Cited by 399Dementia and Cognitive Impairment ResearchAlzheimer's disease research and treatmentsGenetic Associations and Epidemiology

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Risk Estimates of Dementia by Apolipoprotein E Genotypes From a Population-Based Incidence Study: The Rotterdam Study

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Slooter, Arjen J. C., Cruts, Marc, Kalmijn, Sandra, Hofman, Albert, Breteler, Monique M. B., Van Broeckhoven, Christine, van Duijn, Cornelia M.·1998·Archives of Neurology

DOI 10.1001/archneur.55.7.964

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Abstract

OBJECTIVES: To provide risk estimates of dementia and Alzheimer disease as a function of the apolipoprotein E (APOE) genotypes and to assess the proportion of dementia that is attributable to the APOE genotypes. DESIGN: Case-control study nested in a population-based cohort study with a mean (SD) follow-up of 2.1 (0.9) years. SETTING: General population in Rotterdam, the Netherlands. PARTICIPANTS: A total of 134 patients with incident dementia and a random sample of 997 nondemented control subjects. No participant had dementia at baseline. MAIN OUTCOME MEASURES: Odds ratios for dementia and Alzheimer disease, the fraction of dementia attributable to the APOE epsilon4 allele, and the proportion of the variance in age at the onset of dementia explained by the APOE genotypes. RESULTS: Persons with the epsilon4/4 genotype had a more than 10-fold higher risk of dementia (odds ratio, 11.2; 95% confidence interval, 3.6-35.2), and subjects with the epsilon3/4 genotype had a 1.7-fold increased risk of dementia (95% confidence interval, 1.0-2.9) as compared with persons with the epsilon3/3 genotype. The proportion of patients with dementia that is attributable to the epsilon4 allele was estimated to be 20%. The APOE genotypes explained up to 10% of the variance in age at the onset of dementia. The association between the epsilon4 allele and dementia was strongest in the youngest age category and in those with a family history of dementia. CONCLUSIONS: The APOE genotype is an important determinant of the risk of dementia. At a population level, however, other factors than the APOE genotype may play an important role in the cause of dementia.

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Narrative video scene description task discriminates between levels of cognitive impairment in Alzheimer’s disease.
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“…21 (immediate and delayed recall), Benson Complex Figure Copy (immediate and delayed recall), Number Span Test (forwards and backwards), Category Fluency (animals and vegetables), Trail Making Test A and B, Multilingual Naming Test (MINT), and Verbal Fluency (“F” and “L”) (Slooter et al., 1998).”
Background
Associations between apolipoprotein E gene polymorphisms and Alzheimer’s disease risk in a large Chinese Han population
Sun, Y., Wu, P., Li, H., Liu, Z., Tao, Q., Guo, Q., Hong, Z., & Xu, M. (2015) · Clinical Interventions in Aging · doi:10.2147/cia.s73396 · Cited by 14
Genomics of Alzheimer's disease: Value of high-throughput genomic technologies to dissect its etiology
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Cross Talk Between Aluminum and Genetic Susceptibility and Epigenetic Modification in Alzheimer’s Disease
Liang, R. (2018) · Advances in experimental medicine and biology · doi:10.1007/978-981-13-1370-7_10 · Cited by 16
Update on Alzheimer's disease: recent findings and treatments
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Exercise, but not antioxidants, reversed ApoE4-associated motor impairments in adult GFAP-ApoE mice
Chaudhari, K., Wong, J. M., Vann, P. H., & Sumien, N. (2016) · Behavioural Brain Research · doi:10.1016/j.bbr.2016.02.014 · Cited by 14
APOE Genotype in Relation to Sporadic and Alzheimer-Related CAA
McCarron, M. O., & Nicoll, J. A. R. (2000) · Springer eBooks · doi:10.1007/978-94-017-1007-7_5 · Cited by 14
Social network and the risk for developing mild cognitive impairment and dementia among older adults
Eymundsdóttir, H., SIGURDARDOTTIR, S. T., Ramel, A., Jónsson, P. V., Gudnason, V. G., Launer, L. J., & Chang, M. (2022) · Aging Clinical and Experimental Research · doi:10.1007/s40520-022-02150-8 · Cited by 13
The screening of Alzheimer’s patients with CSF biomarkers, modulates the distribution of APOE genotype: impact on clinical trials
Dumurgier, J., Laplanche, J., Mouton‐Liger, F., Lapalus, P., Indart, S., Prévot, M., Peoc’h, K., Hugon, J., & Paquet, C. (2014) · Journal of Neurology · doi:10.1007/s00415-014-7335-6 · Cited by 14
“The apolipoprotein E gene (APOE) is the most important susceptibility gene for AD with a population attributable risk estimated at 20 % [11].”
Background
Bridges to Life
Kurzweil, R., & Grossman, T. (2010) · Springer eBooks · doi:10.1007/978-90-481-3999-6_1 · Cited by 14
Development and validation of risk index for cognitive decline using blood-derived markers
Nettiksimmons, J., Ayonayon, H. N., Harris, T. B., Phillips, C., Rosano, C., Satterfield, S., Yaffe, K. S., Study, F. T. H. A., Cummings, S. R., Garcia, M. E., et al. (2015) · Neurology · doi:10.1212/wnl.0000000000001263 · Cited by 13
Variants regulating ZBTB4 are associated with age‐at‐onset of Alzheimer's disease
Blue, E., Yu, C., Thornton, T. A., Chapman, N. H., Kernfeld, E. M., Jiang, N., Shively, K. M., Buckingham, K. J., Marvin, C. T., Bamshad, M. J., et al. (2017) · Genes Brain & Behavior · doi:10.1111/gbb.12429 · Cited by 12
Role of TOMM40 rs10524523 Polymorphism in Onset of Alzheimer's Disease Caused by the PSEN1 M146L Mutation
Bernardi, L., Gallo, M., Anfossi, M., Conidi, M. E., Colao, R., Puccio, G., Curcio, S. A. M., Frangipane, F., Clodomiro, A., Mirabelli, M., et al. (2013) · Journal of Alzheimer s Disease · doi:10.3233/jad-130119 · Cited by 13
APOE and ACE polymorphisms and dementia risk in the older population over prolonged follow-up: 10 years of incidence in the MRC CFA Study
Keage, H. A. D., Matthews, F. E., Yip, A. G., Gao, L., McCracken, C., McKeith, I. G., Rubinsztein, D. C., Brayne, C., & Study, M. C. F. A. A. (2009) · Age and Ageing · doi:10.1093/ageing/afp210 · Cited by 13
Polymorphisms in LMNA and near a SERPINA gene cluster are associated with cognitive function in older people
Cluett, C., Brayne, C., Clarke, R., Evans, G., Matthews, F., Rubinsztein, D. C., Huppert, F., Llewellyn, D. J., Rice, N., Henley, W., et al. (2010) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2008.08.020 · Cited by 12
“However, the ApoE haplotype only explains about 7–15% of the heritability of LOAD ([Bennett et al., 1995], [Daw et al., 2000], [Farrer et al., 1991], [Rao et al., 1996], [Slooter et al., 1998]).”
Background
Public Willingness to Undergo Presymptomatic Genetic Testing for Alzheimer’s Disease
Alanazy, M. H., Alghsoon, K. A., Alkhodairi, A. F., Binkhonain, F. K., Alsehli, T. N., Altukhaim, F., Alkhodair, I. M., & Muayqil, T. A. (2019) · Neurology Research International · doi:10.1155/2019/2570513 · Cited by 12
“[16] reported that 25% of the general population aged 55 years and older have a first-degree relative with dementia.”
Background
KIBRA gene polymorphism has no association with verbal or visual episodic memory performance
Franks, K. H., Summers, M. J., & Vickers, J. C. (2014) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2014.00270 · Cited by 12
“The association of genes such as brain-derived neurotrophic factor (BDNF) and apolipoprotein-E (ApoE) with cognitive decline and late-onset Alzheimer’s disease (AD) has been investigated (e.g., Corder et al., 1993; Slooter et al., 1998; Hariri et al., 2003; Cosentino et al., 2008).”
Background
DNMBP is genetically associated with Alzheimer dementia in the Belgian population
Bettens, K., Brouwers, N., Engelborghs, S., Pooter, T. D., Deyn, P. P. D., Sleegers, K., & Broeckhoven, C. V. (2008) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2008.02.003 · Cited by 11
Matrix metalloproteinase 3 haplotypes and dementia and Alzheimer's disease
Reitz, C., van Rooij, F. J. A., de Maat, M. P. M., den Heijer, T., Albert Hofman, D., Witteman, J. C. M., & Breteler, M. M. B. (2007) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2007.01.001 · Cited by 11
“Apolipoprotein E (APOE) enotype was assessed on coded DNA samples using polyerase chain reaction without knowledge of the dementia iagnosis (Slooter et al., 1998). After excluding persons with he APOE 2/ 4 genotype, we dichotomized APOE genotype nto presence or absence of the apolipoproteinE 4 (APOE 4) llele. f t s o…”
MethodSelf-citation
Dementia in Germany: Past Trends and Future Developments
Ziegler, U. (2011) · DZNE Pub · doi:10.18453/rosdok_id00000815 · Cited by 11
The role of Apolipoprotein E4 on cognitive impairment in Parkinson’s disease and Parkinsonisms
Rosal, A. E., Martin, S. L., & Strafella, A. P. (2025) · Frontiers in Neuroscience · doi:10.3389/fnins.2025.1515374 · Cited by 10
Direct to Consumer Biomarker Testing for Alzheimer Disease—Are We Ready for the Insurance Consequences?
Arias, J. J., Manchester, M., & Lah, J. J. (2023) · JAMA Neurology · doi:10.1001/jamaneurol.2023.4811 · Cited by 10
The ZARADEMP Project on the incidence, prevalence and risk factors of dementia (and depression) in the elderly community: I. The context and the objectives
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Investigation of triggering receptor expressed on myeloid cells 2 variant in the Wisconsin Registry for Alzheimer's Prevention
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Effect of ApoE4 Genotype on the Association Between Metabolic Phenotype and Subclinical Atherosclerosis in Postmenopausal Women
Sriprasert, I., Mack, W. J., Hodis, H. N., Allayee, H., Brinton, R. D., & Karim, R. (2019) · The American Journal of Cardiology · doi:10.1016/j.amjcard.2019.06.022 · Cited by 9
Age-related mild cognitive deficit: a ready-to-use concept?
Gilles, C. (2003) · Dialogues in Clinical Neuroscience · doi:10.31887/dcns.2003.5.1/cgilles · Cited by 9
“In this study, 6 of 12 MCI subjects had a neuropathological diagnosis of possible AD according to the criteria of the Consortium to Establish a Registry for Alzheimer’s Disease (CERAD).47 In a third study,45 neurofibrillary tangles (NFTs) and neuropil threads (NTs) were present in perirhinal cortex and ERC in NCs, MCI…”
BackgroundInfluential
Association between DCHS2 gene and mild cognitive impairment and Alzheimer's disease in an elderly Brazilian sample
Vieira, R. N., de Ávila, R. T., de Paula, J. J., Cintra, M. T. G., de Souza, R. P., Nicolato, R., Malloy‐Diniz, L. F., de Miranda, D. M., de Moraes, E. N., Marco, L. A. D., et al. (2016) · International Journal of Geriatric Psychiatry · doi:10.1002/gps.4440 · Cited by 9
“The ε4 allele of the APOE gene influences the AAO in a dosedependent manner being responsible for 4% of the variation (Slooter et al., 1998; Tunstall et al., 2000).”
Background
Apolipoprotein E ϵ4 allele is associated with left ventricular systolic dysfunction
Bleumink, G. S., van Duijn, C. M., Kingma, J. H., Witteman, J. C. M., Albert Hofman, D., & Stricker, B. H. C. (2004) · American Heart Journal · doi:10.1016/j.ahj.2003.11.016 · Cited by 9
Epidemiological aspects of frontotemporal dementia
Swieten, J. C. V., & Rosso, S. M. (2008) · Handbook of clinical neurology · doi:10.1016/s0072-9752(07)01232-8 · Cited by 7
“Although the ApoE4 allele has consistently been associated with AD in many studies (Slooter et al., 1998), its association with FTD is controversial as several studies have shown conflicting results (Stevens et al.”
Result
Panel of Genetic Variations as a Potential Non-invasive Biomarker for Early Diagnosis of Alzheimer's Disease
Ma, S. L., & LAM, L. C. W. (2011) · Clinical Psychopharmacology and Neuroscience · doi:10.9758/cpn.2011.9.2.54 · Cited by 8
Lack of Association between Apolipoprotein E Polymorphism with Age at Onset of Subcortical Vascular Dementia
Ryu, H. G., Youn, S. W., & Kwon, O. D. (2012) · Dementia and Geriatric Cognitive Disorders Extra · doi:10.1159/000335494 · Cited by 8
Neurology
Burneo, J. G., Jenkins, M. E., & Demaerschalk, B. M. (2011) · Springer eBooks · doi:10.1007/978-0-387-88555-1 · Cited by 8
Genetic Components of Late-Onset Alzheimer's Disease with Special Emphasis on ApoE, IL- 6, CYP46, SERPINA3 and PPARγ
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Genetic Factors in Early- and Late-Onset Alzheimer’s Disease
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Self-citation
Novel Susceptibility Loci for Alzheimer's DXSisease
Reitz, C. (2015) · Future Neurology · doi:10.2217/fnl.15.42 · Cited by 10
My Healthy Brain: Rationale and Case Report of a Virtual Group Lifestyle Program Targeting Modifiable Risk Factors for Dementia
Mace, R. A., Hopkins, S. W., Reynolds, G., & Vranceanu, A. (2022) · Journal of Clinical Psychology in Medical Settings · doi:10.1007/s10880-022-09843-2 · Cited by 8
“Approximately 40% of dementia cases may be explained by modifiable lifestyle risk factors including lack of exercise, poor diet, inadequate sleep, elevated alcohol and tobacco use, and limited social and mental stimulation (Ashford & Mortimer, 2002; Barnes & Yaffe, 2011; Slooter et al., 1998).”
Background
Impacts of APOE-ε4 and exercise training on brain microvascular endothelial cell barrier function and metabolism
Weber, C. M., Moiz, B., Pena, G. S., Kheradmand, M., Wunderler, B., Kettula, C., Sangha, G. S., Smith, J. C., & Clyne, A. M. (2024) · EBioMedicine · doi:10.1016/j.ebiom.2024.105487 · Cited by 9
Prevention of Alzheimer’s Disease: Intervention Studies
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“Individuals with two APOE ε4 alleles have a more than seven times increased risk of developing AD compared with those with APOE ε3 alleles and approximately 15 to 20 percent of AD cases are attributable to the APOE ε4 allele [25-28].”
Background
Genome scan of age‐at‐onset in the NIMH Alzheimer disease sample uncovers multiple loci, along with evidence of both genetic and sample heterogeneity
Choi, Y., Blue, E., Bird, T. D., Steinbart, E. J., Blacker, D., & Wijsman, E. M. (2011) · American Journal of Medical Genetics Part B Neuropsychiatric Genetics · doi:10.1002/ajmg.b.31220 · Cited by 7
“Only 10–20% of the genetic variance forLOADrisk [Bennett et al., 1995; Slooter et al., 1998] andvariance in age-at-onset [Daw et al.”
Background
Association of cognitive function with tooth loss and mitochondrial variation in adult subjects: a community‐based study in Beijing, China
Gao, W., Wang, X., Wang, X., Cai, Y., & Luan, Q. (2016) · Oral Diseases · doi:10.1111/odi.12529 · Cited by 7
“Oral Diseases 700 Gene apolipoprotein (APOE) e4 allele is not only known to be correlated with both mild cognitive impairment and sporadic Alzheimer’s disease, but also affects conversion from mild cognitive impairment to dementia (Slooter et al, 1998; Reitz and Mayeux, 2010; Stein et al, 2010).”
Background
TheTNFRSF6 gene is not implicated in familial early-onset Alzheimer's disease
Theuns, J., Feuk, L., Dermaut, B., Del‐Favero, J., Roks, G., den Bossche, D. V., Corsmit, E., den Broeck, M. V., van Duijn, C. M., Cruts, M., et al. (2001) · Human Genetics · doi:10.1007/s004390100508 · Cited by 7
Self-citation
Candidate Gene Discovery Procedure after Follow‐Up Confirmatory Analyses of Candidate Regions of Interests for Alzheimer’s Disease in the NIMH Sibling Dataset
Baye, T. M., Perry, R. T., Wiener, H. W., Chen, Z., Harrell, L. E., & Go, R. C. P. (2008) · Disease Markers · doi:10.1155/2008/736409 · Cited by 7
“Keywords: Alzheimer, linkage, QTL, STR, SNP, Genomic scan, Candidate gene, bioinformatics, gene ontology, GO, Alzforum, Alzgene database”

Authors: Slooter, A. J. C., Cruts, M., Kalmijn, S., Hofman, A., Breteler, M. M. B., Van Broeckhoven, C., & van Duijn, C. M.
Affiliations: Erasmus MC (NL)
University of Antwerp (BE)
ORCID: Slooter, Arjen J. C.
Cruts, Marc
Breteler, Monique M. B.
Venue: Archives of Neurology
Publisher: American Medical Association (AMA)
Published: 1998-07-01
Volume: 55
Issue: 7
Pages: 964
ISSN: 0003-9942 (ISSN-L)
DOI: 10.1001/archneur.55.7.964
OpenAlex: W2134448489
Cited by: 399
References: 31
Citations by year: 2026: 3 · 2025: 9 · 2024: 7 · 2023: 8 · 2022: 14 · 2021: 10 · 2020: 16 · 2019: 9 · 2018: 9 · 2017: 15 · 2016: 10 · 2015: 18 · 2014: 18 · 2013: 25 · 2012: 15
FWCI: 8.48
Type: journal article
Language: en
Open access: green
pure.eur.nl
Locations: Archives of Neurology (publishedVersion)
PubMed (publishedVersion)
EUR Research Repository (Erasmus University Rotterdam) (submittedVersion)
RePub (Erasmus University Rotterdam) (submittedVersion, other-oa)
Topics: Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
Keywords: dementia, Alzheimer's disease, apolipoprotein E, APOE ε4, genetic risk factors, dementia incidence, attributable fraction, family history of dementia, Rotterdam Study
MeSH terms: Aged, Aged, 80 and over, Alzheimer Disease, Apolipoproteins E, Dementia, Female, Genotype, Humans, Male, Middle Aged, Netherlands, Incidence, Odds Ratio, Case-Control Studies, Risk Assessment

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Risk Estimates of Dementia by Apolipoprotein E Genotypes From a Population-Based Incidence Study: The Rotterdam Study

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