The DOI matches its Crossref record; 30 of the 31 references it cites were found in a registry or an index.
Risk Estimates of Dementia by Apolipoprotein E Genotypes From a Population-Based Incidence Study: The Rotterdam Study
Open accessAbstract
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.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
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?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“To date, APOE remains the only locus repeatedly associated with AAO8,9, but PICALM and BIN1 have also been reported to affect AAO6,10,11.”
From A common haplotype lowers PU.1 expression in myeloid cells and delays onset of Alzheimer's disease (2017) · cites this paper as [9]
Experimental — accuracy not yet measuredIn the citing paper
“Genetic studies show that a number of genes that have been linked to early-onset AD risk are expressed primarily in microglia.”
From Microglial signatures and their role in health and disease (2018) · cites this paper as [130]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
McKhann, G., Drachman, D., Folstein, M., Katzman, R., Price, D., & Stadlan, E. M. (1984) · Neurology · doi:10.1212/wnl.34.7.939 · Cited by 27,915
McKhann, G., Drachman, D., Folstein, M., Katzman, R., Price, D. L., & Stadlan, E. (2011) · Neurology · doi:10.1212/01.wnl.0000400650.92875.cf · Cited by 9,882
Corder, E. H., Saunders, A. M., Strittmatter, W. J., Schmechel, D. E., Gaskell, P. C., Small, G. W., Roses, A. D., Haines, J. L., & Pericak-Vance, M. A. (1993) · Science · doi:10.1126/science.8346443 · Cited by 9,429
Román, G. C., Tatemichi, T. K., Erkinjuntti, T., Cummings, J. L., Masdeu, J. C., Garcia, J. H., Amaducci, L., Orgogozo, J.-M., Brun, A., Hofman, A., et al. (1993) · Neurology · doi:10.1212/wnl.43.2.250 · Cited by 4,921
Protective effect of apolipoprotein E type 2 allele for late onset Alzheimer disease
Corder, E. H., Saunders, A. M., Risch, N. J., Strittmatter, W. J., Schmechel, D. E., Gaskell, P. C., Rimmler, J. B., Locke, P. A., Conneally, P. M., Schmader, K. E., et al. (1994) · Nature Genetics · doi:10.1038/ng0694-180 · Cited by 1,920
Determinants of disease and disability in the elderly: The Rotterdam elderly study
Albert Hofman, D., Grobbee, D. E., de Jong, P. T. V. M., & Ouweland, F. A. V. D. (1991) · European Journal of Epidemiology · doi:10.1007/bf00145007 · Cited by 1,120
Apolipoprotein E genotyping by one-stage PCR
Wenham, P. R., Price, W. H., & Blundell, G. (1991) · The Lancet · doi:10.1016/0140-6736(91)92823-k · Cited by 1,070
Diagnostic and Statistical Manual of Mental Disorders, Third Edition, Revised
Kobylski, T. P. (1988) · Psychosomatics · doi:10.1016/s0033-3182(88)72438-x · Cited by 1,058
Ott, A., Breteler, M. M. B., van Harskamp, F., Claus, J. J., van der Cammen, T. J. M., Grobbee, D. E., & Hofman, A. (1995) · BMJ · doi:10.1136/bmj.310.6985.970 · Cited by 792
Self-citationApolipoprotein E4 allele in a population–based study of early–onset Alzheimer's disease
van Duijn, C. M., de Knijff, P., Cruts, M., Wehnert, A., Havekes, L. M., Albert Hofman, D., & Broeckhoven, C. V. (1994) · Nature Genetics · doi:10.1038/ng0594-74 · Cited by 459
Self-citation
Flagged first, then by citations
1 of the 31 references couldn’t be matched to a known paper.
Research works printed but not linked: 1
- Altman DG. Multiple regression. In: Practical Statistics for Medical Research. Lon- don, England: Chapman & Hall; 1991:345-346.
Cited by
Sorted by citations
Items 101–200 of 397
Higher Estrogen Levels Are Not Associated With Larger Hippocampi and Better Memory Performance
den Heijer, T., Geerlings, M. I., Albert Hofman, D., de Jong, F. H., Launer, L. J., Pols, H. A. P., & Breteler, M. M. B. (2003) · Archives of Neurology · doi:10.1001/archneur.60.2.213 · Cited by 81
Self-citationSwaminathan, S., Huentelman, M. J., Corneveaux, J. J., Myers, A., Faber, K. M., Foroud, T., Mayeux, R. P., Shen, L., Kim, S., Turk, M., et al. (2012) · PLoS ONE · doi:10.1371/journal.pone.0050640 · Cited by 80
“However it is estimated that the APOE e4 allele accounts for approximately 20% and the non-APOE loci cumulatively account for as much as 35% of the AD risk [10,13].”
BackgroundAPOE 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
“However, the proportion of variance in age-at-onset attributable to APOE is estimated to be only 10–20% [Bennett et al., 1995; Slooter et al., 1998], leaving ample room for the involvement of additional loci.”
BackgroundVitamin 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
“However, 50% of late-onset AD patients do not carry the APOE 4 allele, indicating the existence of additional genetic factors for late-onset AD (Daw et al., 2000; Slooter et al., 1998).”
BackgroundLunnon, K., & Mill, J. (2013) · American Journal of Medical Genetics Part B: Neuropsychiatric Genetics · doi:10.1002/ajmg.b.32201 · Cited by 78
Hypercholesterolaemia-induced oxidative stress at the blood–brain barrier
Dias, I. H. K., Polidori, M. C., & Griffiths, H. R. (2014) · Biochemical Society Transactions · doi:10.1042/bst20140164 · Cited by 78
Finckh, 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
Cognitive Impairment in Alzheimer’s Disease Is Modified by APOE Genotype
van der Vlies, A. E., Pijnenburg, Y. A. L., Koene, T., Klein, M., Kok, A., Scheltens, P., & van der Flier, W. M. (2007) · Dementia and Geriatric Cognitive Disorders · doi:10.1159/000104467 · Cited by 78
“The apolipoprotein E gene (APOE) is an important risk factor for AD [”
BackgroundHow can elderly apolipoprotein E ε4 carriers remain free from dementia?
Ferrari, C., Xu, W., Wang, H., Winblad, B. G., Sorbi, S., Qiu, C., & Fratiglioni, L. (2012) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2012.03.003 · Cited by 79
“The proportion of patients with dementia that is attributable to the APOE 4 is estimated to be 20% in people aged 55 years (Slooter et al., 1998) and 12.”
BackgroundDeterminants, MRI Correlates, and Prognosis of Mild Cognitive Impairment: The Rotterdam Study
de Bruijn, R. F. A. G., Akoudad, S., Cremers, L. G. M., Albert Hofman, D., Niessen, W. J., van der Lugt, A., Koudstaal, P. J., Vernooij, M. W., & Ikram, M. A. (2014) · Journal of Alzheimer s Disease · doi:10.3233/jad-132558 · Cited by 79
“This method has 119 been described in detail previously [19, 20].”
APOA1 polymorphism influences risk for early-onset nonfamiliar AD
Vollbach, H., Heun, R., Morris, C. M., Edwardson, J. A., McKeith, I. G., Jessen, F., Schulz, A., Maier, W., & Kölsch, H. (2005) · Annals of Neurology · doi:10.1002/ana.20593 · Cited by 75
“However, one study estimates that APOE accounts for 50% of the “predicted total genetic effect” in nonfamilial AD,(4) whereas others estimate that APOE accounts for 10 to 15% of the total variance in age at onset.(5,6) So the existence of additional genetic risk factors for AD is suggested.”
BackgroundAssociation of CLU and PICALM variants with Alzheimer's disease
Kamboh, M. I., Minster, R. L., Demirci, F. Y., Ganguli, M., DeKosky, S. T., López, O. L., & Barmada, M. M. (2010) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2010.04.015 · Cited by 77
“Although APOE has emerged as the strongest susceptibility marker for LOAD, it accounts for 30% of the disease risk (Slooter et al., 1998).”
Telomere Length and the Risk of Alzheimer’s Disease: The Rotterdam Study
Fani, L., Hilal, S., Sedaghat, S., Broer, L., Licher, S., Arp, P., van Meurs, J. B. J., Ikram, M. K., & Ikram, M. A. (2019) · Journal of Alzheimer s Disease · doi:10.3233/jad-190759 · Cited by 72
“APOE genotype was determined using polymerase chain reaction on coded DNA samples in the baseline cohort [17] and with a bi-allelic Tacqman assay (rs7412 and rs429358) in the extensions of the Rotterdam Study [13].”
MethodRukhsana Sultana, A., Marzia Perluigi, A., & Butterfield, D. A. (2005) · Journal of Chromatography B · doi:10.1016/j.jchromb.2005.09.024 · Cited by 72
Genetics of Alzheimer’s Disease in Caribbean Hispanic and African American Populations
Reitz, C., & Mayeux, R. P. (2013) · Biological Psychiatry · doi:10.1016/j.biopsych.2013.06.003 · Cited by 69
“It is thought that in non-Hispanic whites, APOE may account for as much as 20% to 50% of LOAD risk (7,35).”
BackgroundF‐box/ LRR ‐repeat protein 7 is genetically associated with Alzheimer's disease
Tosto, G., Fu, H., Vardarajan, B. N., Lee, J. H., Cheng, R., Reyes‐Dumeyer, D., Lantigua, R., Medrano, M. Z., Jiménez‐Velázquez, I. Z., Elkind, M. S. V., et al. (2015) · Annals of Clinical and Translational Neurology · doi:10.1002/acn3.223 · Cited by 71
“The most common genetic risk factor is the APOE-ɛ4 allele with an attributable risk of LOAD of 10–15%.(2) The International Genomics of Alzheimer’s Project (IGAP) replicated eight known LOADsusceptibility loci (CLU, PICALM, CR1, and BIN1, MS4A4A/MS4A4E/MS4A6E cluster, ABCA7, CD2AP, and EPHA1) found in previous genome-…”
BackgroundShi, H., Koronyo, Y., Fuchs, D.-T. S., Sheyn, J., Wawrowsky, K., Lahiri, S., Black, K. L., & Koronyo‐Hamaoui, M. (2020) · Acta Neuropathologica Communications · doi:10.1186/s40478-020-01076-4 · Cited by 71
REM sleep behaviour disorder associated with a neurinoma of the left pontocerebellar angle
Zambelis, T. (2002) · Journal of Neurology Neurosurgery & Psychiatry · doi:10.1136/jnnp.72.6.821 · Cited by 70
Dynamin-binding protein gene on chromosome 10q is associated with late-onset Alzheimer's disease
Kuwano, R., Miyashita, A., Arai, H., Asada, T., Imagawa, M., Shoji, M., Higuchi, S., Urakami, K., Kakita, A., Takahashi, H., et al. (2006) · Human Molecular Genetics · doi:10.1093/hmg/ddl142 · Cited by 70
“However, about 50% of AD patients do not carry the APOE-14 allele, and only 20% of AD patients and ,10% of the variance in AAO appear to be explained by the APOE-14 allele (4,5).”
BackgroundProgranulin polymorphism rs5848 is associated with increased risk of Alzheimer's disease
Sheng, J., Su, L., Xu, Z., & Chen, G. (2014) · Gene · doi:10.1016/j.gene.2014.03.041 · Cited by 64
“Therefore, APOE and PGRN proteins may modulate the pathogenesis of AD via different pathways.”
BackgroundInfluentialCornelius, C., Fastbom, J., Winblad, B. G., & Viitanen, M. H. (2004) · Neuroepidemiology · doi:10.1159/000075957 · Cited by 66
Association between apolipoprotein E polymorphism and Alzheimer disease in Tehran, Iran
Vaisi‐Raygani, A., Zahrai, M., Raygani, A. V., Doosti, M., Javadi, E., رضایی, م., & Pourmotabbed, T. (2004) · Neuroscience Letters · doi:10.1016/j.neulet.2004.10.073 · Cited by 64
The Role of Cerebrovascular Disease in Dementia
DeCarli, C. S. (2003) · The Neurologist · doi:10.1097/00127893-200305000-00001 · Cited by 64
“This may particularly be true for ApoE4, which not only increases the risk for AD but also modulates the effects of vascular disease on the brain (10, 174).”
BackgroundTrajectories of Cognitive and Motor Function Between Ages 45 and 90 Years: A Population-Based Study
van der Willik, K. D., Licher, S., Vinke, E. J., Knol, M. J., Darweesh, S. K. L., van der Geest, J. N., Schagen, S. B., Ikram, M. K., Luik, A. I., & Ikram, M. A. (2020) · The Journals of Gerontology Series A · doi:10.1093/gerona/glaa187 · Cited by 63
“APOE genotype was determined using polymerase chain reaction on coded DNA samples in the initial cohort and with a bi-allelic TaqMan assay in the 2 extensions (36,37).”
MethodPolygenic risk scores in familial Alzheimer disease
Tosto, G., Bird, T. D., Tsuang, D. W., Bennett, D., Boeve, B. F., Cruchaga, C., Faber, K. M., Foroud, T., Farlow, M. R., Goate, A., et al. (2017) · Neurology · doi:10.1212/wnl.0000000000003734 · Cited by 63
Dose dependent effect of APOE ε4 on behavioral symptoms in frontal lobe dementia
Engelborghs, S., Dermaut, B., Mariën, P., Symons, A., Vloeberghs, E., Maertens, K., Somers, N., Goeman, J., Rademakers, R., den Broeck, M. V., et al. (2006) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2005.02.005 · Cited by 64
Dam, D. V., Vloeberghs, E., Abramowski, D., Staufenbiel, M., & Deyn, P. P. D. (2005) · CNS Spectrums · doi:10.1017/s1092852900010051 · Cited by 62
Serum Levels of Pregnancy Zone Protein are Elevated in Presymptomatic Alzheimer’s Disease
IJsselstijn, L., Dekker, L. J. M., Stingl, C., van der Weiden, M. M., Albert Hofman, D., Kros, J. M., Koudstaal, P. J., Smitt, P. A. E. S., Ikram, M. A., Breteler, M. M. B., et al. (2011) · Journal of Proteome Research · doi:10.1021/pr200270z · Cited by 62
Self-citationGenetic association of ubiquilin with Alzheimer's disease and related quantitative measures
Kamboh, M. I., Minster, R. L., Feingold, E., & DeKosky, S. T. (2005) · Molecular Psychiatry · doi:10.1038/sj.mp.4001775 · Cited by 62
Familial Alzheimer disease in Latinos
Rippon, G. A., Tang, M., Lee, J. H., Lantigua, R., Medrano, M. A., & Mayeux, R. P. (2006) · Neurology · doi:10.1212/01.wnl.0000191300.38571.3e · Cited by 61
Robinson, R. A. S., Lange, M. L. B., Rukhsana Sultana, A., Galván, V., Fombonne, J., Gorostiza, O. F., Zhang, J., Warrier, G., Cai, J., Pierce, W. M. J., et al. (2011) · Neuroscience · doi:10.1016/j.neuroscience.2011.01.005 · Cited by 61
The effect of apoE on dementia is not through atherosclerosis: The Rotterdam Study
Knittweis, J. W., McMullen, W., Romas, S. N., Mayeux, R. P., Slooter, A. J. C., Ruitenberg, A., van Duijn, C. M., Breteler, M. M. B., & Liu, H. C. (2000) · Neurology · doi:10.1212/wnl.54.12.2356-a · Cited by 61
Self-citationA data-driven study of Alzheimer's disease related amyloid and tau pathology progression
Aksman, L., Oxtoby, N. P., Scelsi, M. A., Wijeratne, P. A., Young, A. L., Alves, I. L., Collij, L. E., Vogel, J. W., Barkhof, F., Alexander, D. C., et al. (2023) · Brain · doi:10.1093/brain/awad232 · Cited by 69
“42,43 Although we expected earlier A β deposition in ϵ 4 carriers versus non-carriers, 44 we did not observe this in the PET-based analysis (Fig.”
Cathepsin D gene and the risk of Alzheimer's disease: A population-based study and meta-analysis
Schuur, M., Ikram, M. A., Swieten, J. C. V., Isaacs, A. J., Vergeer, J. M., Albert Hofman, D., Oostra, B. A., Breteler, M. M. B., & van Duijn, C. M. (2009) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2009.10.011 · Cited by 61
Self-citationDias, I. H. K., Mistry, J. J., Fell, S., Reis, A., Spickett, C. M., Polidori, M. C., Lip, G. Y. H., & Griffiths, H. R. (2014) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2014.07.012 · Cited by 61
Kamboh, M. I., Minster, R. L., Kenney, M., Öztürk, A., Desai, P. P., Kammerer, C. M., & DeKosky, S. T. (2005) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2005.07.015 · Cited by 60
“However, the APOE genetic variation explains only 4 to 9% of the variation in AAO [2,21].”
BackgroundReitz, C., & Mayeux, R. P. (2010) · Journal of Alzheimer s Disease · doi:10.3233/jad-2010-1255 · Cited by 60
“[38,39]”
BackgroundGenetic susceptibility testing for neurodegenerative diseases: Ethical and practice issues
Roberts, J. S., & Uhlmann, W. R. (2013) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2013.02.005 · Cited by 62
Marra, C., Bizzarro, A., Daniele, A., Luca, L. D., Ferraccioli, M., Valenza, A., Brahe, C., Tiziano, F. D., Gainotti, G., & Masullo, C. (2004) · Dementia and Geriatric Cognitive Disorders · doi:10.1159/000079191 · Cited by 59
Yang, A. C., Huang, C., Liu, M., Liou, Y.-J., Hong, C., Lo, M., Huang, N. E., Peng, C., Lin, C., & Tsai, S. (2013) · Human Brain Mapping · doi:10.1002/hbm.22398 · Cited by 56
“[Hallman et al., 1991; Hong et al., 1996; Myers et al., 1996; Slooter et al., 1998]. fMRI Scanning and Imaging Processing fMRI scanning was performed at National Yang-Ming University using a 3.0-”
MethodInfluentialGenetics of Early-Onset Alzheimer Dementia
Rademakers, R., Cruts, M., & Broeckhoven, C. V. (2003) · The Scientific World JOURNAL · doi:10.1100/tsw.2003.39 · Cited by 58
“patients with dementia that is attributable to the APOEε4 allele was estimated to be 7– 20%[90,91].”
BackgroundSelf-citationvan der Flier, W. M., Staekenborg, S. S., Pijnenburg, Y. A. L., Gillissen, F., Romkes, R., Kok, A., Bouwman, F. H., & Scheltens, P. (2006) · Dementia and Geriatric Cognitive Disorders · doi:10.1159/000096682 · Cited by 56
“However, risk factors for the occurrence of neuropsychiatric and behavioral symptoms in AD are largely unknown. It is conceivable that known genetic risk factors for AD, such as apoliprotein E (APOE) [ ,”
BackgroundVascular cognitive impairment: epidemiology, subtypes, diagnosis and management
Black, S. E. (2011) · The Journal of the Royal College of Physicians of Edinburgh · doi:10.4997/jrcpe.2011.121 · Cited by 61
Apolipoprotein E genotype and progression of Alzheimer's disease: the Rotterdam Study
Slooter, A. J. C., Houwing‐Duistermaat, J. J., van Harskamp, F., Cruts, M., Broeckhoven, C. V., Breteler, M. M. B., Albert Hofman, D., Stijnen, T., & van Duijn, C. M. (1999) · Journal of Neurology · doi:10.1007/s004150050351 · Cited by 56
“The APOE genotype was determined on coded DNA samples, as described in detail elsewhere [ 21 ].”
BackgroundMethodInfluentialSelf-citationPredictors of mortality among demented elderly in primary care
Schäufele, M., Bickel, H., & Weyerer, S. B. (1999) · International Journal of Geriatric Psychiatry · doi:10.1002/(sici)1099-1166(199911)14:11 · Cited by 48
The impact of APOE on myocardial infarction, stroke, and dementia
Slooter, A. J. C., Cruts, M., Albert Hofman, D., Koudstaal, P. J., van der Kuip, D. A. M., de Ridder, M. A. J., Witteman, J. C. M., Breteler, M. M. B., Broeckhoven, C. V., & van Duijn, C. M. (2004) · Neurology · doi:10.1212/01.wnl.0000118302.66674.e1 · Cited by 55
“Prevalent dementia, n (%) 3 (6) 40 (5) 10 (5) 178 (5) 100 (6) 20 (12)‡”
Self-citationEffects of ApoE4 and maternal history of dementia on hippocampal atrophy
Andrawis, J. P., Hwang, K. S., Green, A. E., Kotlerman, J., Elashoff, D., Morra, J. H., Cummings, J. L., Toga, A. W., Thompson, P. M., & Apostolova, L. G. (2012) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2010.07.020 · Cited by 54
Serum apolipoprotein E level is not increased in Alzheimer's disease: the Rotterdam study
Slooter, A. J. C., de Knijff, P., Albert Hofman, D., Cruts, M., Breteler, M. M. B., Broeckhoven, C. V., Havekes, L. M., & van Duijn, C. M. (1998) · Neuroscience Letters · doi:10.1016/s0304-3940(98)00339-5 · Cited by 54
Self-citationSultana, R., Newman, S. F., Abdul, H. M., Cai, J., Pierce, W. M., Klein, J. B., Merchant, M., & Butterfield, D. A. (2006) · Journal of Neuroscience Research · doi:10.1002/jnr.20876 · Cited by 53
“Furthermore, there also is an association between AD and allele 4 of the apolipoprotein E (APOE) gene (Levy-Lahad et al., 1995; Slooter et al., 1998), the endothelial nitric oxide synthase-3 gene (Dahiyat et al.”
BackgroundGünther, C., Hadeln, K. V., Müller-Thomsen, T., Alberici, A., Binetti, G., Hock, C., Nitsch, R. M., Stoppe, G., Reiss, J., Gal, A., et al. (2004) · Neuroscience Letters · doi:10.1016/j.neulet.2004.07.070 · Cited by 53
Jahrling, J. B., & Laberge, R.-M. (2015) · Current Topics in Medicinal Chemistry · doi:10.2174/1568026615666150610125856 · Cited by 55
“the e-4 allele have a higher risk than those who carry only one copy, and both groups have a higher risk than those who carry only the e-2 or e-3 forms [8].”
BackgroundEEG abnormalities in early and late onset Alzheimer's disease: understanding heterogeneity
de Waal, H., Stam, C. J., Blankenstein, M. A., Pijnenburg, Y. A. L., Scheltens, P., & van der Flier, W. M. (2010) · Journal of Neurology Neurosurgery & Psychiatry · doi:10.1136/jnnp.2010.216432 · Cited by 53
“Since it has been shown before that the effect of age at onset may be modified by APOE genotype,(7; 8; 20) we examined if there was an interaction between age at onset and APOE ε4 genotype on the prevalence of EEG abnormalities.”
BackgroundFamilial influence on variation in age of onset and behavioural phenotype in Alzheimer's disease
Tunstall, N., Owen, M. J., Williams, J. H., Rice, F. J., Carty, S., Lillystone, S., Fraser, L. S. M., Kehoe, P. G., Neill, D., Rudrasingham, V., et al. (2000) · The British Journal of Psychiatry · doi:10.1192/bjp.176.2.156 · Cited by 53
ApoE genotype in relation to AD and cholesterol
Liu, H. C., Hong, C. J., Wang, S. J., Fuh, J., WANG, P., Shyu, H.-Y., & Teng, E. L. (1999) · Neurology · doi:10.1212/wnl.53.5.962 · Cited by 53
Fine mapping of 10q and 18q for familial Alzheimer's disease in Caribbean Hispanics
Lee, J. H., Mayeux, R. P., Mayo, D., Mo, J., Santana, V., Williamson, J., Flaquer, A., Ciappa, A., Rondon, H. Z., Estevez, P., et al. (2004) · Molecular Psychiatry · doi:10.1038/sj.mp.4001538 · Cited by 53
“1 but this variant explains only 20p of the attributable risk”
Guo, Z., Fratiglioni, L., Viitanen, M. H., Lannfelt, L., Basun, H., Fastbom, J., & Winblad, B. G. (2001) · American Journal of Epidemiology · doi:10.1093/aje/153.3.225 · Cited by 53
Ramakers, I. H. G. B., Visser, P. J., Aalten, P., Bekers, O., Sleegers, K., Broeckhoven, C. V., Jolles, J., & Verhey, F. R. J. (2008) · Dementia and Geriatric Cognitive Disorders · doi:10.1159/000144072 · Cited by 55
“Primacy Effect. Ratio of the number of words remembered from the first 3 words of the list divided by 3. Recency Effect. Ratio of the number of words remembered from the last 3 words of the list divided by 3. APOE Genotyping APOE genotype was determined on genomic DNA extracted form EDTA-anticoagulated blood using the…”
MethodDonepezil for behavioural disorders associated with Lewy bodies: a case series
Lanctôt, K. L., & Herrmann, N. (2000) · International Journal of Geriatric Psychiatry · doi:10.1002/(sici)1099-1166(200004)15:4 · Cited by 105
Self-citationAssociation of progranulin polymorphism rs5848 with neurodegenerative diseases: a meta-analysis
Chen, Y., Li, S., Su, L., Sheng, J., Lv, W., Chen, G., & Xu, Z. (2015) · Journal of Neurology · doi:10.1007/s00415-014-7630-2 · Cited by 50
Sacuiu, S. F. (2016) · Handbook of clinical neurology · doi:10.1016/b978-0-12-802973-2.00008-2 · Cited by 57
Apathy and APOE in mild behavioral impairment, and risk for incident dementia
Vellone, D. A., Ghahremani, M., Goodarzi, Z., Forkert, N. D., Smith, E. E., & Ismail, Z. (2022) · Alzheimer s & Dementia Translational Research & Clinical Interventions · doi:10.1002/trc2.12370 · Cited by 51
Genetic Testing and Counseling in the Diagnosis and Management of Young-Onset Dementias
Goldman, J. S. (2015) · Psychiatric Clinics of North America · doi:10.1016/j.psc.2015.01.008 · Cited by 52
Beck, T. N., Nicolas, E., Kopp, M. C., & Golemis, E. A. (2014) · Oncoscience · doi:10.18632/oncoscience.64 · Cited by 50
“Additionally, a significant difference (genotype: P = 0.047; allele frequency: P = 0.024) between the two groups was maintained even if only subjects without the APOE ε4 allele were considered [13].”
BackgroundInfluentialNon-apolipoprotein E and apolipoprotein E genetics of sporadic Alzheimer's disease
Seripa, D., Panza, F., Franceschi, M., D’Onofrio, G., Solfrizzi, V., Dallapiccola, B., & Pilotto, A. (2009) · Ageing Research Reviews · doi:10.1016/j.arr.2008.12.003 · Cited by 50
Genetic, Physiological, and Lifestyle Predictors of Mortality in the General Population
Walter, S., Mackenbach, J. P., Vokó, Z., Lhachimi, S. K., Ikram, M. A., Uitterlinden, A. G., Newman, A. B., Murabito, J. M., Garcia, M. E., Gudnason, V. G., et al. (2012) · American Journal of Public Health · doi:10.2105/ajph.2011.300596 · Cited by 51
Diagnostic accuracy of the Preclinical AD Scale (PAS) in cognitively mildly impaired subjects
Visser, P. J., Verhey, F. R. J., Scheltens, P., Cruts, M., Ponds, R., Broeckhoven, C. V., & JOLLES, J. (2002) · Journal of Neurology · doi:10.1007/s004150200011 · Cited by 49
“APOE genotyping was performed by a polymerase chain reaction [22].”
MethodSelf-citationWhat does heritability of Alzheimer’s disease represent?
Baker, E. A., Leonenko, G., Schmidt, K. M., Hill, M., Myers, A., Shoai, M., de Rojas, I., Tesi, N., Holstege, H. H., van der Flier, W. M., et al. (2023) · PLoS ONE · doi:10.1371/journal.pone.0281440 · Cited by 55
“There are no patents or patents, products in development or marketed products associated with this research to declare. variance when studying incident AD [22].”
Rademakers, R., Cruts, M., Sleegers, K., Dermaut, B., Theuns, J., Aulchenko, Y. S., Weckx, S., Pooter, T. D., den Broeck, M. V., Corsmit, E., et al. (2005) · The American Journal of Human Genetics · doi:10.1086/491749 · Cited by 51
“For ∼7%– 20% of patients, AD is attributable to APOE 4 (Slooter et al. 1998; Warwick et al. 2000).”
BackgroundSelf-citationMicroglia Signatures: A Cause or Consequence of Microglia-Related Brain Disorders?
Mirarchi, A., Albi, E., & Arcuri, C. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms252010951 · Cited by 52
“…ε 4 These genes include those encoding TREM2, ATP-binding casse tt e subfamily A member 7 (ABCA7) [75], members of the membrane-spanning 4-domains subfamily A (MS4A) 74, CD133 [76], the ε 4 allele of APOE (APOE4) [77,78], PU.1 [79], and others. allele of APOE (APOE4) [77,78], PU.1 [79], and others.”
BackgroundAziz, A.-L., Giusiano, B., Joubert, S., Duprat, L., Didic, M., Guériot, C., Koric, L., Boucraut, J., Félician, O., Ranjeva, J., et al. (2017) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2017.02.010 · Cited by 48
McDonough, I. M., Wood, M. M., & Miller, W. S. (2019) · Europe PMC (PubMed Central) · Cited by 45
Cholesterol and apolipoprotein E in Alzheimer's disease
Reiss, A. B. (2005) · American Journal of Alzheimer s Disease & Other Dementias® · doi:10.1177/153331750502000208 · Cited by 46
Energy and the Alzheimer brain
Mamelak, M. (2017) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2017.02.001 · Cited by 47
“Carriage f the APOe2 genotype decreases the risk of Alzheimer’s disease Slooter et al., 1998; Verghese et al., 2011).”
BackgroundTheuns, J. (2003) · Human Molecular Genetics · doi:10.1093/hmg/ddg098 · Cited by 45
“3-fold increase of the E4 allele in EOAD patients (7,8).”
BackgroundHigh APOE epsilon 4 allele frequencies associated with Alzheimer disease in a Tunisian population
Achouri-Rassas, A., Khiari, H. M., Fredj, S. H., Sahnoun, S., Batti, H., Zakraoui, N. O., Cherif, A., Anane, N., Benali, N., Messaoud, T. B., et al. (2011) · Neurological Sciences · doi:10.1007/s10072-011-0663-8 · Cited by 45
“It has been estimated that the population-attributable risk for AD caused by APOE e4 allele ranges from 20 to 70% [ 41 ].”
BackgroundUnderstanding the link between cancer and neurodegeneration
Driver, J. A. (2011) · Journal of Geriatric Oncology · doi:10.1016/j.jgo.2011.11.007 · Cited by 46
Young Alzheimer patients show distinct regional changes of oscillatory brain dynamics
de Waal, H., Stam, C. J., de Haan, W., van Straaten, E. C. W., Scheltens, P., & van der Flier, W. M. (2011) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2011.10.013 · Cited by 45
A Mathematical Model of Alzheimer's Disease and the Apoe Gene
Macdonald, A. S., & Pritchard, D. (2000) · Astin Bulletin · doi:10.2143/ast.30.1.504627 · Cited by 44
“(d) The weakest associations between ApoE and AD were reported in the two prospective studies, those by Evans et al. (1997) and Slooter et al. (1998).”
The GAB2 Gene and the Risk of Alzheimer's Disease: Replication and Meta-Analysis
Ikram, M. A., Liu, F., Oostra, B. A., Albert Hofman, D., van Duijn, C. M., & Breteler, M. M. B. (2009) · Biological Psychiatry · doi:10.1016/j.biopsych.2008.11.014 · Cited by 44
Self-citationVariations in estrogen receptor α gene and risk of dementia, and brain volumes on MRI
den Heijer, T., Schuit, S. C. E., Pols, H. A. P., van Meurs, J. B. J., Albert Hofman, D., Koudstaal, P. J., van Duijn, C. M., Uitterlinden, A. G., & Breteler, M. M. B. (2004) · Molecular Psychiatry · doi:10.1038/sj.mp.4001553 · Cited by 43
“8 APOE genotype was determined in 5281 participants of the total cohort and in 404 participants of the subset with MRI examination”
Self-citationOlarte, L., Schupf, N., Lee, J. H., Tang, M.-X., Santana, V., Williamson, J., Maramreddy, P., Tycko, B., & Mayeux, R. (2006) · Archives of Neurology · doi:10.1001/archneur.63.11.1586 · Cited by 42
ABCA7 gene and the risk of Alzheimer's disease in Han Chinese in Taiwan
Liao, Y., Lee, W., Hwang, J.-P., Wang, Y.-F., Tsai, C.-F., Wang, P., Wang, S., & Fuh, J. (2014) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2014.05.009 · Cited by 46
“However, it only accounts for 20%e30% of Alzheimer’s disease (AD) risks (Slooter et al., 1998).”
BackgroundAssociating Alzheimer’s disease pathology with its cerebrospinal fluid biomarkers
Bridel, C., Somers, C., Sieben, A., Rozemüller, A. J. M., Niemantsverdriet, E., Struyfs, H., Vermeiren, Y., Broeckhoven, C. V., Deyn, P. P. D., Bjerke, M., et al. (2022) · Brain · doi:10.1093/brain/awac013 · Cited by 39
Genome scan on Swedish Alzheimer's disease families
Sillén, A., Forsell, C., Lilius, L., Axelman, K., Björk, B. F., Onkamo, P., Kere, J., Winblad, B. G., & Graff, C. (2005) · Molecular Psychiatry · doi:10.1038/sj.mp.4001772 · Cited by 42
Risk factors and early signs of Alzheimer's disease in a family study sample
Heun, R., Kölsch, H., & Jessen, F. (2005) · European Archives of Psychiatry and Clinical Neuroscience · doi:10.1007/s00406-005-0596-4 · Cited by 42
Öztürk, A., DeKosky, S. T., & Kamboh, M. I. (2005) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2005.08.024 · Cited by 41
“Despite the evidence for substantial genetic effect in the etiology of LOAD, to date APOE that accounts for 20–30 % of AD risk [16,17], is the only established risk factor for LOAD.”
BackgroundDementia—Epidemiological Considerations, Nomenclature, and a Tacit Consensus Definition
Breitner, J. C. S. (2006) · Journal of Geriatric Psychiatry and Neurology · doi:10.1177/0891988706291081 · Cited by 41
Distribution of APOE Genotypes in a Memory Clinic Cohort
van der Flier, W. M., Pijnenburg, Y. A. L., Schoonenboom, S. N. M., Dik, M. G., Blankenstein, M. A., & Scheltens, P. (2008) · Dementia and Geriatric Cognitive Disorders · doi:10.1159/000124750 · Cited by 41
“However, not all patients presenting with subjective complaints at a memory clinic will develop dementia. Therefore, from a clinical point of view, it is highly important to identify additional risk factors to mark initially nondemented patients that should be monitored more carefully.The apolipoprotein E gene (APOE)…”
BackgroundLipoprotein‐associated phospholipase A2 is associated with risk of dementia
van Oijen, M., van der Meer, I. M., Albert Hofman, D., Witteman, J. C. M., Koudstaal, P. J., & Breteler, M. M. B. (2005) · Annals of Neurology · doi:10.1002/ana.20721 · Cited by 40
“A polymerase chain reaction was performed.(19) Two groups were formed on the basis of presence or absence of an APOE ε4”
MethodSelf-citationAlzheimer's disease risk genes and the age-at-onset phenotype
Thambisetty, M., An, Y., & Tanaka, T. (2013) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2013.05.028 · Cited by 43
Goldman, J. S. (2012) · Current Neurology and Neuroscience Reports · doi:10.1007/s11910-012-0296-1 · Cited by 40
“The apolipoprotein E gene (APOE) is associated with the greatest risk of developing the disease, accounting for 20 %–29 % of late-onset AD risk [23–25].”
Scuteri, D., Rombolà, L., Tridico, L., Mizoguchi, H., Watanabe, C., Sakurada, T., Sakurada, S., Corasaniti, M. T., Bagetta, G., & Morrone, L. A. (2018) · Current Medicinal Chemistry · doi:10.2174/0929867325666180307115546 · Cited by 40
Pezzolo, E., Mutlu, Ü., Vernooij, M. W., Dowlatshahi, E. A., Gisondi, P., Girolomoni, G., Nijsten, T. E. C., Ikram, M. A., & Wakkee, M. (2018) · Journal of the American Academy of Dermatology · doi:10.1016/j.jaad.2018.07.046 · Cited by 40
Redox proteomics in some age-related neurodegenerative disorders or models thereof
Butterfield, D. A., Abdul, H. M., Newman, S. F., & Reed, T. T. (2006) · NeuroRx · doi:10.1016/j.nurx.2006.05.003 · Cited by 37
“been definitely identified, the epsilon 4 allele of the APOE gene.(3)”
BackgroundConfirmation of association between D10S583 and Alzheimer's disease in a case–control sample
Ait‐Ghezala, G., Abdullah, L. I., Crescentini, R. M., Crawford, F., Town, T., Singh, S., Richards, D., Duara, R., & MULLAN, M. J. (2002) · Neuroscience Letters · doi:10.1016/s0304-3940(02)00243-4 · Cited by 36
Healthcare services relaxing natural selection may contribute to increase of dementia incidence
You, W., Henneberg, R. J., & Henneberg, M. (2022) · Scientific Reports · doi:10.1038/s41598-022-12678-4 · Cited by 37
Gene Expression and Methylation Analysis of ABCA7 in Patients with Alzheimer’s Disease
Yamazaki, K., Yoshino, Y., Mori, T., Yoshida, T., Ozaki, Y., Sao, T., Mori, Y., Ochi, S., Iga, J., & Ueno, S. (2017) · Journal of Alzheimer s Disease · doi:10.3233/jad-161195 · Cited by 37
No association of SORL1 SNPs with Alzheimer's disease
Minster, R. L., DeKosky, S. T., & Kamboh, M. I. (2008) · Neuroscience Letters · doi:10.1016/j.neulet.2008.05.082 · Cited by 36
The effect of APOE on dementia is not through atherosclerosis: The Rotterdam Study
Slooter, A. J. C., Cruts, M., Ott, A., Bots, M. L., Witteman, J. C. M., Hofman, A., Broeckhoven, C. V., Breteler, M. M. B., & van Duijn, C. M. (1999) · Neurology · doi:10.1212/wnl.53.7.1593 · Cited by 36
Self-citationThe Impact of Apolipoprotein E (APOE) Epigenetics on Aging and Sporadic Alzheimer’s Disease
Lozupone, M., Dibello, V., Sardone, R., Castellana, F., Zupo, R., Lampignano, L., Bortone, I., Daniele, A., Bellomo, A., Solfrizzi, V., et al. (2023) · Biology · doi:10.3390/biology12121529 · Cited by 39
“Indeed, according to the notion of stochastic risk or protective factors and although it is known that APOE ε 4/ ε 4-carriers developed dementia about 10 years earlier than APOE ε 2 carriers [96], there was still significant discrepancy in the age of onset for APOE ε 4/ ε 4-carriers [22].”
Background
Metadata
- 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)
- Venue
- Archives of Neurology
- Publisher
- American Medical Association (AMA)
- Published
- 1998-07-01
- Volume
- 55
- Issue
- 7
- Pages
- 964
- ISSN
- 0003-9942 (ISSN-L)
- 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
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
