% of age-matched healthy controls.5,11”
From AAVrh.10-Mediated APOE2 Central Nervous System Gene Therapy for APOE4-Associated Alzheimer's Disease (2018) · cites this paper as [5]
The Statistical analysis table reports that APOE ε4 is more frequent in late-onset and sporadic AD groups than in controls. But its figures are allele frequencies, not percentages of people carrying at least one ε4 allele: it reports 0.36–0.42 for the AD groups and 0.16 for CEPH controls. The claimed 45%–50% versus 15% carrier comparison is therefore not established by this paper. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThe major risk factor for Alzheimer's disease is inheritance of the E4 allele of apolipoprotein E (APOE).
“The major risk factor for AD is inheritance of the E4 allele of apolipoprotein E (APOE).5,6”
From AAVrh.10-Mediated APOE2 Central Nervous System Gene Therapy for APOE4-Associated Alzheimer's Disease (2018) · cites this paper as [5]
The Abstract and the section labelled Statistical analysis report an association between APOE ε4 and late-onset familial and sporadic Alzheimer’s disease, and describe ε4 as a possible susceptibility gene or risk factor. They do not establish that it is the major risk factor for Alzheimer’s disease generally; the paper also reports no significant association in its combined early-onset familial groups. The indexed passages provide no page number. (LLM, conf=0.86)
Experimental — accuracy not yet measuredThe APOE ε4 allele is the strongest genetic risk factor for late-onset, sporadic Alzheimer's disease.
“The apolipoprotein E (APOE) ε4 allele is the strongest genetic risk factor for late-onset, sporadic Alzheimer’s disease (AD).”
From Human ApoE isoforms differentially regulate brain amyloid-β peptide clearance (2011) · cites this paper as [3]
The Abstract reports a significant association between APOE ε4 and sporadic Alzheimer’s disease, and the Statistical analysis section describes ε4 as a possible susceptibility gene or risk factor. Neither passage compares it with other genetic risk factors or establishes that it is the strongest. (LLM, conf=0.89)
Experimental — accuracy not yet measuredThe APOE ε4 allele dramatically increases AD risk and decreases age of onset by 10 to 15 years.
“the presence of which dramatically increases risk for developing AD and decreases age of onset by 10 to 15 years”
From Human ApoE isoforms differentially regulate brain amyloid-β peptide clearance (2011) · cites this paper as [3]
The Abstract and Results report a significant association between APOE ε4 and late-onset familial and sporadic AD, supporting the increased-risk portion of the claim. They do not report that ε4 decreases age of onset by 10–15 years; the discussion instead links earlier onset to APP mutations. Passage page numbers are not provided in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measured
Variables available from the CCSMA included age of dementia onset, gender, education, and presence of one or two APOE ε4 alleles, determined from buccal DNA.
“Variables available from the CCSMA included age of dementia onset, gender, education, and presence of one or two APOE ε4 alleles, determined from buccal DNA.(24)”
From Progression of Cognitive, Functional, and Neuropsychiatric Symptom Domains in a Population Cohort With Alzheimer Dementia: The Cache County Dementia Progression Study (2011) · cites this paper as [24]
The Methods and Genomic DNA sections describe age-of-onset information and APOE genotyping, supporting those elements of the sentence. They do not describe CCSMA variables, gender or education data, or buccal DNA; the paper instead reports DNA from blood samples and brain tissue. (LLM, conf=0.85)
Experimental — accuracy not yet measuredAPOE ε4 allele is the highest genetic risk factor for LOAD.
“Among these genes, apolipoprotein E ( APOE ; especially the APOE ε 4 allele) is the highest genetic risk factor for LOAD [23,24].”
From Is there a role for B cells in Alzheimer's disease? (2026) · cites this paper as [23]
The Abstract and Statistical analysis section report an association between APOE ε4 and late-onset familial and sporadic Alzheimer’s disease, and describe ε4 as a possible susceptibility gene or risk factor. They do not establish that it is the highest genetic risk factor relative to other genes. Page numbers are not available in our copy. (LLM, conf=0.87)
Experimental — accuracy not yet measuredAPOE4 increases Alzheimer's disease susceptibility and APOE2 offers protection.
“The three primary APOE isoforms (APOE2, APOE3, and APOE4) have distinct effects on AD onset and age-related progression, with APOE4 increasing susceptibility and APOE2 offering protection (Corder et al., 1993; Saunders et al., 1993; Wolf et al., 2013).”
From Isogenic human stem cell models reveal mutation-dependent protective mechanisms of APOE3 Christchurch (2026) · cites this paper as Saunders et al., 1993
The paper’s Discussion reports an association between APOE ε4 and late-onset familial and sporadic Alzheimer’s disease, supporting the susceptibility portion of the claim. Our copy identifies ε2 as an allele but does not say it offers protection; it also does not establish distinct effects of all three isoforms on age-related progression. (LLM, conf=0.90)
Experimental — accuracy not yet measuredAPOE ε4 is the strongest genetic risk factor for late-onset Alzheimer's disease.
“the ε4 allele is the strongest genetic risk factor for late-onset AD”
From ApoE4 reduction: An emerging and promising therapeutic strategy for Alzheimer's disease (2022) · cites this paper as Saunders et al 1993
The Abstract reports a significant association between APOE ε4 and late-onset familial and sporadic Alzheimer’s disease. The discussion (indexed as “Statistical analysis”; page not provided) describes ε4 as a susceptibility gene or risk factor, but does not establish that it is the strongest genetic risk factor. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThe risk for AD is 3-4-fold higher in individuals carrying one APOE ε4 allele and about 10-15-fold higher in those carrying two APOE ε4 alleles.
“The risk for AD is 3–4-fold higher in individuals carrying one APOE ε4 allele and about 10–15-fold higher in those carrying two APOE ε4 alleles”
From ApoE4 reduction: An emerging and promising therapeutic strategy for Alzheimer's disease (2022) · cites this paper as Saunders et al 1993
The Statistical analysis table reports higher APOE ε4 allele frequencies in late-onset and sporadic AD groups than in controls, and the discussion calls ε4 a possible risk factor. The paper does not report AD risk separately for people carrying one versus two ε4 alleles, so it does not support the stated 3–4-fold and 10–15-fold estimates. (LLM, conf=0.88)
Experimental — accuracy not yet measuredAPOE4 is the strongest genetic risk factor for AD with high prevalence.
“In conclusion, APOE4 is the strongest genetic risk factor for AD with high prevalence (Saunders et al 1993, Sims et al 2020).”
From ApoE4 reduction: An emerging and promising therapeutic strategy for Alzheimer's disease (2022) · cites this paper as Saunders et al 1993
The Statistical analysis section reports significantly higher APOE4 allele frequencies in late-onset familial and sporadic AD groups than in controls (0.36–0.42 versus 0.16), supporting its association with AD and its frequency in those patient groups. It does not establish APOE4 as the strongest genetic risk factor for AD overall; the same section reports no significant association in the combined early-onset familial AD group. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThe greatest risk factors for Alzheimer's dementia are older age, genetics - especially the e4 form of the apolipoprotein E (APOE) gene - and having a family history of Alzheimer's dementia.
“The greatest risk factors for Alzheimer's dementia are older age, 70 , 71 genetics — especially the e4 form of the apolipoprotein E (APOE) gene 72 , 73 — and having a family history of Alzheimer's dementia.”
From 2024 Alzheimer's disease facts and figures (2024) · cites this paper as [72]
The APOE ε2 allele confers protection against developing AD.
“in contrast, the APOE ε2 allele confers protection against developing AD (2-5).”
From Human ApoE isoforms differentially regulate brain amyloid-β peptide clearance (2011) · cites this paper as [3]
The Abstract and Statistical analysis passages associate APOE ε4 with increased susceptibility to late-onset AD, but do not say that ε2 protects against developing AD. A search for ε2 allele frequencies and protective effects found only a passage describing how ε2 is identified in genotyping, not its relationship to AD risk. (LLM, conf=0.76)
Experimental — accuracy not yet measuredVariants of the apolipoprotein E allele account for most cases of late-onset Alzheimer's disease.
“Variants of the apolipoprotein E allele appear to account for most cases of late-onset Alzheimer's disease”
From Preclinical Evidence of Alzheimer's Disease in Persons Homozygous for the ε4 Allele for Apolipoprotein E (1996) · cites this paper as [3]
The e4 allele is associated with an increased risk of Alzheimer's disease.
“the e4 allele has been associated with an increased risk of Alzheimer's disease, 1-7”
From Preclinical Evidence of Alzheimer's Disease in Persons Homozygous for the ε4 Allele for Apolipoprotein E (1996) · cites this paper as [3]
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- Authors
- 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., Hulette, C., Crain, B., Goldgaber, D., & Roses, A. D.
- Affiliations
- Duke University (US)
- Departments of Medicine [Neurology] (Drs. Saunders, Strittmatter, Schmechel, Pericak-Vance, Alberts, and Roses, and S. Joo and B. Rosi), Neurobiology (Drs. Strittmatter, Schmechel, and Roses), and Pathology (Drs. Hulette and Crain), Joseph and Kathleen Bryan Alzheimer's Disease Research Center, Duke University Medical Center, Durham, NC; the Department of Medicine [Neurology] (Drs. St. George-Hyslop and Crapper-MacLachlan), Centre for Research in Neurodegenerative Disease, University of Toronto,...
- Venue
- Neurology
- Published
- 1993-08
- Volume
- 43
- Issue
- 8
- Pages
- 1467-1467
- ISSN
- 0028-3878 (ISSN-L)
- 1526-632X
- OpenAlex
- W1999631936
- Cited by
- 3,786
- References
- 29
- Citations by year
- 2026: 46 · 2025: 67 · 2024: 96 · 2023: 75 · 2022: 83 · 2021: 107 · 2020: 101 · 2019: 89 · 2018: 93 · 2017: 74 · 2016: 86 · 2015: 93 · 2014: 102 · 2013: 95 · 2012: 119
- FWCI
- 105.77
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Neurology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Alzheimer's Association
- American Health Assistance Foundation
- Medical Research Council Canada
- National Institutes of Health (MO1-RR-30)
- Medical Research Council
- National Institute on Aging (NIA AG05128, NIA AG 07922)
- National Institute of Neurological Disorders and Stroke
- National Center for Research Resources (M01 RR 30)
- 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 › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Keywords
- apolipoprotein E, APOE ε4, Alzheimer's disease, sporadic Alzheimer's disease, genetic susceptibility, amyloid-beta, APOE isoforms, allele frequency, genetic association
- MeSH terms
- Aged, Alleles, Alzheimer Disease, Apolipoproteins E, Female, Gene Amplification, Gene Frequency, Humans, Male, Middle Aged, Mutation
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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