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
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
Epidemiology of Alzheimer's disease: occurrence, determinants, and strategies toward intervention
Qiu, C., Kivipelto, M., & von Strauss, E. (2009) · Dialogues in Clinical Neuroscience · doi:10.31887/dcns.2009.11.2/cqiu · Cited by 1,261
Alzheimer disease: Epidemiology, diagnostic criteria, risk factors and biomarkers
Reitz, C., & Mayeux, R. P. (2014) · Biochemical Pharmacology · doi:10.1016/j.bcp.2013.12.024 · Cited by 1,271
Microglial signatures and their role in health and disease
Butovsky, O., & Weiner, H. L. (2018) · Nature Reviews Neuroscience · doi:10.1038/s41583-018-0057-5 · Cited by 1,046
Wada, K., Tanaka, K., & Nakashima, K. (2011) · PubMed · Cited by 1,132
Dietary Intake of Antioxidants and Risk of Alzheimer Disease
Engelhart, M. J. (2002) · JAMA · doi:10.1001/jama.287.24.3223 · Cited by 1,080
“Alcohol intake None 1113 (21) 1 drink/wk 1156 (21) 1 drink/wk − 1 drink/d 1518 (28) 1-4 drinks/d 1443 (27) 4 drinks/d 165 (3) Educational level†‡ Low 1854 (35) Intermediate 1538 (28) High 2003 (37) Smoking‡ Current 1257 (23) Former 2305 (43) Never 1808 (34) Pack-years of smoking, median (interquartile range) Current 2…”
Epidemiology of Alzheimer DiseasePreprint
Mayeux, R. P., & Stern, Y. (2012) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a006239 · Cited by 1,127
“The population attributable risk related to APOE-14 has been estimated at 20% (Slooter et al. 1998).”
How Does it STAC Up? Revisiting the Scaffolding Theory of Aging and Cognition
Reuter‐Lorenz, P. A., & Park, D. C. (2014) · Neuropsychology Review · doi:10.1007/s11065-014-9270-9 · Cited by 1,054
“Even one copy of the gene, which is carried by roughly 20 % of the population, substantially increases the risk of an Alzheimer’s diagnosis in one’s lifetime (by a factor of 1.7; (Slooter et al. 1998)).”
BackgroundInfluentialDementia and Alzheimer Disease Incidence: A Prospective Cohort Study
Kukull, W. A., Higdon, R., Bowen, J. D., McCormick, W. C., Teri, L., Schellenberg, G. D., van Belle, G., Jolley, L., & Larson, E. B. (2002) · Archives of Neurology · doi:10.1001/archneur.59.11.1737 · Cited by 806
Apolipoprotein E Genotype and Sex Risk Factors for Alzheimer Disease: A Meta-analysis
Neu, S. C., Pa, J., Kukull, W., Beekly, D., Kuzma, A., Gangadharan, P., Wang, L.-S., Romero, K., Arneric, S. P., Redolfi, A., et al. (2017) · JAMA Neurology · doi:10.1001/jamaneurol.2017.2188 · Cited by 674
Mapping complex disease loci in whole-genome association studies
Carlson, C. S., Eberle, M. A., Kruglyak, L., & Nickerson, D. A. (2004) · Nature · doi:10.1038/nature02623 · Cited by 623
“For example, the PAF for the Apo€4, allele in late-onset Alzheimer's disease has been estimated at 20p (ref”
BackgroundThe probabilistic model of Alzheimer disease: the amyloid hypothesis revised
Frisoni, G. B., Altomare, D., Thal, D. R., Ribaldi, F., van der Kant, R., Ossenkoppele, R., Blennow, K., Cummings, J., van Duijn, C., Nilsson, P. M., et al. (2022) · Nature Reviews Neuroscience · doi:10.1038/s41583-021-00533-w · Cited by 513
E PIDEMIOLOGY OF N EURODEGENERATION
Mayeux, R. P. (2003) · Annual Review of Neuroscience · doi:10.1146/annurev.neuro.26.043002.094919 · Cited by 531
Type 2 diabetes and atrophy of medial temporal lobe structures on brain MRI
den Heijer, T., Vermeer, S. E., van Dijk, E. J., Prins, N. D., Koudstaal, P. J., Albert Hofman, D., & Breteler, M. M. B. (2003) · Diabetologia · doi:10.1007/s00125-003-1235-0 · Cited by 512
“Apolipoprotein E (APOE) genotyping yielded the following alleles: ε2, ε3, and ε4 [24].”
BackgroundSelf-citationA common haplotype lowers PU.1 expression in myeloid cells and delays onset of Alzheimer's disease
The International Genomics of Alzheimer's Project, Huang, K.-L., Initiative, T. A. D. N., Marcora, E., Pimenova, A. A., Di Narzo, A. F., Kapoor, M., Jin, S. C., Harari, O., Bertelsen, S., et al. (2017) · Nature Neuroscience · doi:10.1038/nn.4587 · Cited by 423
Haan, M. N. (1999) · JAMA · doi:10.1001/jama.282.1.40 · Cited by 457
“Apolipoprotein E e4 alleles may account for 13% to 20% of dementia cases.(25,26) Although APOE genotype is not a specific disease locus, it may create host susceptibility that affects the rate of disease progression.”
BackgroundReitz, C., Jun, G., Naj, A., Rajbhandary, R., Vardarajan, B. N., Wang, L.-S., Valladares, O., Lin, C.-F., Larson, E. B., Graff-Radford, N. R., et al. (2013) · JAMA · doi:10.1001/jama.2013.2973 · Cited by 431
“As much as 20% of the disease-attributable risk is related to the ε4 variant in APOE.(2) A series of large genome-wide association studies (GWASs) identified several additional variants that affect disease susceptibility in non-Hispanic whites of European ancestry, including CR1, CLU, PICALM, BIN1, CD2AP, CD33, EPHA1,…”
Vascular risk factors and dementia: How to move forward?
Viswanathan, A., Rocca, W. A., & Tzourio, C. (2009) · Neurology · doi:10.1212/01.wnl.0000341271.90478.8e · Cited by 414
Goldman, J. S., Hahn, S. E., Catania, J. W., Larusse-Eckert, S., Butson, M. B., Rumbaugh, M., Strecker, M. N., Roberts, J. S., Burke, W., Mayeux, R., et al. (2011) · Genetics in Medicine · doi:10.1097/gim.0b013e31821d69b8 · Cited by 393
The epigenetics of aging and neurodegeneration
Lardenoije, R., Iatrou, A., Kenis, G., Kompotis, K., Steinbusch, H. W. M., Mastroeni, D., Coleman, P., Lemere, C. A., Hof, P. R., van den Hove, D. L. A., et al. (2015) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2015.05.002 · Cited by 381
“Although these genetic risk factors may be informative in screening for populations at risk to develop sAD, it has not yet been discovered how they exactly affect AD development (Slooter et al., 1998).”
BackgroundInfluentialAlzheimer's Disease and the Amyloid Cascade Hypothesis: A Critical Review
Reitz, C. (2012) · International Journal of Alzheimer s Disease · doi:10.1155/2012/369808 · Cited by 398
Oxidative stress in Alzheimer's disease brain: New insights from redox proteomics
Butterfield, D. A., Perluigi, M., & Sultana, R. (2006) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2006.06.026 · Cited by 363
Loy, C. T., Schofield, P. R., Turner, A. M., & Kwok, J. B. (2014) · The Lancet · doi:10.1016/s0140-6736(13)60630-3 · Cited by 342
Cholesterol in Alzheimer's disease
Shobab, L. A., Hsiung, G. R., & Feldman, H. (2005) · The Lancet Neurology · doi:10.1016/s1474-4422(05)70248-9 · Cited by 351
Systemic markers of inflammation and cognitive decline in old age
Schram, M. T., Euser, S. M., De Craen, A. J. M., Witteman, J. C., Frölich, M., Hofman, A., Jolles, J., Breteler, M. M. B., & Westendorp, R. G. J. (2007) · Journal of the American Geriatrics Society · doi:10.1111/j.1532-5415.2007.01159.x · Cited by 326
Self-citationClinical aspects of Alzheimer's disease
Zvěřová, M. (2019) · Clinical Biochemistry · doi:10.1016/j.clinbiochem.2019.04.015 · Cited by 308
Does This Patient Have Dementia?
Holsinger, T., Deveau, J., Boustani, M. A., & Williams, J. W. (2007) · JAMA · doi:10.1001/jama.297.21.2391 · Cited by 308
Cognitive change and the APOE ɛ4 allele
Deary, I. J., Whiteman, M. C., Pattie, A., Starr, J. M., Hayward, C., Wright, A. F., Carothers, A. D., & Whalley, L. J. (2002) · Nature · doi:10.1038/418932a · Cited by 296
The 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
“One study estimates that apoE accounts for 50% of the “predicted total genetic effect” (Roses et al. 1995), whereas others estimate that apoE accounts for 10%–15% of the total variance in age at onset (Bennett et al. 1995; Slooter et al. 1998).”
BackgroundDeelen, J., Beekman, M., Uh, H., Helmer, Q., Kuningas, M., Christiansen, L., Kremer, D., van der Breggen, R., Suchiman, H. E. D., Lakenberg, N., et al. (2011) · Aging Cell · doi:10.1111/j.1474-9726.2011.00705.x · Cited by 285
“For the RS GWAS controls and Danish replication study cases, previously measured data were used (Slooter et al., 1998; Jacobsen et al., 2010).”
Dietary Antioxidants and Long-term Risk of Dementia
Devore, E. E., Grodstein, F., van Rooij, F. J. A., Albert Hofman, D., Stampfer, M. J., Witteman, J. C. M., & Breteler, M. M. B. (2010) · Archives of Neurology · doi:10.1001/archneurol.2010.144 · Cited by 286
“Without knowledge of dementia diagnosis, the apolipoprotein (APOE) genotype was assessed on coded DNA samples using polymerase chain reaction.(29)”
MethodSelf-citationRukhsana Sultana, A., Marzia Perluigi, A., & Butterfield, D. A. (2006) · Antioxidants and Redox Signaling · doi:10.1089/ars.2006.8.2021 · Cited by 261
“among others, apolipoprotein E genotype (120, 195), hyper-”
BackgroundDietary fatty acids and the risk of Parkinson disease
de Lau, L. M. L., Bornebroek, M., Witteman, J. C. M., Albert Hofman, D., Koudstaal, P. J., & Breteler, M. M. B. (2005) · Neurology · doi:10.1212/01.wnl.0000166038.67153.9f · Cited by 260
Self-citationTraumatic Brain Injury as a Risk Factor for Alzheimer's Disease: A Review
Lye, T. C., & Shores, E. A. (2000) · Neuropsychology Review · doi:10.1023/a:1009068804787 · Cited by 259
Corneveaux, J. J., Myers, A. J., Allen, A. N., Pruzin, J. J., Ramirez, M., Engel, A., Nalls, M. A., Chen, K., Lee, W., Chewning, K., et al. (2010) · Human Molecular Genetics · doi:10.1093/hmg/ddq221 · Cited by 237
High Blood Pressure and Cerebral White Matter Lesion Progression in the General Population
Verhaaren, B. F. J., Vernooij, M. W., de Boer, R., Albert Hofman, D., Niessen, W. J., van der Lugt, A., & Ikram, M. A. (2013) · Hypertension · doi:10.1161/hypertensionaha.111.00430 · Cited by 236
“Apolipoprotein E (ApoE)-ε4 genotyping was performed as previously described.(30)”
MethodAPOE Genotype Effects on Alzheimer's Disease Onset and Epidemiology
Ashford, J. W. (2004) · Journal of Molecular Neuroscience · doi:10.1385/jmn:23:3:157 · Cited by 239
Genetics of Alzheimer's Disease: A Centennial Review
Ertekin‐Taner, N. (2007) · Neurologic Clinics · doi:10.1016/j.ncl.2007.03.009 · Cited by 243
“The population attributable risk for AD or dementia due to the ApoE ε4 allele was estimated to be between 20–70% [97, 99].”
BackgroundResultWijsman, E. M., Pankratz, N., Choi, Y., Rothstein, J. H., Faber, K. M., Cheng, R., Lee, J. H., Bird, T. D., Bennett, D. A., Diaz-Arrastia, R. R., et al. (2011) · PLoS Genetics · doi:10.1371/journal.pgen.1001308 · Cited by 229
“There is incomplete lifetime penetrance even in the highest-risk APOE genotypes [18], and the fraction of genetic variance for LOAD risk attributed to APOE is estimated as only 10–20% [19,20].”
BackgroundMolecular genetics of Alzheimer's disease: An update
Brouwers, N., Sleegers, K., & Broeckhoven, C. V. (2008) · Annals of Medicine · doi:10.1080/07853890802186905 · Cited by 213
“Except for APOE, not much is known about other risk genes contributing to late-onset AD, though several such risk genes must exist with effect sizes equal to or even larger than the APOE o4 allele (6,7).”
BackgroundCognitive and Behavioral Neurology
Finger, E. C., & Daffner, K. R. (2011) · Springer eBooks · doi:10.1007/978-0-387-88555-1_8 · Cited by 201
Relation between smoking and risk of dementia and Alzheimer disease
Reitz, C., den Heijer, T., van Duijn, C. M., Albert Hofman, D., & Breteler, M. M. B. (2007) · Neurology · doi:10.1212/01.wnl.0000271395.29695.9a · Cited by 200
Self-citationThe Apolipoprotein E ϵ4 Allele and Decline in Different Cognitive Systems During a 6-Year Period
Wilson, R. S., Schneider, J. A., Barnes, L. L., Beckett, L. A., Aggarwal, N. T., Cochran, E. J., Berry‐Kravis, E., Bach, J., Fox, J. H., Evans, D. A., et al. (2002) · Archives of Neurology · doi:10.1001/archneur.59.7.1154 · Cited by 192
Arendt, T. (2003) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2003.09.007 · Cited by 189
Can Dementia Be Prevented? Brain Aging in a Population-Based Context
Haan, M. N., & Wallace, R. B. (2004) · Annual Review of Public Health · doi:10.1146/annurev.publhealth.25.101802.122951 · Cited by 191
Microglia as Dynamic Cellular Mediators of Brain Function
Wright-Jin, E. C., & Gutmann, D. H. (2019) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2019.08.013 · Cited by 197
Javaid, F. Z., Brenton, J., Guo, L., & Cordeiro, M. F. (2016) · Frontiers in Neurology · doi:10.3389/fneur.2016.00055 · Cited by 179
“Amyloid-β(1-42) alters structure and function of retinal pigmented epithelial cells.”
BackgroundMolecular Genetics of Late‐Onset Alzheimer's Disease
Kamboh, M. I. (2004) · Annals of Human Genetics · doi:10.1046/j.1529-8817.2004.00110.x · Cited by 170
“The risk attributable to the APOE∗4 allele is 20–29% (Seshadri et al. 1995; Slooter et al. 1998).”
BackgroundQian, J., Wolters, F. J., Beiser, A., Haan, M., Ikram, M. A., Karlawish, J., Langbaum, J. B., Neuhaus, J. M., Reiman, E. M., Roberts, J. S., et al. (2017) · PLOS Medicine · doi:10.1371/journal.pmed.1002254 · Cited by 169
Current status on Alzheimer disease molecular genetics: from past, to present, to future
Bettens, K., Sleegers, K., & Broeckhoven, C. V. (2010) · Human Molecular Genetics · doi:10.1093/hmg/ddq142 · Cited by 173
“Nonetheless, APOE 14 does not account for all genetic variation in AD (8,9).”
BackgroundHippocampal, amygdalar, and global brain atrophy in different apolipoprotein E genotypes
den Heijer, T., Oudkerk, M., Launer, L. J., van Duijn, C. M., Albert Hofman, D., & Breteler, M. M. B. (2002) · Neurology · doi:10.1212/wnl.59.5.746 · Cited by 169
Self-citationSchiepers, O. J. G., Harris, S. E., Gow, A. J., Pattie, A., Brett, C. E., Starr, J. M., & Deary, I. J. (2011) · Molecular Psychiatry · doi:10.1038/mp.2010.137 · Cited by 170
Non-familial Alzheimer's disease is mainly due to genetic factors
Ashford, J. W., & Mortimer, J. A. (2002) · Journal of Alzheimer s Disease · doi:10.3233/jad-2002-4307 · Cited by 151
“A few studies focusing on population incidence of AD have found substantially lower estimates for population attributable risk associated with the APOE-ε 4 allele [14,16,25,54].”
Johnson, S. C., Schmitz, T. W., Trivedi, M. A., Ries, M. L., Torgerson, B. M., Carlsson, C. M., Asthana, S., Hermann, B. P., & Sager, M. A. (2006) · Journal of Neuroscience · doi:10.1523/jneurosci.0959-06.2006 · Cited by 154
Prince, J. A., Feuk, L., Sawyer, S. L., Gottfries, J., Ricksten, A., Nägga, K., Bogdanović, N., Blennow, K., & Brookes, A. J. (2001) · European Journal of Human Genetics · doi:10.1038/sj.ejhg.5200651 · Cited by 141
Chui, H. C., Zheng, L., Reed, B., Vinters, H. V., & Mack, W. J. (2011) · Alzheimer s Research & Therapy · doi:10.1186/alzrt98 · Cited by 145
Neurophysiological Markers of Alzheimer’s Disease: Quantitative EEG Approach
Smailović, U., & Jelić, V. (2019) · Neurology and Therapy · doi:10.1007/s40120-019-00169-0 · Cited by 152
On Jim Watson's APOE status: genetic information is hard to hide
Nyholt, D. R., Yu, C., & Visscher, P. M. (2008) · European Journal of Human Genetics · doi:10.1038/ejhg.2008.198 · Cited by 137
APOE Genotype, Family History of Dementia, and Alzheimer Disease Risk
Huang, W., Qiu, C., Strauss, E. I. V., Winblad, B. G., & Fratiglioni, L. (2004) · Archives of Neurology · doi:10.1001/archneur.61.12.1930 · Cited by 134
“Because of the old age of our study sample, the estimated relative risks in our study were lower than those of previous studies.(3,6,15) Thus, our findings may not be generalizable to the younger-old population.”
BackgroundResultInfluentialBäcker‐Koduah, P., Paul, F., & Dörr, J.-M. (2017) · The EPMA Journal · doi:10.1007/s13167-017-0120-8 · Cited by 134
“However, not all AD patients express the APOEε4 allele which points to additional causative factors [165, 166].”
BackgroundThe apolipoprotein E varepsilon2 allele and decline in episodic memory
Wilson, R. S. (2002) · Journal of Neurology, Neurosurgery & Psychiatry · doi:10.1136/jnnp.73.6.672 · Cited by 161
How to Use an Article About Genetic Association
Attia, J., Ioannidis, J. P. A., Thakkinstian, A., McEvoy, M., Scott, R. J., Minelli, C., Thompson, J. R., Infante‐Rivard, C., & Guyatt, G. H. (2009) · JAMA · doi:10.1001/jama.2008.946 · Cited by 131
Analyses of the National Institute on Aging Late-Onset Alzheimer's Disease Family Study
Lee, J. H. (2008) · Archives of Neurology · doi:10.1001/archneur.65.11.1518 · Cited by 126
“A LTHOUGH THE APOLIPOPROtein E ε4 allele (APOE ε4) (OMIM 107741) is the most consistently replicated genetic variant influencing the risk of late-onset Alzheimer disease (LOAD),(1) it explains only 20% of the attributable genetic risk.(2) Daw et al(3) reported that there may be 4 additional genes influencing LOAD risk.”
Developmental and vascular risk factors for Alzheimer's disease
Borenstein, A. R., Wu, Y., Mortimer, J. A., Schellenberg, G. D., McCormick, W. C., Bowen, J. D., McCurry, S. M., & Larson, E. B. (2004) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2004.04.010 · Cited by 127
APOE-ε4 is associated with memory decline in cognitively impaired elderly
Dik, M. G., Jonker, C., Bouter, L. M., Geerlings, M. I., van Kamp, G. J., & Deeg, D. J. H. (2000) · Neurology · doi:10.1212/wnl.54.7.1492 · Cited by 128
Genome-wide Association Studies in Alzheimer’s Disease: A Review
Tosto, G., & Reitz, C. (2013) · Current Neurology and Neuroscience Reports · doi:10.1007/s11910-013-0381-0 · Cited by 131
“Although the population attributable risk of APOE ε4 is estimated at 20–50 % [30], the presence of ε4 is neither necessary nor sufficient for development of the disease [31].”
BackgroundPankratz, N., & Foroud, T. (2007) · Genetics in Medicine · doi:10.1097/gim.0b013e31815bf97c · Cited by 129
Insulin resistance in Alzheimer's disease
Dineley, K. T., Jahrling, J. B., & Denner, L. A. (2014) · Neurobiology of Disease · doi:10.1016/j.nbd.2014.09.001 · Cited by 125
Genetic diagnosis and prognosis of Alzheimer’s disease: challenges and opportunities
Reitz, C. (2015) · Expert Review of Molecular Diagnostics · doi:10.1586/14737159.2015.1002469 · Cited by 125
“While the population attributable risk for APOE"4 is estimated at 20–50%, [51], the presence of "4 is neither necessary nor sufficient for developing the disease [52].”
BackgroundProspective Belgian study of neurodegenerative and vascular dementia: APOE genotype effects
Engelborghs, S. (2003) · Journal of Neurology Neurosurgery & Psychiatry · doi:10.1136/jnnp.74.8.1148 · Cited by 120
Devanand, D. P., Pelton, G. H., Zamora, D., Liu, X., Tabert, M. H., Goodkind, M. S., Scarmeas, N., Braun, I. M., Stern, Y., & Mayeux, R. P. (2005) · Archives of Neurology · doi:10.1001/archneur.62.6.975 · Cited by 122
“In studies that compared patients who had AD with healthy controls, the mean odds ratio for heterozygotes was approximately 4 in clinical samples and approximately 2 in community samples, with considerable variability across studies.(2,3) The APOE ε4 allele’s association with AD is not influenced by sex, diminishes af…”
BackgroundRole of Cholesterol in APP Metabolism and Its Significance in Alzheimer’s Disease Pathogenesis
Maulik, M., Westaway, D. A., Jhamandas, J. H., & Kar, S. (2012) · Molecular Neurobiology · doi:10.1007/s12035-012-8337-y · Cited by 121
“compared to individuals with the ε3 or ε2 forms [40, 41].”
BackgroundDufouil, C., Tzourio, C., Brayne, C., Berr, C., Amouyel, P., & Alpérovitch, A. (2000) · Epidemiology · doi:10.1097/00001648-200005000-00009 · Cited by 118
The keystone of Alzheimer pathogenesis might be sought in Aβ physiology
Puzzo, D., Gulisano, W., Arancio, O., & Palmeri, A. (2015) · Neuroscience · doi:10.1016/j.neuroscience.2015.08.039 · Cited by 116
“…but apolipoprotein E (APOE) gene, since subjects with the APOE-e4 allele had a more than 10-fold higher risk of dementia (Corder et al., 1993; Slooter et al., 1998); (iv) studies on animal models have demonstrated that if mutations of APP, PS or secretases leading to an increase of Ab burden…”
Engelborghs, S., Sleegers, K., Cras, P. P., Brouwers, N., Serneels, S., Leenheir, E. D., Martin, J. J., Vanmechelen, E., Broeckhoven, C. V., & Deyn, P. P. D. (2007) · Brain · doi:10.1093/brain/awm136 · Cited by 114
“Genomic DNA was extracted from total blood using standard methods and the APOE genotype was determined as described earlier (Slooter et al., 1998).”
MethodJohnson, S. C., La Rue, A., Hermann, B. P., Xu, G., Koscik, R. L., Jonaitis, E. M., Bendlin, B. B., Hogan, K. J., Roses, A. D., Saunders, A. M., et al. (2011) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2010.11.012 · Cited by 112
“In population studies of frequency of APOE variants among AD cases, the proportion without an 34 allele is 36% to 50% [4–6]; thus, approximately 40% to 50% of AD cases require an explanation beyond APOE 34 [7].”
BackgroundAlzheimer’ s disease, oxidative stress and gammahydroxybutyrate
Mamelak, M. (2006) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2006.06.008 · Cited by 108
Qiu, C. (2004) · Journal of Neurology Neurosurgery & Psychiatry · doi:10.1136/jnnp.2003.021493 · Cited by 115
Advances in the prevention of Alzheimer's Disease
Sindi, S., Mangialasche, F., & Kivipelto, M. (2015) · F1000Prime Reports · doi:10.12703/p7-50 · Cited by 118
“The APOE e4 allele increases the risk for AD in a dose-response manner, where those with homozygous e4 allele (two e4 copies) have a higher risk than individuals with heterozygous e4 allele (a combination of one e4 copy, and an alternative copy: e2 or e3 allele), who in turn have a higher risk than individuals with no…”
Ranson, J. M., Rittman, T., Hayat, S. A., Brayne, C., Jessen, F., Blennow, K., van Duijn, C. M., Barkhof, F., Tang, E. Y. H., Mummery, C. J., et al. (2021) · Alzheimer s Research & Therapy · doi:10.1186/s13195-021-00895-4 · Cited by 123
“, 51–95% in APOE ɛ4/ɛ4 and 22–90% in APOE ɛ4/- [26, 27] and a mean age at dementia onset of 73–74 years in APOE ɛ4/ɛ4 and 75–82 in APOE ɛ4/- [28, 29].”
Most rapid cognitive decline in APOE ε4 negative Alzheimer's disease with early onset
van der Vlies, A. E., Koedam, E., Pijnenburg, Y. A. L., Twisk, J. W. R., Scheltens, P., & van der Flier, W. M. (2009) · Psychological Medicine · doi:10.1017/s0033291709005492 · Cited by 107
“The apolipoprotein E gene (APOE) is an important risk factor for AD (Kuusisto et al. 1994 ; Strittmatter & Roses, 1995 ; Slooter et al. 1998 ; Petersen et al. 2005).”
BackgroundPrestroke Cognitive Performance, Incident Stroke, and Risk of Dementia
Reitz, C., Bos, M. J., Albert Hofman, D., Koudstaal, P. J., & Breteler, M. M. B. (2007) · Stroke · doi:10.1161/strokeaha.107.490334 · Cited by 108
Self-citationGenetics of Alzheimer disease in the pre- and post-GWAS era
Ertekin‐Taner, N. (2010) · Alzheimer s Research & Therapy · doi:10.1186/alzrt26 · Cited by 112
“PAR esti mates may have an upward bias in family-based studies and younger populations given that APOE has a stronger eff ect in younger ages (from younger than age 70 to eighties) and longitudinal studies may provide more accurate estimates of PAR of APOE where estimates of 20% were obtained [35,37,38].”
BackgroundAlzheimer’s Disease: Mechanism and Approach to Cell Therapy
Amemori, T., Jendelová, P., Růžička, J., Urdzíková, L. M., & Syková, E. (2015) · International Journal of Molecular Sciences · doi:10.3390/ijms161125961 · Cited by 110
“[20,21]; however, in sporadic cases its estimated prevalence risk is only 10%–20% [22].”
BackgroundGenome-wide association analysis of age-at-onset in Alzheimer's disease
Kamboh, M. I., Barmada, M. M., Demirci, F. Y., Minster, R. L., Carrasquillo, M. M., Pankratz, V. S., Younkin, S. G., Saykin, A. J., Initiative, T. A. D. N., Sweet, R. A., et al. (2012) · Molecular Psychiatry · doi:10.1038/mp.2011.135 · Cited by 100
The effect of APOE genotype on clinical phenotype in Alzheimer disease
van der Flier, W. M., Schoonenboom, S. N. M., Pijnenburg, Y. A. L., Fox, N. C., & Scheltens, P. (2006) · Neurology · doi:10.1212/01.wnl.0000228222.17111.2a · Cited by 98
“8 Amyloid (1-42) (A 42), total tau, and tau phosphorylated at threonine-181 (Ptau-181) were measured by sandwich ELISA (Innotest -amyloid[1-42], Innotest hTAU-Ag, and Innotest Phosphotau(181P); Innogenetics, Ghent, Belgium).”
MethodHolmquist, S., Nordström, A., & Nordström, P. (2020) · PLoS Medicine · doi:10.1371/journal.pmed.1003016 · Cited by 98
van der Willik, K. D., Fani, L., Rizopoulos, D., Licher, S., Fest, J., Schagen, S. B., Ikram, M. K., & Ikram, M. A. (2019) · Journal of Neuroinflammation · doi:10.1186/s12974-019-1454-z · Cited by 96
Evidence for a novel late-onset Alzheimer disease locus on chromosome 19p13.2.
Wijsman, E. M., Daw, E. W., Yu, C.-E., Payami, H., Steinbart, E. J., Nochlin, D., Conlon, E. M., Bird, T. D., & Schellenberg, G. D. (2004) · The American Journal of Human Genetics · doi:10.1086/423393 · Cited by 71
Luck, T., Riedel-Heller, S. G., Luppa, M., Wiese, B., Köhler, M., Jessen, F., Bickel, H., Weyerer, S., Pentzek, M., König, H.-H., et al. (2014) · Psychological Medicine · doi:10.1017/s0033291713001918 · Cited by 93
“The ε4 allele of apolipoprotein E (APOE) is the most important currently known genetic risk factor for lateonset Alzheimer’s disease (AD) dementia (Paulson & Igo, 2011), and is thought to account for around 20–50% of the attributable total risk for dementia (Slooter et al. 1998; Ashford, 2004).”
BackgroundWhite Matter Microstructure in Relation to Education in Aging and Alzheimer's Disease1
Teipel, S. J., Meindl, T., Wagner, M., Kohl, T., Bürger, K., Reiser, M. F., Herpertz, S. C., Möller, H., & Hampel, H. J. (2009) · Journal of Alzheimer s Disease · doi:10.3233/jad-2009-1077 · Cited by 92
“Important risk factors for AD that are not accessible to intervention include age, female gender, and apolipoprotein E4 (ApoE4) genotype [11,12].”
BackgroundGenetic susceptibility factors for Alzheimer's disease
Richard, F., & Amouyel, P. (2001) · European Journal of Pharmacology · doi:10.1016/s0014-2999(00)00903-1 · Cited by 92
Dubal, D. B. (2020) · Handbook of clinical neurology · doi:10.1016/b978-0-444-64123-6.00018-7 · Cited by 92
Aerssens, J., Raeymaekers, P., Lilienfeld, S., Geerts, H., Konings, F., & Parys, W. (2001) · Dementia and Geriatric Cognitive Disorders · doi:10.1159/000051238 · Cited by 91
Emerging Link between Alzheimer’s Disease and Homeostatic Synaptic Plasticity
Jang, S.-S., & Chung, H. J. (2016) · Neural Plasticity · doi:10.1155/2016/7969272 · Cited by 93
Cognitive Resilience to Apolipoprotein E ε4
Kaup, A. R., Nettiksimmons, J., Harris, T. B., Sink, K. M., Satterfield, S., Metti, A. L., Ayonayon, H. N., & Yaffe, K. S. (2015) · JAMA Neurology · doi:10.1001/jamaneurol.2014.3978 · Cited by 89
“Future research might explore whether the following differ by race: (1) types of stressors experienced in aging, (2) older adults’ coping styles, and (3) the neurobiological effects of stress on the aging brain.”
Genetic Testing For Alzheimer’s And Long-Term Care Insurance
Taylor, D. H., Cook-Deegan, R. M., Hiraki, S. C., Roberts, J. S., Blazer, D. G., & Green, R. C. (2010) · Health Affairs · doi:10.1377/hlthaff.2009.0525 · Cited by 87
Transcriptional regulation of Alzheimer's disease genes: implications for susceptibility
Theuns, J. (2000) · Human Molecular Genetics · doi:10.1093/hmg/9.16.2383 · Cited by 89
Vascular factors in dementia: an overview
DeCarli, C. S. (2004) · Journal of the Neurological Sciences · doi:10.1016/j.jns.2004.09.005 · Cited by 88
Apolipoprotein E ε4 Allele Differentiates the Clinical Response to Donepezil in Alzheimer’s Disease
Bizzarro, A., Marra, C., Acciarri, A., Valenza, A., Tiziano, F. D., Brahe, C., & Masullo, C. (2005) · Dementia and Geriatric Cognitive Disorders · doi:10.1159/000087371 · Cited by 85
“Apolipoprotein E (APOE) genotype has been demonstrated to be a definite genetic risk factor for Alzheimer’s disease (AD) and the e4 allele has a significantly higher frequency in AD patients compared with healthy subjects [”
BackgroundApolipoprotein E and Carotid Artery Atherosclerosis
Slooter, A. J. C., Bots, M. L., Havekes, L. M., del Sol, A. I., Cruts, M., Grobbee, D. E., Albert Hofman, D., Broeckhoven, C. V., Witteman, J. C. M., & van Duijn, C. M. (2001) · Stroke · doi:10.1161/hs0901.095377 · Cited by 79
Self-citation
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
