The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.
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.
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
“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]
Citations
Cites
The publisher hasn’t deposited this paper’s reference list.
Cited by
Sorted by citations
Items 201–300 of 1,178
Sex differences in Alzheimer’s disease and common neuropathologies of aging
Oveisgharan, S., Arvanitakis, Z., Yu, L., Farfel, J., Schneider, J. A., & Bennett, D. A. (2018) · Acta Neuropathologica · doi:10.1007/s00401-018-1920-1 · Cited by 330
“Published clinical studies found that women had higher odds for Alzheimer’s dementia and this association was stronger among APOE ε4 carriers compared to ε3ε3 carriers [21].”
InfluentialAlzheimer's Disease and Mild Cognitive Impairment
Kelley, B. J., & Petersen, R. C. (2007) · Neurologic Clinics · doi:10.1016/j.ncl.2007.03.008 · Cited by 335
Plasmalogens the neglected regulatory and scavenging lipid species
Wallner, S., & Schmitz, G. (2011) · Chemistry and Physics of Lipids · doi:10.1016/j.chemphyslip.2011.06.008 · Cited by 339
Mosconi, L. (2013) · Clinical and Translational Imaging · doi:10.1007/s40336-013-0026-y · Cited by 328
Cardiovascular disease and Alzheimer's disease: common links
Stampfer, M. J. (2006) · Journal of Internal Medicine · doi:10.1111/j.1365-2796.2006.01687.x · Cited by 340
The NIH Cognitive and Emotional Health Project: Report of the Critical Evaluation Study Committee
Hendrie, H. C., Albert, M. S., Butters, M. A., Gao, S., Knopman, D. S., Launer, L. J., Yaffe, K., Cuthbert, B. N., Edwards, E., & Wagster, M. V. (2006) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2005.11.004 · Cited by 323
Andrews-Zwilling, Y., Bien-Ly, N., Xu, Q., Li, G., Bernardo, A., Yoon, S. Y., Zwilling, D., Yan, T. X., Chen, L., & Huang, Y. (2010) · The Journal of Neuroscience · doi:10.1523/jneurosci.4040-10.2010 · Cited by 326
“Likewise, in humans, women with apoE4 have higher risk than men with apoE4 to develop Alzheimer’s disease (Farrer et al., 1997).”
BackgroundSex differences in Alzheimer risk: Brain imaging of endocrine vs chronologic aging
Mosconi, L., Berti, V., Quinn, C., McHugh, P., Petrongolo, G., Varsavsky, I., Osorio, R. S., Pupi, A., Vallabhajosula, S., Isaacson, R. S., et al. (2017) · Neurology · doi:10.1212/wnl.0000000000004425 · Cited by 319
APOE Genotype and Alzheimer Disease Risk Across Age, Sex, and Population Ancestry
Belloy, M. E., Andrews, S. J., Le Guen, Y., Cuccaro, M., Farrer, L. A., Napolioni, V., & Greicius, M. D. (2023) · JAMA Neurology · doi:10.1001/jamaneurol.2023.3599 · Cited by 320
Self-citationChang, S., Ma, T. R., Miranda, R. D., Balestra, M. E., Mahley, R. W., & Huang, Y. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0508254102 · Cited by 319
Mouse models of Alzheimer's disease
Hall, A. M., & Roberson, E. D. (2012) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2011.11.017 · Cited by 317
Genetics, environmental factors and the emerging role of epigenetics in neurodegenerative diseases
Migliore, L., & Coppedè, F. (2008) · Mutation research. Fundamental and molecular mechanisms of mutagenesis · doi:10.1016/j.mrfmmm.2008.10.011 · Cited by 331
ApoE Cascade Hypothesis in the pathogenesis of Alzheimer’s disease and related dementias
Martens, Y. A., Zhao, N., Liu, C.-C., Kanekiyo, T., Yang, A. J., Goate, A. M., Holtzman, D. M., & Bu, G. (2022) · Neuron · doi:10.1016/j.neuron.2022.03.004 · Cited by 316
Mercury Toxicity and Neurodegenerative Effects
Carocci, A., Rovito, N., Sinicropi, M. S., & Genchi, G. (2013) · Reviews of Environmental Contamination and Toxicology · doi:10.1007/978-3-319-03777-6_1 · Cited by 334
A novel Alzheimer disease locus located near the gene encoding tau protein
Jun, G., Ibrahim-Verbaas, C. A., Vronskaya, M., Lambert, J.-C., Chung, J., Naj, A. C., Kunkle, B. W., Wang, L.-S., Bis, J. C., Bellenguez, C., et al. (2016) · Molecular Psychiatry · doi:10.1038/mp.2015.23 · Cited by 297
Vascular risk factors, cognitve decline, and dementia
Hanon, O. (2008) · Vascular Health and Risk Management · doi:10.2147/vhrm.s1839 · Cited by 322
“In the same way, the ε 4 allele of the Apo E gene represents a genetic risk factor for atherosclerosis (Wilson et al 1996) and the most important Powered by TCPDF (www.tcpdf.org) genetic risk factor for sporadic AD in the general population (Farrer et al 1997).”
Neurotoxic Effects of Aluminium Among Foundry Workers and Alzheimer’s Disease
Polizzi, S., Pira, E., Ferrara, M., Bugiani, M., Papaleo, A., Albera, R., & Palmi, S. (2002) · NeuroToxicology · doi:10.1016/s0161-813x(02)00097-9 · Cited by 319
Law, A. (2001) · Brain Research Reviews · doi:10.1016/s0165-0173(00)00051-5 · Cited by 314
Jeremic, D., Jiménez-Díaz, L., & Navarro-López, J. D. (2021) · Ageing Research Reviews · doi:10.1016/j.arr.2021.101496 · Cited by 306
“Women bearing ε4 isoform showed steeper cognitive decline than did men APOE-ε4 carriers, and women with high Aβ showed worse cognitive decline than men with high Aβ (Buckley et al., 2018; Farrer et al., 1997).”
BackgroundOxidative Stress in Alzheimer’s Disease: Why Did Antioxidant Therapy Fail?
Persson, T., Popescu, B. O., & Cedazo-Mı́nguez, Á. (2014) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2014/427318 · Cited by 329
Microglia, Lifestyle Stress, and Neurodegeneration
Madore, C., Yin, Z., Leibowitz, J. A., & Butovsky, O. (2020) · Immunity · doi:10.1016/j.immuni.2019.12.003 · Cited by 313
Nature, nurture, and development: from evangelism through science toward policy and practice
Rutter, M. (2002) · Child Development · doi:10.1111/1467-8624.00388 · Cited by 309
“…particular alleles are responsible for thalassaemia (sickle cell disease; see Weatherall & Clegg, 2001); and, for reasons that remain ill understood, the apolipoprotein E4 seems to carry less of a risk for Alzheimer’s disease in individuals of African or Hispanic heritage (Farrer et al., 1997).”
BackgroundRelationship Between ApoE, MRI Findings, and Cognitive Function in the Cardiovascular Health Study
Kuller, L. H., Shemanski, L. R., Manolio, T. A., Haan, M. N., Fried, L. P., Bryan, R. N., Burke, G. L., Tracy, R. P., & Bhadelia, R. A. (1998) · Stroke · doi:10.1161/01.str.29.2.388 · Cited by 313
Mechanisms of protein-folding diseases at a glance
Valastyan, J. S., & Lindquist, S. L. (2014) · Disease Models & Mechanisms · doi:10.1242/dmm.013474 · Cited by 318
“At least one copy of the APOE4 allele is found in 65-80% of individuals with Alzheimer’s disease (AD) (Farrer et al., 1997).”
BackgroundLewczuk, P., Riederer, P. F., O’Bryant, S. E., Verbeek, M. M., Dubois, B., Visser, P. J., Jellinger, K. A., Engelborghs, S., Ramírez, A., Parnetti, L., et al. (2017) · The World Journal of Biological Psychiatry · doi:10.1080/15622975.2017.1375556 · Cited by 318
“For APOE-e2, compelling evidence supports a protective effect and a delaying effect on age of disease onset (Corder et al. 1994; Farrer et al. 1997).”
BackgroundAPOE2: protective mechanism and therapeutic implications for Alzheimer’s disease
Li, Z., Shue, F., Zhao, N., Shinohara, M., & Bu, G. (2020) · Molecular Neurodegeneration · doi:10.1186/s13024-020-00413-4 · Cited by 306
Apolipoprotein E–dependent accumulation of Alzheimer disease–related lesions begins in middle age
Kok, E., Haikonen, S., Luoto, T., Huhtala, H., Goebeler, S., Haapasalo, H., & Karhunen, P. J. (2009) · Annals of Neurology · doi:10.1002/ana.21696 · Cited by 299
Exercise-Induced Neuroplasticity: A Mechanistic Model and Prospects for Promoting Plasticity
El‐Sayes, J., Harasym, D., Turco, C. V., Locke, M. B., & Nelson, A. J. (2018) · The Neuroscientist · doi:10.1177/1073858418771538 · Cited by 335
Astrocytes as Key Regulators of Brain Energy Metabolism: New Therapeutic Perspectives
Béard, E., Lengacher, S., Dias, S., Magistretti, P. J., & Finsterwald, C. (2022) · Frontiers in Physiology · doi:10.3389/fphys.2021.825816 · Cited by 326
van der Lee, S. J., Wolters, F. J., Ikram, M. K., Albert Hofman, D., Ikram, M. A., Amin, N., & van Duijn, C. M. (2018) · The Lancet Neurology · doi:10.1016/s1474-4422(18)30053-x · Cited by 317
Tervo, S., Kivipelto, M., Hänninen, T., Vanhanen, M., Hallikainen, M., Mannermaa, A., & Soininen, H. (2004) · Dementia and Geriatric Cognitive Disorders · doi:10.1159/000076356 · Cited by 298
Fat Intake at Midlife and Risk of Dementia and Alzheimer’s Disease: A Population-Based Study
Laitinen, M. H., Ngandu, T., Rovio, S., Helkala, E.-L., Uusitalo, U. M., Viitanen, M. H., Nissinen, A. M., Tuomilehto, J., Soininen, H. S., & Kivipelto, M. (2006) · Dementia and Geriatric Cognitive Disorders · doi:10.1159/000093478 · Cited by 298
“Alzheimer’s disease (AD), the major form of dementia, is a disease of complex origin. The e4 allele of apolipoprotein E (ApoE), which is involved in cholesterol metabolism, is to date the only genetic risk factor for AD of established general significance [”
BackgroundThe role of TNF and its receptors in Alzheimer's disease
Perry, R. (2001) · Neurobiology of Aging · doi:10.1016/s0197-4580(01)00291-3 · Cited by 301
Genetic variation in PCDH11X is associated with susceptibility to late-onset Alzheimer’s disease
Carrasquillo, M. M., Zou, F., Pankratz, V. S., Wilcox, S. L., Ma, L., Walker, L. P., Younkin, S. G., Younkin, C. S., Younkin, L. H., Bisceglio, G. D., et al. (2009) · Nature Genetics · doi:10.1038/ng.305 · Cited by 296
“Multiple rare mutations in the genes encoding the amyloid β protein precursor, presenilin 1 and presenilin 2 cause an early-onset familial form of Alzheimer's disease with autosomal dominant inheritance, but the only well established susceptibility allele for LOAD is the APOE e4 allel”
BackgroundThe Number of Trait Loci in Late-Onset Alzheimer Disease
Daw, E. W., Payami, H., Nemens, E. J., Nochlin, D., Bird, T. D., Schellenberg, G. D., & Wijsman, E. M. (2000) · The American Journal of Human Genetics · doi:10.1086/302710 · Cited by 295
“…accepted findings of a dose effect for the 4 allele with respect to the 3 allele (Corder et al. 1993) and also found shifts in age at onset of AD that correspond exactly to the order of the liabilities for AD for each genotype found in some previous studies (Jarvik et al. 1995; Farrer et al. 1997).”
BackgroundResultExecutive Functions in Alzheimer Disease: A Systematic Review
Guarino, A., Favieri, F., Boncompagni, I., Agostini, F., Cantone, M., & Casagrande, M. (2019) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2018.00437 · Cited by 280
Multiple cognitive deficits during the transition to Alzheimer's disease
Bäckman, L., Jones, S., Berger, A., Laukka, E. J., & Small, B. J. (2004) · Journal of Internal Medicine · doi:10.1111/j.1365-2796.2004.01386.x · Cited by 309
Changing perspectives regarding late-life dementia
Fotuhi, M., Hachinski, V., & Whitehouse, P. J. (2009) · Nature Reviews Neurology · doi:10.1038/nrneurol.2009.175 · Cited by 291
Shaw, P., Lerch, J. P., Pruessner, J. C., Taylor, K. N., Rose, A. B., Greenstein, D., Clasen, L., Evans, A., Rapoport, J. L., & Giedd, J. N. (2007) · The Lancet Neurology · doi:10.1016/s1474-4422(07)70106-0 · Cited by 257
Neuroprotective Actions of Dietary Choline
Blusztajn, J., Slack, B., & Mellott, T. (2017) · Nutrients · doi:10.3390/nu9080815 · Cited by 293
Chen, X., & Mobley, W. C. (2019) · Frontiers in Neuroscience · doi:10.3389/fnins.2019.00659 · Cited by 302
Mouse models of Alzheimer’s disease
Esquerda-Canals, G., Montoliu-Gaya, L., Güell-Bosch, J., & Villegas, S. (2017) · Journal of Alzheimer’s Disease · doi:10.3233/jad-170045 · Cited by 288
Apolipoprotein E in lipid metabolism and neurodegenerative disease
Yang, L. G., March, Z. M., Stephenson, R. A., & Narayan, P. S. (2023) · Trends in Endocrinology & Metabolism · doi:10.1016/j.tem.2023.05.002 · Cited by 286
Advances in developing novel therapeutic strategies for Alzheimer’s disease
Cao, J., Hou, J., Ping, J., & Cai, D. (2018) · Molecular Neurodegeneration · doi:10.1186/s13024-018-0299-8 · Cited by 283
Apolipoprotein E ε4 allele, AD pathology, and the clinical expression of Alzheimer’s disease
Bennett, D. A., Wilson, R. S., Schneider, J. A., Evans, D. A., Aggarwal, N. T., Arnold, S. E., Cochran, E. J., Berry-Kravis, E., & Bienias, J. L. (2003) · Neurology · doi:10.1212/01.wnl.0000042478.08543.f7 · Cited by 282
Rabinovici, G. D., Furst, A. J., Alkalay, A., Racine, C. A., O’Neil, J. P., Janabi, M., Baker, S. L., Agarwal, N., Bonasera, S. J., Mormino, E. C., et al. (2010) · Brain · doi:10.1093/brain/awp326 · Cited by 289
“M].”
BackgroundMethodResultInfluentialKanekiyo, T., & Bu, G. (2014) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2014.00093 · Cited by 281
“Since the APOE 4 allele increases the risk for late-onset Alzheimer’s disease (AD) compared with the APOE 2 and 3 alleles (Corder et al., 1993; Farrer et al., 1997), LDLR family has been vigorously studied as a target to explore the complex pathogenesis of AD.”
BackgroundAnalysis of European mitochondrial haplogroups with Alzheimer disease risk
van der Walt, J. M., Dementieva, Y. A., Martin, E. R., Scott, W. K., Nicodemus, K. K., Kroner, C. C., Welsh-Bohmer, K. A., Saunders, A. M., Roses, A. D., Small, G. W., et al. (2004) · Neuroscience Letters · doi:10.1016/j.neulet.2004.04.051 · Cited by 280
Buckley, R. F., Mormino, E. C., Amariglio, R. E., Properzi, M. J., Rabin, J. S., Lim, Y. Y., Papp, K. V., Jacobs, H. I. L., Burnham, S., Hanseeuw, B. J., et al. (2018) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2018.04.010 · Cited by 276
Chen, J.-H., Lin, K.-P., & Chen, Y.-C. (2009) · Journal of the Formosan Medical Association · doi:10.1016/s0929-6646(09)60402-2 · Cited by 288
Kimura, R., Kamino, K., Yamamoto, M., Nuripa, A., Kida, T., Kazui, H., Hashimoto, R., Tanaka, T., Kudo, T., Yamagata, H., et al. (2007) · Human Molecular Genetics · doi:10.1093/hmg/ddl437 · Cited by 281
Longitudinal MRI atrophy biomarkers: Relationship to conversion in the ADNI cohort
Risacher, S. L., Shen, L., West, J. D., Kim, S., McDonald, B. C., Beckett, L. A., Harvey, D. J., Jack, C. R., Weiner, M. W., & Saykin, A. J. (2010) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2010.04.029 · Cited by 276
Clearance of cerebral Aβ in Alzheimer’s disease: reassessing the role of microglia and monocytes
Zuroff, L. R., Daley, D. A., Black, K. L., & Koronyo‐Hamaoui, M. (2017) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-017-2463-7 · Cited by 292
Head (2012) · doi:10.1001/archneurol.2011.845 · Cited by 267
Female Sex and Alzheimer's Risk: The Menopause Connection
Scheyer, O., Rahman, A., Hristov, H., Berkowitz, C., Isaacson, R. S., Diaz Brinton, R., & Mosconi, L. (2018) · The Journal of Prevention of Alzheimer's Disease · doi:10.14283/jpad.2018.34 · Cited by 268
“A long with advanced age and apolipoprotein E (APOE)-4 genotype, female sex is one of the major risk factor for developing late-onset Alzheimer’s disease (AD) (1).”
Human APOE Isoform-Dependent Effects on Brain β-Amyloid Levels in PDAPP Transgenic Mice
Bales, K. R., Liu, F., Wu, S., Lin, S., Koger, D., DeLong, C., Hansen, J. C., Sullivan, P. M., & Paul, S. M. (2009) · The Journal of Neuroscience · doi:10.1523/jneurosci.0887-09.2009 · Cited by 274
“The 4 allele of the apolipoprotein E gene is a well established risk factor for late-onset Alzheimer’s disease (AD), even in populations where the 4 allele is under-represented (Saunders et al., 1993; Farrer et al., 1997).”
BackgroundYe, S., Huang, Y., Müllendorff, K., Dong, L., Giedt, G., Meng, E. C., Cohen, F. E., Kuntz, I. D., Weisgraber, K. H., & Mahley, R. W. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0508693102 · Cited by 275
Sexual dimorphism in predisposition to Alzheimer's disease
Fisher, D. W., Bennett, D. A., & Dong, H. (2018) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2018.04.004 · Cited by 270
Naismith, S. L., Norrie, L. M., Mowszowski, L., & Hickie, I. B. (2012) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2012.05.009 · Cited by 282
APOE genotype as a risk factor for ischemic cerebrovascular disease
McCarron, M. O., DeLong, D. M., & Alberts, M. J. (1999) · Neurology · doi:10.1212/wnl.53.6.1308 · Cited by 270
Damoiseaux, J. S., Seeley, W. W., Zhou, J., Shirer, W. R., Coppola, G., Karydas, A., Rosen, H. J., Miller, B. L., Kramer, J. H., Greicius, M. D., et al. (2012) · Journal of Neuroscience · doi:10.1523/jneurosci.0305-12.2012 · Cited by 267
“Gender Modulates the APOE 4 Effect in Healthy Older”
InfluentialThe biological pathways of Alzheimer disease: a review
Calabrò, M., Rinaldi, C., Santoro, G., & Crisafulli, C. (2020) · AIMS neuroscience · doi:10.3934/neuroscience.2021005 · Cited by 287
Autosomal Recessive Causes Likely in Early-Onset Alzheimer Disease
Wingo, T. S. (2012) · Archives of Neurology · doi:10.1001/archneurol.2011.221 · Cited by 265
Snyder, H. M., Asthana, S., Bain, L., Brinton, R., Craft, S., Dubal, D. B., Espeland, M. A., Gatz, M., Mielke, M. M., Raber, J., et al. (2016) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2016.08.004 · Cited by 262
Cerebrovascular atherosclerosis correlates with Alzheimer pathology in neurodegenerative dementias
Yarchoan, M. M., Xie, S. X., Kling, M. A., Toledo, J. B., Wolk, D. A., Lee, E. B., Deerlin, V. M. V., Lee, V. M. Y., Trojanowski, J. Q., & Arnold, S. E. (2012) · Brain · doi:10.1093/brain/aws271 · Cited by 268
The Role of Estrogen in Brain and Cognitive Aging
Russell, J. K., Jones, C. K., & Newhouse, P. A. (2019) · Neurotherapeutics · doi:10.1007/s13311-019-00766-9 · Cited by 257
Cerebrovascular Effects of Apolipoprotein E: Implications for Alzheimer Disease
Zlokovic, B. V. (2013) · JAMA Neurology · doi:10.1001/jamaneurol.2013.2152 · Cited by 263
Epigenetic regulation in the pathophysiology of Alzheimer's disease
Chouliaras, L., Rutten, B. P. F., Kenis, G., Peerbooms, O., Visser, P. J., Verhey, F., van Os, J., Steinbusch, H. W. M., & van den Hove, D. L. A. (2010) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2010.01.002 · Cited by 262
Sando, S. B., Melquist, S., Cannon, A., Hutton, M. L., Sletvold, O., Saltvedt, I., White, L. R., Lydersen, S., & Aasly, J. O. (2008) · BMC Neurology · doi:10.1186/1471-2377-8-9 · Cited by 261
Lim, A. S. P., Yu, L., Kowgier, M. E., Schneider, J. A., Buchman, A. S., & Bennett, D. A. (2013) · JAMA Neurology · doi:10.1001/jamaneurol.2013.4215 · Cited by 269
Gender, sex steroid hormones, and Alzheimer’s disease
Vest, R. S., & Pike, C. J. (2013) · Hormones and Behavior · doi:10.1016/j.yhbeh.2012.04.006 · Cited by 260
Neuropsychological Measures in Normal Individuals That Predict Subsequent Cognitive Decline
Blacker, D., Lee, H., Muzikansky, A., Martin, E. C., Tanzi, R. E., McArdle, J. J., Moss, M. B., & Albert, M. (2007) · Archives of Neurology · doi:10.1001/archneur.64.6.862 · Cited by 269
Ostan, R., Monti, D., Gueresi, P., Bussolotto, M., Franceschi, C., & Baggio, G. (2016) · Clinical Science · doi:10.1042/cs20160004 · Cited by 270
Physical Activity and Alzheimer’s Disease: A Systematic Review
Stephen, R., Hongisto, K., Solomon, A., & Lönnroos, E. (2017) · The Journals of Gerontology Series A: Biological Sciences and Medical Sciences · doi:10.1093/gerona/glw251 · Cited by 262
“The impact of apolipoprotein E allele on AD and dementia seems to become weaker at older ages (52) and also the impact of physical inactivity may be lower among APOE4 carriers who survive to old age (50).”
BackgroundAssociation of Apolipoprotein E ε4 With Medial Temporal Tau Independent of Amyloid-β
Therriault, J., Benedet, A. L., Pascoal, T. A., Mathotaarachchi, S., Chamoun, M., Savard, M., Thomas, E., Kang, M. S., Lussier, F., Tissot, C., et al. (2020) · JAMA Neurology · doi:10.1001/jamaneurol.2019.4421 · Cited by 256
Sex, Apolipoprotein E ε4 Status, and Hippocampal Volume in Mild Cognitive Impairment
Fleisher, A. (2005) · Archives of Neurology · doi:10.1001/archneur.62.6.953 · Cited by 268
The role of APOE -ε4 in longitudinal cognitive decline
Bretsky, P., Guralnik, J. M., Launer, L. J., Albert, M., & Seeman, T. E. (2003) · Neurology · doi:10.1212/01.wnl.0000055875.26908.24 · Cited by 258
Potential occupational risks for neurodegenerative diseases
Park, R. M., Schulte, P. A., Bowman, J. D., Walker, J. T., Bondy, S. C., Yost, M. G., Touchstone, J. A., & Dosemeci, M. (2005) · American Journal of Industrial Medicine · doi:10.1002/ajim.20178 · Cited by 256
“…against the effects of oxidative stressors [Behl and Holsboer, 1998], and a genetic polymorphism in metabolism or detoxification of a neurotoxin could have different distributions in white and black workers [Agzndez et al., 1995; Farrer et al., 1997; Hubble et al., 1998; Headrie et al., 2001].”
BackgroundHussain, B., Fang, C., & Chang, J. (2021) · Frontiers in Neuroscience · doi:10.3389/fnins.2021.688090 · Cited by 255
Stonehouse, W., Conlon, C. A., Podd, J., Hill, S. R., Minihane, A. M., Haskell, C., & Kennedy, D. (2013) · The American Journal of Clinical Nutrition · doi:10.3945/ajcn.112.053371 · Cited by 252
Esposito, L., Raber, J., Kekonius, L., Yan, F., Yu, G.-Q., Bien-Ly, N., Puoliväli, J., Scearce-Levie, K., Masliah, E., & Mucke, L. (2006) · The Journal of Neuroscience · doi:10.1523/jneurosci.0482-06.2006 · Cited by 254
A Comprehensive Genetic Association Study of Alzheimer Disease in African Americans
Logue, M. W. (2011) · Archives of Neurology · doi:10.1001/archneurol.2011.646 · Cited by 250
Genomic Priorities and Public Health
Merikangas, K. R., & RISCH, N. J. (2003) · Science · doi:10.1126/science.1091468 · Cited by 251
The Epidemiology of Common Late-Life Mental Disorders in the Community: Themes for the New Century
Gallo, J. J., & Lebowitz, B. D. (1999) · Psychiatric Services · doi:10.1176/ps.50.9.1158 · Cited by 248
Endoplasmic Reticulum Ca2+ Handling in Excitable Cells in Health and Disease
Stutzmann, G. E., & Mattson, M. P. (2011) · Pharmacological Reviews · doi:10.1124/pr.110.003814 · Cited by 255
Harmonizing Genetic Ancestry and Self-identified Race/Ethnicity in Genome-wide Association Studies
Fang, H., Hui, Q., Lynch, J. A., Honerlaw, J. P., Assimes, T. L., Huang, J., Vujković, M., Damrauer, S. M., Pyarajan, S., Gaziano, J. M., et al. (2019) · The American Journal of Human Genetics · doi:10.1016/j.ajhg.2019.08.012 · Cited by 226
Jia, J., Zhao, T., Liu, Z., Liang, Y., Li, F., Li, Y., Liu, W., Li, F., Shi, S., Zhou, C., et al. (2023) · BMJ · doi:10.1136/bmj-2022-072691 · Cited by 252
Ioannidis, J. P. A., Trikalinos, T. A., & Khoury, M. J. (2006) · American Journal of Epidemiology · doi:10.1093/aje/kwj259 · Cited by 248
“Finally, our analyzed sample did not include any of the very few genetic variants that have been identified to date with a postulated odds ratio exceeding 3. The only such meta-analysis published in the time frame of our literature search (the apolipoprotein E gene (APOE) and Alzheimer’s disease ( 16 )) did not provid…”
BackgroundAge-related macular degeneration (AMD): Alzheimer's disease in the eye?
Kaarniranta, K., Salminen, A., Haapasalo, A., Soininen, H., & Hiltunen, M. (2011) · Journal of Alzheimer s Disease · doi:10.3233/jad-2011-101908 · Cited by 248
“In contrast to AMD, the APOE-ε4 polymorphism represents the strongest thus far identified risk factor for AD, whereas the APOE- ε2 allele carriers have a reduced risk for developing AD (http://www.alzgene.org) [53] [54] [55] [56] [57].”
BackgroundMild Cognitive Impairment: A Systematic Review
Mariani, E., Monastero, R., & Mecocci, P. (2007) · Journal of Alzheimer s Disease · doi:10.3233/jad-2007-12104 · Cited by 248
Ungar, L., Altmann, A., & Greicius, M. D. (2014) · Brain Imaging and Behavior · doi:10.1007/s11682-013-9272-x · Cited by 246
“In studies with long-lived subjects, the APOE4 effect is detectable in age of onset but is diminished in terms of overall risk, such that beyond age 80 there is little additional risk attributable to APOE4 (Blacker et al. 1997; Dickson et al. 2008; Farrer et al. 1997; Khachaturian et al. 2004).”
InfluentialKnopman, D. S., Boeve, B. F., & Petersen, R. C. (2003) · Mayo Clinic Proceedings · doi:10.4065/78.10.1290 · Cited by 257
Health Behavior Changes After Genetic Risk Assessment for Alzheimer Disease: The REVEAL Study
Chao, S. H.-L., Roberts, J. S., Marteau, T. M., Silliman, R. A., Cupples, L. A., & Green, R. C. (2008) · Alzheimer Disease & Associated Disorders · doi:10.1097/wad.0b013e31815a9dcc · Cited by 243
Huang, Y., Weisgraber, K. H., Mucke, L., & Mahley, R. W. (2004) · Journal of Molecular Neuroscience · doi:10.1385/jmn:23:3:189 · Cited by 242
The genetics and neuropathology of Alzheimer’s disease
Schellenberg, G. D., & Montine, T. J. (2012) · Acta Neuropathologica · doi:10.1007/s00401-012-0996-2 · Cited by 256
Luis, C. A., Loewenstein, D., Acevedo, A., Barker, W. W., & Duara, R. (2003) · Neurology · doi:10.1212/01.wnl.0000080366.90234.7f · Cited by 247
Fusar‐Poli, P., Cappucciati, M., Rutigliano, G., Schultze‐Lutter, F., Bonoldi, I., Borgwardt, S., Riecher‐Rössler, A., Addington, J., Perkins, D., Woods, S. W., et al. (2015) · World Psychiatry · doi:10.1002/wps.20250 · Cited by 234
Kukull, W. A., & Ganguli, M. (2012) · Neurology · doi:10.1212/wnl.0b013e318258f812 · Cited by 239
Complexity of Work and Risk of Alzheimer's Disease: A Population-Based Study of Swedish Twins
Andel, R., Crowe, M., Pedersen, N., Mortimer, J. A., Crimmins, E. M., Johansson, B. E. A., & Gatz, M. (2005) · The Journals of Gerontology Series B · doi:10.1093/geronb/60.5.p251 · Cited by 240
Mosconi, L., De Santi, S., Brys, M., Tsui, W. H., Pirraglia, E., Glodzik-Sobanska, L., Rich, K. E., Switalski, R., Mehta, P. D., Pratico, D., et al. (2008) · Biological Psychiatry · doi:10.1016/j.biopsych.2007.05.030 · Cited by 238
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
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
