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Effects of Age, Sex, and Ethnicity on the Association Between Apolipoprotein E Genotype and Alzheimer Disease: A Meta-analysis
Abstract
Objective. —To examine more closely the association between apolipoprotein E (APOE) genotype and Alzheimer disease (AD) by age and sex in populations of various ethnic and racial denominations. Data Sources. —Forty research teams contributed data onAPOEgenotype, sex, age at disease onset, and ethnic background for 5930 patients who met criteria for probable or definite AD and 8607 controls without dementia who were recruited from clinical, community, and brain bank sources. Main Outcome Measures. —Odds ratios (ORs) and 95% confidence intervals (Cls) for AD, adjusted for age and study and stratified by major ethnic group (Caucasian, African American, Hispanic, and Japanese) and source, were computed forAPOEgenotypes ∈2/∈2,∈2/∈3,∈2/∈4,∈3/∈4 and ∈4/∈4 relative to the ∈3/∈3 group. The influence of age and sex on the OR for each genotype was assessed using logistic regression procedures. Results. —Among Caucasian subjects from clinic- or autopsy-based studies, the risk of AD was significantly increased for people with genotypes ∈2/∈4 (OR=2.6, 95% Cl=1.6-4.0), ∈3/∈4 (OR=3.2, 95% Cl=2.8-3.8), and ∈4/∈4 (OR=14.9, 95% CI=10.8-20.6); whereas, the ORs were decreased for people with genotypes ∈2/∈2 (OR=0.6, 95% Cl=0.2-2.0) and ∈2/∈3 (OR=0.6, 95% Cl=0.5-0.8). TheAPOE∈4-AD association was weaker among African Americans and Hispanics, but there was significant heterogeneity in ORs among studies of African Americans (P<.03). TheAPOE∈4—AD association in Japanese subjects was stronger than in Caucasian subjects (∈3/∈4: OR=5.6, 95% Cl=3.9-8.0; ∈4/∈4: OR=33.1, 95% Cl=13.6-80.5). The ∈2/∈3 genotype appears equally protective across ethnic groups. We also found that among Caucasians,APOEgenotype distributions are similar in groups of patients with AD whose diagnoses were determined clinically or by autopsy. In addition, we found that theAPOE∈4 effect is evident at all ages between 40 and 90 years but diminishes after age 70 years and that the risk of AD associated with a given genotype varies with sex. Conclusions. —TheAPOE∈4 allele represents a major risk factor for AD in all ethnic groups studied, across all ages between 40 and 90 years, and in both men and women. The association betweenAPOE∈4 and AD in African Americans requires clarification, and the attenuated effect ofAPOE∈4 in Hispanics should be investigated further.
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In the citing paper
“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 [65]
In the citing paper
“such that APOE4 homozygotes are at the highest risk”
From Exceptionally low likelihood of Alzheimer’s dementia in APOE2 homozygotes from a 5,000-person neuropathological study (2020) · cites this paper as [4]
In the citing paper
“Also, previous studies of clinically and neuropathologically characterized cases and controls may have been too small to demonstrate that APOE2 homozygotes have an even lower OR than the relatively low-risk APOE2/3 group due to the paucity of APOE2 homozygotes, who comprise <1% of the general population1,4.”
From Exceptionally low likelihood of Alzheimer’s dementia in APOE2 homozygotes from a 5,000-person neuropathological study (2020) · cites this paper as [4]
In the citing paper
“Compared to the most common APOE3/3 genotype, each additional copy of the APOE4 allele is associated with a higher risk of Alzheimer’s dementia and a younger mean age at dementia onset, such that APOE4 homozygotes are at the highest risk”
From Exceptionally low likelihood of Alzheimer’s dementia in APOE2 homozygotes from a 5,000-person neuropathological study (2020) · cites this paper as [4]
In the citing paper
“Apolipoprotein E (APOE), the major susceptibility gene for late-onset Alzheimer’s disease (AD), has three common alleles (APOE2, 3, and 4), giving rise to six genotypes (APOE2/2, 2/3, 3/3, 2/4, 3/4, and 4/4).”
From Exceptionally low likelihood of Alzheimer’s dementia in APOE2 homozygotes from a 5,000-person neuropathological study (2020) · cites this paper as [4]
In the citing paper
“while the presence of one or two copies of the APOE2 allele is associated with a lower risk of Alzheimer’s dementia and an older mean age at dementia onset1–4.”
From Exceptionally low likelihood of Alzheimer’s dementia in APOE2 homozygotes from a 5,000-person neuropathological study (2020) · cites this paper as [4]
In the citing paper
“Fourth, findings from our non-Hispanic White groups cannot yet be extended to other ethnic and racial groups4.”
From Exceptionally low likelihood of Alzheimer’s dementia in APOE2 homozygotes from a 5,000-person neuropathological study (2020) · cites this paper as [4]
In the citing paper
“APOE is genetically linked to late-onset sporadic Alzheimer’s disease (LOAD), with APOE4 being a significant risk factor, APOE3 considered the “neutral” allele, and APOE2 exerting a protective role against LOAD [6, 7].”
In the citing paper
“In addition, APOE4 is linked to hypercholesterolemia and increased risk of cardiovascular disorders (CVD) [7, 41]”
In the citing paper
“Compared to ε3 homozygotes, individuals with one or two ε4 alleles harbor approximately 3 and 15 times increased risk, respectively”
From Effects of APOE2 and APOE4 on brain microstructure in older adults: modification by age, sex, and cognitive status (2024) · cites this paper as [1]
In the citing paper
“whereas carriers of the protective ε2 allele have an estimated 1.7 times decreased risk [1]”
From Effects of APOE2 and APOE4 on brain microstructure in older adults: modification by age, sex, and cognitive status (2024) · cites this paper as [1]
In the citing paper
“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 [11]
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 [5]
In the citing paper
“In humans, the APOE2/4 genotype confers an intermediate risk, higher than that of APOE3/3 but lower than APOE3/4 and APOE4/4 5,6 .”
From APOE2 attenuates APOE4-associated amyloid pathology and related toxicity in a mouse model of Alzheimer’s disease (2026) · cites this paper as [5]
In the citing paper
“Population studies have demonstrated that the ε4 allele increases the risk of developing AD by either 3-fold (1 allele) or 12-fold (2 alleles) [6]”
From In Vivo Human Apolipoprotein E Isoform Fractional Turnover Rates in the CNS (2012) · cites this paper as [6]
In the citing paper
“ApoE4, found in 65–80% of cases of sporadic and familial Alzheimer's disease, increases the occurrence of AD by ∼12 fold in two ɛ4 allele carriers, compared with those with no ɛ4 allele (Farrer et al., 1997).”
From Apolipoprotein E in Synaptic Plasticity and Alzheimer’s Disease: Potential Cellular and Molecular Mechanisms (2014) · cites this paper as Farrer et al., 1997
In the citing paper
“The APOE4 allele is a major genetic risk factor for late-onset AD and was previously shown to accelerate AD progression in humans and in mouse models 6-11 .”
From APOE4 impairs the microglial response in Alzheimer’s disease by inducing TGFβ-mediated checkpoints (2023) · cites this paper as [6]
In the citing paper
“The APOE4 allele is the strongest genetic risk factor for late-onset Alzheimer's disease (AD).”
From APOE4 impairs the microglial response in Alzheimer’s disease by inducing TGFβ-mediated checkpoints (2023) · cites this paper as [6]
In the citing paper
“Epidemiologic studies show sex differences in clinical risk are largely discernable within the context of APOE ε4,11,42,43 particularly between the ages of 65 to 75 years compared with APOE ε4 clinically normal male carriers.44”
From Sex Differences in the Association of Global Amyloid and Regional Tau Deposition Measured by Positron Emission Tomography in Clinically Normal Older Adults (2019) · cites this paper as [43]
In the citing paper
“Separately, clinical studies have reported that women APOE ε4 carriers had a higher risk of Alzheimer’s dementia than men carriers [21].”
From Sex differences in Alzheimer’s disease and common neuropathologies of aging (2018) · cites this paper as [21]
In the citing paper
“Furthermore, a recent meta-analysis of 58000 participants showed that APOE ε3/ε4 women have the same increased odds of AD dementia as APOE ε3ε4 men have, in contrast to a previous meta-analysis which reported APOE ε4 women to carry a higher risk of Alzheimer’s dementia compared to APOE ε4 men [21].”
From Sex differences in Alzheimer’s disease and common neuropathologies of aging (2018) · cites this paper as [21]
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 [18]
In the citing paper
“The initial intriguing observation that the APOEε4 allele increases AD risk differentially across races and ethnicities, with the greatest increase in risk seen in East Asian people, followed by white, then Black, then Hispanic people6, has now been confirmed by a larger meta-analysis using not only self-reported race and ethnicity but also global genetic ancestry to ascertain the biological basis”
From Multifaceted roles of APOE in Alzheimer disease (2024) · cites this paper as [6]
In the citing paper
“Rather, age and sex moderate the effects of the APOE genotype on AD risk so that the risk associated with the APOEε3/ε4 genotype is highest in women of ages 60–70 years (or 70–80 years according to ref. 6) but decreases in older women and equalizes to that of non-Hispanic White, Black and Hispanic men of the same age10.”
From Multifaceted roles of APOE in Alzheimer disease (2024) · cites this paper as [6]
In the citing paper
“The APOE polymorphism is the most studied, successfully replicated, and well-established risk factor for AD where APOE*2 is the protective allele and APOE*4 is the risk allele as compared to APOE*3 [7–10].”
From Genome-wide analysis identifies novel loci influencing plasma apolipoprotein E concentration and Alzheimer’s disease risk (2023) · cites this paper as [8]
In the citing paper
“The original association study implicating L28P with LOAD risk was carried out in a relatively small sample size.”
From Investigation of the independent role of a rare APOE variant (L28P; APOE*4Pittsburgh) in late-onset Alzheimer disease (2023) · cites this paper as [9]
In the citing paper
“due to the complete linkage disequilibrium of L28P with APOE*4 (C112R)”
From Investigation of the independent role of a rare APOE variant (L28P; APOE*4Pittsburgh) in late-onset Alzheimer disease (2023) · cites this paper as [9]
In the citing paper
“it was associated with an elevated risk for AD [9]”
From Investigation of the independent role of a rare APOE variant (L28P; APOE*4Pittsburgh) in late-onset Alzheimer disease (2023) · cites this paper as [9]
In the citing paper
“In 1999, two groups independently identified a novel and rare missense mutation in the APOE gene [9, 10] in which the leucine residue is replaced by proline at codon 28 (L28P; rs769452).”
From Investigation of the independent role of a rare APOE variant (L28P; APOE*4Pittsburgh) in late-onset Alzheimer disease (2023) · cites this paper as [9]
In the citing paper
“with the East Asian population having a higher risk of AD associated with the APOE ε4 allele”
From Genetics of Alzheimer’s disease: An East Asian perspective (2023) · cites this paper as [11]
In the citing paper
“while the effect of APOE ε4 is weaker in African American and Hispanic populations”
From Genetics of Alzheimer’s disease: An East Asian perspective (2023) · cites this paper as [11]
In the citing paper
“The AD risk associated with common APOE alleles ε4 1 and ε2 2 is well established in European-ancestry individuals but varies considerably across other ancestries (Table 1). 3”
From Association of African Ancestry–Specific APOE Missense Variant R145C With Risk of Alzheimer Disease (2023) · cites this paper as [3]
In the citing paper
“Among the AD susceptibility genes/loci identified to date, APOE remains the most significant genetic risk factor across populations.”
From Association of rare APOE missense variants with Alzheimer's disease in the Japanese population (2025) · cites this paper as [8]
In the citing paper
“Although there is only about 20% of the population carrying the APOE ε4, this isoform is vastly enriched in AD patients with over 60% of symptomatic AD patients carrying at least one APOE ε4 allele”
From ApoE4 reduction: An emerging and promising therapeutic strategy for Alzheimer's disease (2022) · cites this paper as Farrer et al 1997
In the citing paper
“The ε4 allele of apolipoprotein E (APOE) is the dominant genetic risk factor for late-onset Alzheimer’s disease (AD).”
From APOE4 is Associated with Differential Regional Vulnerability to Bioenergetic Deficits in Aged APOE Mice (2020) · cites this paper as [5]
In the citing paper
“The genetic polymorphism of human apolipoprotein E (ApoE) has been shown to confer differential susceptibility to late-onset AD, which accounts for the majority of the AD cases (Farrer et al., 1997).”
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 Farrer et al., 1997
In the citing paper
“occurs in approximately two-thirds of all cases [1–3]”
From Neuronal Apolipoprotein E4 Expression Results in Proteome-Wide Alterations and Compromises Bioenergetic Capacity by Disrupting Mitochondrial Function (2019) · cites this paper as [2]
In the citing paper
“Apolipoprotein (apo) E4 is the major genetic risk factor for Alzheimer’s disease (AD)”
From Neuronal Apolipoprotein E4 Expression Results in Proteome-Wide Alterations and Compromises Bioenergetic Capacity by Disrupting Mitochondrial Function (2019) · cites this paper as [2]
In the citing paper
“In contrast, APOE3 is defined as risk-neutral while APOE2 represents the strongest genetic protective factor (Corder et al., 1994; Farrer et al., 1997; Reiman et al., 2020).”
From APOE genotype-dependent differences in human astrocytic energy metabolism (2025) · cites this paper as Farrer et al., 1997
In the citing paper
“Since then, numerous studies have confirmed that possession of the ε4 allele is the strongest genetic risk factor for both AD and CAA, or a combination of both disorders (Bertram et al., 2007; Farrer et al., 1997).”
From The role of apolipoprotein E in Alzheimer's disease (2009) · cites this paper as Farrer et al., 1997
In the citing paper
“However, in certain ethnic groups, the apoE ε4 allele seems to have either a weaker effect or no clear effect on AD (Farrer et al., 1997; Kalaria et al., 2008; Mayeux, 2003; Tang et al., 1998).”
From The role of apolipoprotein E in Alzheimer's disease (2009) · cites this paper as Farrer et al., 1997
In the citing paper
“Finally, it is important to note that the ε2 allele of apoE is associated with a lower risk for AD (Corder et al., 1994; Farrer et al., 1997).”
From The role of apolipoprotein E in Alzheimer's disease (2009) · cites this paper as Farrer et al., 1997
In the citing paper
“APOE genotypes were in Hardy-Weinberg equilibrium in both cases and controls; their frequencies (Table 4) were similar to previous reports for the relevant age groups (44;47;48).”
From Association of ALS with head injury, cigarette smoking and APOE genotypes (2010) · cites this paper as [47]
In the citing paper
“The ε4 allele of apolipoprotein E (APOE) is the strongest genetic risk factor for sporadic Alzheimer's Disease (AD).”
From APOE loss-of-function variants: Compatible with longevity and associated with resistance to Alzheimer’s disease pathology (2024) · cites this paper as [4]
In the citing paper
“An APOE ε4/ε4 individual of European ancestry has a sixteen-fold increase in AD risk and eighteen year earlier age at AD onset compared to a European ancestry individual carrying two copies of the more prevalent APOE ε3 allele 4 .”
From APOE loss-of-function variants: Compatible with longevity and associated with resistance to Alzheimer’s disease pathology (2024) · cites this paper as [4]
In the citing paper
“The global frequency of the human ε4 allele is 13.7%, and the frequency of ε4 carriers is increased to 40% in AD patients [452, 453].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [453]
In the citing paper
“Clinical incidence and average age of AD onset was found to be 91% at 68 years of age in ε4 homozygous carriers, 47% at 76 years of age in ε4 heterozygous carriers, and 20% at 84 years of age in non-ε4 individuals [453].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [453]
In the citing paper
“ApoE4 is present in roughly 20–25% of the human population, and apoE4 carriers account for 60–75% of AD cases in most clinical studies [11], highlighting the importance of apoE4 in AD pathogenesis.”
From Apolipoprotein E4, inhibitory network dysfunction, and Alzheimer’s disease (2019) · cites this paper as [11]
In the citing paper
“ApoE4 increases the risk and decreases the age of onset of AD in a gene dose dependent manner [4–11].”
From Apolipoprotein E4, inhibitory network dysfunction, and Alzheimer’s disease (2019) · cites this paper as [11]
In the citing paper
“the effect of APOEε4 has been reported to differ across ethnicities [58–61]”
From Genetic architecture of Alzheimer's disease (2020) · cites this paper as [58]
In the citing paper
“the association between ε4 and disease is reported to be weaker among African-American and Hispanic individuals [58, 61, 62] and nonexistent among Nigerian individuals [63].”
From Genetic architecture of Alzheimer's disease (2020) · cites this paper as [58]
In the citing paper
“APOEε2/APOEε4 individuals are still at increased risk for AD, suggesting the APOEε4 isoform exhibits some dominant effect over the APOEε2 isoform [58].”
From Genetic architecture of Alzheimer's disease (2020) · cites this paper as [58]
In the citing paper
“Several studies have demonstrated APOE genotype has an exacerbated effect on disease risk in females [58]”
From Genetic architecture of Alzheimer's disease (2020) · cites this paper as [58]
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Items 901–1,000 of 1,178
Apolipoprotein E4, cholinergic integrity and the pharmacogenetics of Alzheimer’s disease
Poirier, J., & Sevigny, P. (1998) · Journal of neural transmission. Supplementum · doi:10.1007/978-3-7091-6467-9_18 · Cited by 81
The Complex Role of Apolipoprotein E in Alzheimer’s Disease: an Overview and Update
Mahoney‐Sanchez, L., Belaidi, A. A., Bush, A. I., & Ayton, S. (2016) · Journal of Molecular Neuroscience · doi:10.1007/s12031-016-0839-z · Cited by 84
“Reciprocally, carriage of the ε2 isoform lowers the risk of AD and delays the age of onset (Corder et al. 1994; Farrer et al. 1997; Suri et al. 2013).”
BackgroundThe role of APOE in transgenic mouse models of AD
Balu, D., Karstens, A. J., Loukenas, E., Maldonado Weng, J., York, J. M., Valencia-Olvera, A. C., & LaDu, M. J. (2019) · Neuroscience Letters · doi:10.1016/j.neulet.2019.134285 · Cited by 81
Analysis of Copy Number Variation in Alzheimer’s Disease: The NIALOAD/ NCRAD Family Study
Swaminathan, S., Shen, L., Kim, S., Inlow, M. H., West, J. D., Faber, K. M., Foroud, T., Mayeux, R. P., & Saykin, A. J. (2012) · Current Alzheimer Research · doi:10.2174/156720512802455331 · Cited by 85
ApoE isoforms and measures of anxiety in probable AD patients and Apoe−/− mice
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Prospective memory and apolipoprotein e in healthy aging and early stage Alzheimer's disease.
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Dementia and Cerebrovascular Disease
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A cross-ethnic analysis of risk factors for AD in white Hispanics and white non-Hispanics
Harwood, D. G., Barker, W. W., Loewenstein, D., Ownby, R. L., George‐Hyslop, P. S., MULLAN, M. J., & Duara, R. (1999) · Neurology · doi:10.1212/wnl.52.3.551 · Cited by 81
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“It is well established that ApoE plays an important role in the genetics of LOAD (4, 5 ).”
BackgroundIncidence of Dementia in Relation to Stroke and the Apolipoprotein E ε4 Allele in the Very Old
Zhu, L., Fratiglioni, L., Guo, Z., Basun, H., Corder, E. H., Winblad, B. G., & Viitanen, M. H. (2000) · Stroke · doi:10.1161/01.str.31.1.53 · Cited by 81
APOE ε4 associates with microglial activation independently of Aβ plaques and tau tangles
Ferrari-Souza, J. P., Lussier, F. Z., Leffa, D. T., Therriault, J., Tissot, C., Bellaver, B., Ferreira, P. C. L., Malpetti, M., Wang, Y.-T., Povala, G., et al. (2023) · Science Advances · doi:10.1126/sciadv.ade1474 · Cited by 81
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Sex and gender considerations in Alzheimer’s disease: The Women’s Brain Project contribution
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Systematic review and meta-analysis of the effects of menopause hormone therapy on cognition
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DLB and PDD: a role for mutations in dementia and Parkinson disease genes?
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Negative Life Events and Cognitive Performance in a Population of Older Adults
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“Similar such examples have been provided in the association study of adult macular degeneration ( 34 , 35).”
BackgroundVariability of Familial Risk of Alzheimer Disease Across the Late Life Span
Silverman, J. M., Ciresi, G., Smith, C. J., Marin, D. B., & Beeri, M. S. (2005) · Archives of General Psychiatry · doi:10.1001/archpsyc.62.5.565 · Cited by 80
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20-Year prevalence projections for dementia and impact of preventive policy about risk factors
Jacqmin‐Gadda, H., Alpérovitch, A., Montlahuc, C., Commenges, D., Leffondré, K., Dufouil, C., Elbaz, A., Tzourio, C., Ménard, J., Dartigues, J., et al. (2013) · European Journal of Epidemiology · doi:10.1007/s10654-013-9818-7 · Cited by 80
Hernández, D., Rooney, L. A., Daniszewski, M., Gulluyan, L. M., Liang, H. H., Cook, A. L., Hewitt, A. W., & Pébay, A. (2021) · Stem Cell Reviews and Reports · doi:10.1007/s12015-021-10147-5 · Cited by 79
Is the Urea Cycle Involved in Alzheimer's Disease?
Hansmannel, F., Sillaire, A. R., Kamboh, M. I., Lendon, C. L., Pasquier, F., Hannequin, D., Laumet, G. O., Mounier, A., Ayral, A., DeKosky, S. T., et al. (2010) · Journal of Alzheimer s Disease · doi:10.3233/jad-2010-100630 · Cited by 82
Apolipoprotein E isoform-dependent effects on anxiety and cognition in female TR mice
Siegel, J. A., Haley, G. E., & Raber, J. (2010) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2010.03.002 · Cited by 82
“…AD patients (Robertson et al., 2005) and the risk to develop AD and cognitive impairments in nondemented healthy elderly (Berteau-Pavy et al., 2007; Farrer et al., 1997; Greenwood et al., 2005a; Greenwood et al., 2005b; Saunders et al., 1993), little is known about the potential relationship…”
Sundar, P. D., Feingold, E., Minster, R. L., DeKosky, S. T., & Kamboh, M. I. (2006) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2006.04.005 · Cited by 78
Apolipoprotein E 2 genotype delays onset of dementia with Lewy bodies in a Norwegian cohort
Berge, G., Sando, S. B., Rongve, A., Aarsland, D., & White, L. R. (2014) · Journal of Neurology Neurosurgery & Psychiatry · doi:10.1136/jnnp-2013-307228 · Cited by 79
Effect of Alzheimer disease genetic risk disclosure on dietary supplement use
Vernarelli, J. A., Roberts, J. S., Hiraki, S. C., Chen, C. A., Cupples, L. A., & Green, R. C. (2010) · American Journal of Clinical Nutrition · doi:10.3945/ajcn.2009.28981 · 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
“…et al., 2003]: the e4 allele is associated with reduced ageat-onset in a dose-dependent manner [Corder et al., 1993, 1998; Daw et al., 2000], and the e2 allele is associated with increased age-at-onset [Corder et al., 1994, 1998; Farrer et al., 1997; Daw et al., 2000], relative to the e3 allele.”
BackgroundKamboh, M. I., Ferrell, R. E., & DeKosky, S. T. (1998) · Neuroscience Letters · doi:10.1016/s0304-3940(98)00141-4 · Cited by 79
Fan, J., Tao, W., Li, X., Li, H., Zhang, J., Wei, D., Chen, Y., & Zhang, Z. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20051177 · Cited by 87
Anthocyanin as a therapeutic in Alzheimer’s disease: A systematic review of preclinical evidences
Suresh, S., Begum, R. F., Ankul Singh, S., & Chitra, V. (2022) · Ageing Research Reviews · doi:10.1016/j.arr.2022.101595 · Cited by 81
Vitamin D receptor and Alzheimer's disease: a genetic and functional study
Wang, L., Hara, K., Baaren, J. M. V., Price, J. C., Beecham, G. W., Gallins, P. J., Whitehead, P. L., Wang, G., Lu, C., Slifer, M. A., et al. (2012) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2011.12.038 · Cited by 79
“For late-onset AD, apolipoprotein E (APOE) gene has been universally established as a susceptibility gene (Corder et al., 1993; Farrer et al., 1997; Saunders et al., 1993).”
BackgroundCrivello, F., Lemaître, H., Dufouil, C., Grassiot, B., Delcroix, N., Tzourio‐Mazoyer, N., Tzourio, C., & Mazoyer, B. M. (2010) · NeuroImage · doi:10.1016/j.neuroimage.2009.12.116 · Cited by 78
“While the ɛ2 protective effect on AD is now well established (Corder et al., 1993; Farrer et al., 1997), the biological basis of such protective effect for the ɛ3 remains uncertain.”
InfluentialGenetic heterogeneity of Alzheimer's disease: Complexity and advances
Lambert, J., & Amouyel, P. (2007) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2007.05.015 · Cited by 81
Rusanen, M., Rovio, S., Ngandu, T., Nissinen, A. M., Tuomilehto, J. O., Soininen, H. S., & Kivipelto, M. (2010) · Dementia and Geriatric Cognitive Disorders · doi:10.1159/000320484 · Cited by 77
“Therefore, keeping in mind the harmful effects of smoking, it would not be surprising if this habit as well increased the disease risk particularly among genetically susceptible persons. The mixed findings regarding the interaction between smoking and APOE may be due to many factors. It has been suggested that the eff…”
BackgroundIslet amyloid polypeptide: Another key molecule in Alzheimer’s pathogenesis?
Zhang, Y., & Song, W. (2017) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2017.03.001 · Cited by 79
“Moreover, ApoE-e4 heterozygotes and homozygotes are reported to have an increased risk of sporadic AD by three and fifteen fold, respectively (Farrer et al., 1997).”
BackgroundFinckh, U., van Hadeln, K., Müller‐Thomsen, T., Alberici, A., Binetti, G. G., Hock, C., Nitsch, R. M., Stoppe, G., Reiss, J., & Gal, A. (2003) · Neurogenetics · doi:10.1007/s10048-003-0157-9 · Cited by 78
Midlife cardiovascular risk factors and late cognitive impairment
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Cognitive reserve and cortical thickness in preclinical Alzheimer’s disease
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“Eight individuals with one APOE-4 and one APOE-2 allele were excluded from all analyses, since the APOE-4 allele increases dementia risk whereas the APOE-2 allele reduces dementia risk (Corder et al. 1994; Farrer et al. 1997).”
BackgroundLi, Q. S., Sun, Y., & Wang, T. (2020) · Clinical Epigenetics · doi:10.1186/s13148-020-00944-z · Cited by 84
Korecka, M., & Shaw, L. M. J. (2021) · Journal of Neurochemistry · doi:10.1111/jnc.15465 · Cited by 82
“The human ApoE gene possesses three major alleles: ε2, ε3, and ε4, with a worldwide frequency of approximately 8%, 78%, and 14%, respectively (Farrer et al., 1997).”
BackgroundA “multi-omics” analysis of blood–brain barrier and synaptic dysfunction in APOE4 mice
Barisano, G., Kisler, K., Wilkinson, B., Nikolakopoulou, A. M., Sagare, A. P., Wang, Y., Gilliam, W., Huuskonen, M. T., Hung, S.-T., Ichida, J. K., et al. (2022) · Journal of Experimental Medicine · doi:10.1084/jem.20221137 · Cited by 78
Effects of sex and APOE ε4 on object recognition and spatial navigation in the elderly
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APOE ε4 and cognitive function in early life: A meta-analysis.
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Prasad, K. N., Cole, W. C., & Prasad, K. C. (2002) · Journal of the American College of Nutrition · doi:10.1080/07315724.2002.10719249 · Cited by 76
How can elderly apolipoprotein E ε4 carriers remain free from dementia?
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Ethnic Differences in Dementia and Alzheimer's Disease
Anderson, N. B., Bulatao, R. A. B., & Cohen, B. (2004) · Cited by 78
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APOE effects on regional tau in preclinical Alzheimer’s disease
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Presence of ApoE ε4 Allele Associated with Thinner Frontal Cortex in Middle Age
Fennema‐Notestine, C., Panizzon, M. S., Thompson, W., Chen, C., Eyler, L. T., Fischl, B. R., Franz, C. E., Grant, M. D., Jak, A. J., Jernigan, T. L., et al. (2011) · Journal of Alzheimer s Disease · doi:10.3233/jad-2011-0002 · Cited by 79
“The resulting map is exploratory in nature and provides guidance for future studies.”
BackgroundGenetic Markers of Alzheimer’s Disease
Perković, M. N., & Pivac, N. (2019) · Advances in experimental medicine and biology · doi:10.1007/978-981-32-9721-0_3 · Cited by 82
Exosome Production Is Key to Neuronal Endosomal Pathway Integrity in Neurodegenerative Diseases
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Cerebral Amyloid Angiopathy: A Common Cause of Cerebral Hemorrhage
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The Role of Genetics in Advancing Precision Medicine for Alzheimer’s Disease—A Narrative Review
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APOE and Alzheimer’s Disease: Neuroimaging of Metabolic and Cerebrovascular Dysfunction
Brandon, J. A., Farmer, B. C., Williams, H. C., & Johnson, L. A. (2018) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2018.00180 · Cited by 75
“Conversely, E2 is associated with increased longevity and a decreased risk of AD (Farrer et al., 1997; Garatachea et al., 2014).”
BackgroundDeary, I. J., Whiteman, M. C., Pattie, A., Starr, J. M., Hayward, C., Wright, A. F., Visscher, P. M., Tynan, M. C., & Whalley, L. J. (2004) · Psychology and Aging · doi:10.1037/0882-7974.19.2.367 · Cited by 76
“They also agree with the suggested protective effect of the 2 allele on memory (Farrer et al., 1997; Wilson, Bienias, et al., 2002).”
Insulin Resistance in Peripheral Tissues and the Brain: A Tale of Two Sites
Rhea, E. M., Banks, W. A., & Raber, J. (2022) · Biomedicines · doi:10.3390/biomedicines10071582 · Cited by 76
Exosomes in the Diseased Brain: First Insights from In vivo Studies
Levy, E. (2017) · Frontiers in Neuroscience · doi:10.3389/fnins.2017.00142 · Cited by 79
“…risk of being affected by AD than men, regardless of longevity and other disease mortality factors (Payami et al., 1994; Buckwalter et al., 1996; Farrer et al., 1997; Andersen et al., 1999; Bretsky et al., 1999; Lobo et al., 2000; Mortensen and Hogh, 2001; Brookmeyer et al., 2002; Barnes et…”
Wolters, F. J., Yang, Q., Biggs, M. L., Jakobsdottir, J., Li, S., Evans, D. S., Bis, J. C., Harris, T. B., Vasan, R. S., Zilhao, N. R., et al. (2019) · PLOS ONE · doi:10.1371/journal.pone.0219668 · Cited by 74
APOE-ε4 Genotype and Dementia Before and After Transient Ischemic Attack and Stroke
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“1,2 Allelic frequencies in whites are 15% for APOE-ε4 and 8% for APOE-ε2 with the remainder being APOE-ε3.”
BackgroundResultInfluentialAPOE4 confers transcriptomic and functional alterations to primary mouse microglia
Machlovi, S. I., Neuner, S. M., Hemmer, B. M., Khan, R., Liu, Y., Huang, M., Zhu, J. D., Castellano, J. M., Cai, D., Marcora, E., et al. (2022) · Neurobiology of Disease · doi:10.1016/j.nbd.2022.105615 · Cited by 73
“APOE ε4 increases risk in a semi-dominant manner, with one copy increasing risk ~3 fold and two copies increasing risk ~15 fold relative to the ε3/ε3 genotype (Genin et al., 2011), which is the most common in all populations studied (Farrer et al., 1997; Liu et al., 2013).”
BackgroundRemembering your A, B, C's: Alzheimer's disease and ABCA1
Lewandowski, C. T., Laham, M. S., & Thatcher, G. R. J. (2022) · Acta Pharmaceutica Sinica B · doi:10.1016/j.apsb.2022.01.011 · Cited by 76
Genetics of Vascular Dementia: Systematic Review and Meta-Analysis
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Object recognition analysis in mice using nose-point digital video tracking
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“BRAIN A JOURNAL OF NEUROLOGY Assessment and familial aggregation of psychosis in Alzheimer’s disease from the National Institute on Aging Late Onset Alzheimer’s Disease”
BackgroundUpdate on Biomarkers For Amyloid Pathology in Alzheimer’s Disease
Ashton, N. J., Schöll, M., Heurling, K., Gkanatsiou, E., Portelius, E., Höglund, K., Brinkmalm, G., Hye, A., Blennow, K., & Zetterberg, H. (2018) · Biomarkers in Medicine · doi:10.2217/bmm-2017-0433 · Cited by 78
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Prasad, K. N., Hovland, A. R., Cole, W. C., Prasad, K. C., Nahreini, P., Edwards‐Prasad, J., & Andreatta, C. P. (2000) · Clinical Neuropharmacology · doi:10.1097/00002826-200001000-00002 · Cited by 75
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“The apolipoprotein E (APOE) e4 allele is a major genetic risk factor for sporadic Alzheimer’s disease (AD) accounting for 40–80% of cases (Farrer et al, 1997).”
BackgroundMeng, Y., Baldwin, C. T., Bowirrat, A., Waraska, K., Inzelberg, R., Friedland, R. P., & Farrer, L. A. (2006) · The American Journal of Human Genetics · doi:10.1086/503687 · Cited by 72
Self-citationPostgenomics, uncertain futures, and the familiarization of susceptibility genes
Chilibeck, G., Lock, M. M., & Sehdev, M. (2010) · Social Science & Medicine · doi:10.1016/j.socscimed.2010.01.053 · Cited by 74
“On the other hand, ApoE 4 is significantly associated with dementia among African Americans, although less so than in white American populations (Farrer et al., 1997).”
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Sex- and APOE Isoform-Dependent Effects of Radiation on Cognitive Function
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Genetic risk of Alzheimer's disease: advising relatives
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Parkinson's Disease and Apolipoprotein E: Possible Association with Dementia but not Age at Onset
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Sorl1 as an Alzheimer’s Disease Predisposition Gene?
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APOE2 orchestrated differences in transcriptomic and lipidomic profiles of postmortem AD brain
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The role of amyloids in Alzheimer's and Parkinson's diseases
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Apolipoprotein E Genotype Modifies the Phenotype of Alzheimer Disease
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“Some prior research on hippocampal volume (Farrer et al., 1997; Lemaitre et al., 2005) also found that when comparing the heterozygous and homozygous APOE e4 groups, the right hippocampus may have more pronounced atrophy than the left side.”
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Early identification and heritability of mild cognitive impairment
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“In AD patients APOE4-induced risk is greater in females [2, 19, 20, 41, 45] consistent with our finding that E4FADF are cognitively impaired compared to all other groups tested at 8 months.”
Result
Metadata
- Authors
- Farrer, L. A.
- Corresponding author
- Farrer, Lindsay A.
- ORCID
- Farrer, Lindsay A.
- Venue
- JAMA
- Publisher
- American Medical Association (AMA)
- Published
- 1997-10-22
- Volume
- 278
- Issue
- 16
- Pages
- 1349
- ISSN
- 0002-9955 (ISSN-L)
- 0098-7484
- OpenAlex
- W7028228764
- Cited by
- 124
- References
- 0
- Citations by year
- 2026: 16 · 2025: 8 · 2024: 6 · 2023: 12 · 2022: 12 · 2021: 11 · 2020: 12 · 2019: 7 · 2018: 5 · 2017: 7 · 2016: 3 · 2015: 5 · 2014: 4 · 2013: 1 · 2012: 4
- FWCI
- 0.82
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- JAMA (publishedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (submittedVersion)
- Florence Research (University of Florence) (submittedVersion)
- 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
- apolipoprotein E, APOE ε4, Alzheimer's disease, genetic risk, age of onset, sex differences, ethnic differences, African Americans, Hispanic population, Japanese population, genetic heterogeneity, dementia risk
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