The DOI matches its Crossref record; 130 of the 131 references it cites were found in a registry or an index.
Molecular Genetics of Late‐Onset Alzheimer's Disease
Open accessAbstract
Summary: Late‐onset Alzheimer's disease (AD) is a complex and multifactorial disease with the possible involvement of several genes. Apolipoprotein E (APOE), especially the APOE*4 allele, has been established as a strong susceptibility marker that accounts for nearly 30% of the risk in late‐onset AD. However, as the APOE*4 allele is neither necessary nor sufficient for the development of AD, it emphasizes the involvement of other genetic and/or environmental factors which, alone or in conjunction with APOE*4, can modify the risk of AD. Recently, genome‐wide linkage or linkage disequilibrium studies on late‐onset AD have provided informative data for the existence of multiple putative genes for AD on several chromosomes, with the strongest evidence on chromosomes 12, 10, 9 and 6. This paper attempts to review the current progress on the identification of additional genetic loci for late‐onset AD.
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 cited source says what the claim attributes to it.
In the citing paper
“The APOE polymorphism is the most studied, successfully replicated, and well-established risk factor for AD where APOE*2 is the protective allele and APOE*4 is the risk allele as compared to APOE*3 [7–10].”
From Genome-wide analysis identifies novel loci influencing plasma apolipoprotein E concentration and Alzheimer’s disease risk (2023) · cites this paper as [9]
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
Sørlie, T., Perou, C. M., Tibshirani, R. J., Aas, T., Geisler, S. B., Johnsen, H., Hastie, T. J., Eisen, M. B., van de Rijn, M., Jeffrey, S. S., et al. (2001) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.191367098 · Cited by 11,506
Goate, A., Chartier-Harlin, M.-C., Mullan, M., Brown, J., Crawford, F., Fidani, L., Giuffra, L., Haynes, A., Irving, N., James, L., et al. (1991) · Nature · doi:10.1038/349704a0 · Cited by 4,659
Cloning of a gene bearing missense mutations in early-onset familial Alzheimer's disease
Sherrington, R., Rogaev, E. I., Liang, Y., Rogaeva, E. A., Levesque, G., Ikeda, M., Chi, H., Lin, C., Li, G., Holman, K., et al. (1995) · Nature · doi:10.1038/375754a0 · Cited by 4,051
Candidate gene for the chromosome 1 familial Alzheimer’s disease locus
Levy-Lahad, E., Wasco, W., Poorkaj, P., Romano, D. M., Oshima, J., Pettingell, W. H., Yu, C.-E., Jondro, P. D., Schmidt, S. D., Wang, K., et al. (1995) · Science · doi:10.1126/science.7638622 · Cited by 2,577
Exploring the new world of the genome with DNA microarrays
Brown, P. O., & Botstein, D. (1999) · Nature Genetics · doi:10.1038/4462 · Cited by 2,430
Rogaev, E. I., Sherrington, R., Rogaeva, E. A., Levesque, G., Ikeda, M., Liang, Y., Chi, H., Lin, C., Holman, K., Tsuda, T., et al. (1995) · Nature · doi:10.1038/376775a0 · Cited by 2,052
Deficiency of presenilin-1 inhibits the normal cleavage of amyloid precursor protein
De Strooper, B., Saftig, P., Craessaerts, K., Vanderstichele, H., Guhde, G., Annaert, W., Von Figura, K., & Van Leuven, F. (1998) · Nature · doi:10.1038/34910 · Cited by 1,818
Berge, K. E., Tian, H., Graf, G. A., Yu, L., Grishin, N. V., Schultz, J. R., Kwiterovich, P. O., Shan, B., Barnes, R., & Hobbs, H. H. (2000) · Science · doi:10.1126/science.290.5497.1771 · Cited by 1,645
Enhanced neurofibrillary degeneration in transgenic mice expressing mutant tau and APP
Lewis, J., Dickson, D. W., Lin, W.-L., Chisholm, L., Corral, A., Jones, G., Yen, S.-H., Sahara, N., Skipper, L., Yager, D., et al. (2001) · Science · doi:10.1126/science.1058189 · Cited by 1,611
Formation of Neurofibrillary Tangles in P301L Tau Transgenic Mice Induced by Aβ42 Fibrils
Götz, J., Chen, F., van Dorpe, J., & Nitsch, R. M. (2001) · Science · doi:10.1126/science.1062097 · Cited by 1,526
Research works printed but not linked: 4
- Holmans P., 2003, Evidence of interaction between susceptibility loci on chromosomes 1, 10 and 12 in late‐onset Alzheimer's disease (LOAD), Am J Hum Genet, 73, 184
- Roses A. D., 1995, Alzheimer's disease as a model of molecular gerontology, J NIH Res, 7, 51
- Stanton K. C., 2003, Further evidence of linkage of Alzheimer's disease on chromosome 12, Am J Hum Genet, 73, 471
- Xu P.‐T., 2002, Characterization and analyses of AD candidate genes P16 and MTAP on chromosome 9p21, Am J Hum Genet, 71, A490
Cited by
Sorted by citations
Review Article: Genetics of Alzheimer Disease
Bekris, L. M., Yu, C.-E., Bird, T. D., & Tsuang, D. W. (2010) · Journal of Geriatric Psychiatry and Neurology · doi:10.1177/0891988710383571 · Cited by 1,029
Devi, L., Prabhu, B. M., Galati, D. F., Avadhani, N. G., & Anandatheerthavarada, H. K. (2006) · The Journal of Neuroscience · doi:10.1523/jneurosci.1469-06.2006 · Cited by 792
Epigenetic mechanisms in neurogenesis
Yao, B., Christian, K. M., He, C., Jin, P., Ming, G., & Song, H. (2016) · Nature reviews. Neuroscience · doi:10.1038/nrn.2016.70 · Cited by 406
Rosiglitazone attenuates learning and memory deficits in Tg2576 Alzheimer mice
Pedersen, W. A., McMillan, P. J., Kulstad, J. J., Leverenz, J. B., Craft, S., & Haynatzki, G. R. (2006) · Experimental Neurology · doi:10.1016/j.expneurol.2006.01.018 · Cited by 320
Genetics, environmental factors and the emerging role of epigenetics in neurodegenerative diseases
Migliore, L., & Coppedè, F. (2008) · Mutation research. Fundamental and molecular mechanisms of mutagenesis · doi:10.1016/j.mrfmmm.2008.10.011 · Cited by 331
Metadata
- Authors
- Kamboh, M. I.
- Affiliations
- University of Pittsburgh (US)
- Corresponding author
- Kamboh, M. Ilyas
- ORCID
- Kamboh, M. Ilyas
- Venue
- Annals of Human Genetics
- Publisher
- Wiley
- Published
- 2004-06-28
- Volume
- 68
- Issue
- 4
- Pages
- 381-404
- ISSN
- 0003-4800 (ISSN-L)
- 1469-1809
- OpenAlex
- W2137932456
- Cited by
- 170
- References
- 131
- Citations by year
- 2025: 4 · 2024: 2 · 2023: 4 · 2022: 2 · 2021: 6 · 2020: 4 · 2019: 1 · 2018: 1 · 2017: 5 · 2016: 7 · 2015: 4 · 2014: 7 · 2013: 6 · 2012: 12
- FWCI
- 2.76
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Annals of Human Genetics (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (AG 05-133, P50AG005133, AG13672, R01AG013672)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Keywords
- late-onset Alzheimer's disease, apolipoprotein E, genetic susceptibility, genetic loci, genome-wide linkage analysis, linkage disequilibrium, complex diseases, genetic risk factors
- MeSH terms
- Alzheimer Disease, Apolipoproteins E, Humans, Genetic Linkage, Molecular Biology, Biomarkers
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
