The DOI matches its Crossref record; 24 of the 24 references it cites were found in a registry or an index.
Replication of CLU, CR1, and PICALM Associations With Alzheimer Disease
Open accessAbstract
OBJECTIVE: To test for replication of the association between variants in the CLU, CR1, and PICALM genes with Alzheimer disease. DESIGN: Follow-up case-control association study. SETTING: The Mayo Clinics at Jacksonville, Florida, and Rochester, Minnesota. PARTICIPANTS: Community-based patients of European descent with late-onset Alzheimer disease (LOAD) and controls without dementia who were seen at the Mayo clinics, and autopsy-confirmed cases and controls whose pathology was evaluated at the Mayo Clinic in Jacksonville. Additional samples were obtained from the National Cell Repository for Alzheimer Disease (NCRAD). A total of 1829 LOAD cases and 2576 controls were analyzed. INTERVENTIONS: The most significant single-nucleotide polymorphisms in CLU (rs11136000), CR1 (rs3818361), and PICALM (rs3851179) were tested for allelic association with LOAD. Main Outcome Measure Clinical or pathology-confirmed diagnosis of LOAD. RESULTS: Odds ratios for CLU, CR1, and PICALM were 0.82, 1.15, and 0.80, respectively, comparable in direction and magnitude with those originally reported. P values were 8.6 x 10(-5), .014, and 1.3 x 10(-5), respectively; they remain significant even after Bonferroni correction for the 3 single-nucleotide polymorphisms tested. CONCLUSION: These results show near-perfect replication and provide the first additional evidence that CLU, CR1, and PICALM are associated with the risk of LOAD.
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
“The association of PICALM polymorphisms with late-onset AD has been reported by the majority of GWAS studies (94, 119, 236, 265, 298, 344, 528).”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [94]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Some additional highly replicated risk genes include CR1 , BIN1 , and TREM2 (94, 119, 219, 300, 344, 543).”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [94]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Several GWAS studies have identified CLU as a significant genetic risk factor for sporadic AD (94, 119, 236, 343).”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [94]
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
Association of apolipoprotein E allele ϵ4 with late‐onset familial and sporadic Alzheimer's disease
Saunders, A. M., Strittmatter, W. J., Schmechel, D., St. George-Hyslop, P. H., Pericak-Vance, M. A., Joo, S. H., Rosi, B. L., Gusella, J. F., Crapper-MacLachlan, D. R., Alberts, M. J., et al. (1993) · Neurology · doi:10.1212/wnl.43.8.1467 · Cited by 3,786
Diffusible, nonfibrillar ligands derived from Aβ 1–42 are potent central nervous system neurotoxins
Lambert, M. P., Barlow, A. K., Chromy, B. A., Edwards, C., Freed, R., Liosatos, M., Morgan, T. E., Rozovsky, I., Trommer, B., Viola, K. L., et al. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.11.6448 · Cited by 3,506
Harold, D., Abraham, R., Hollingworth, P., Sims, R., Gerrish, A., Hamshere, M. L., Pahwa, J. S., Moskvina, V., Dowzell, K., Williams, A., et al. (2009) · Nature Genetics · doi:10.1038/ng.440 · Cited by 3,326
Self-citationGenome-wide association study identifies variants at CLU and CR1 associated with Alzheimer's disease
the European Alzheimer's Disease Initiative Investigators, Lambert, J.-C., Heath, S., Even, G., Campion, D., Sleegers, K., Hiltunen, M., Combarros, O., Zelenika, D., Bullido, M. J., et al. (2009) · Nature Genetics · doi:10.1038/ng.439 · Cited by 2,234
Systematic meta-analyses of Alzheimer disease genetic association studies: the AlzGene database
Bertram, L., McQueen, M. B., Mullin, K., Blacker, D., & Tanzi, R. E. (2007) · Nature Genetics · doi:10.1038/ng1934 · Cited by 1,857
Role of Genes and Environments for Explaining Alzheimer Disease
Gatz, M., Reynolds, C. A., Fratiglioni, L., Johansson, B., Mortimer, J. A., Berg, S., Fiske, A., & Pedersen, N. L. (2006) · Archives of General Psychiatry · doi:10.1001/archpsyc.63.2.168 · Cited by 1,798
The neuronal sortilin-related receptor SORL1 is genetically associated with Alzheimer disease
Rogaeva, E., Meng, Y., Lee, J. H., Gu, Y., Kawarai, T., Zou, F., Katayama, T., Baldwin, C. T., Cheng, R., Hasegawa, H., et al. (2007) · Nature Genetics · doi:10.1038/ng1943 · Cited by 1,167
Self-citation
Cited by
Sorted by citations
Items 201–208 of 208
Postoperative Cognitive Dysfunction and Delirium
Newman, M. F., Berger, M., & Mathew, J. P. (2021) · Elsevier eBooks · doi:10.1016/b978-0-323-56724-4.00042-3
Belbin, O., Carrasquillo, M. M., Crump, M. P., Culley, O. J., Hunter, T. A., Ma, L., Bisceglio, G. D., Dickson, D. W., Younkin, S. G., Morgan, K., et al. (2011)
Self-citationThe Future Role of Biomarkers in Alzheimer’s Disease Diagnostics
Richens, J. L., Vafadar-Isfahani, B., Vere, K., Ball, G., Kalsheker, N. A., Rees, R. C., Bajaj, N. P. S., O’Shea, P., & Morgan, K. (2013) · Springer eBooks · doi:10.1007/978-1-4614-7309-1_13
Self-citationTurgut Ozal University Faculty of Medicine 6th International Student Congress
Turgut Ozal University Faculty of Medicine 6th International Student Congress (2015) · Clinical and investigative medicine · doi:10.25011/cim.v38i4.24263
Zhu, X.-C., Dai, W.-Z., & Ma, T. (2020) · Figshare · doi:10.6084/m9.figshare.12949466
Zhu, X.-C., Dai, W.-Z., & Ma, T. (2020) · Figshare · doi:10.6084/m9.figshare.12949469
Rôle des ADAM dans le processus physiopathologique de la maladie d'Alzheimer
Laumet, G. O. (2010) · theses.fr (ABES) · doi:10.70675/94126786zf990z488ezb471z5f1d5686766c
Mahmoudi, A.-E.-R. (2015) · theses.fr (ABES) · doi:10.70675/5f05520ez1713z4991za6c8z055ab117e2bb
Metadata
- Authors
- Carrasquillo, M. M., Belbin, O., Hunter, T. A., Ma, L., Bisceglio, G. D., Zou, F., Crook, J. E., Pankratz, V. S., Dickson, D. W., Graff-Radford, N. R., Petersen, R. C., Morgan, K., & Younkin, S. G.
- Affiliations
- Mayo Clinic in Florida (US)
- Mayo Clinic (US)
- University of Nottingham (GB)
- ORCID
- Venue
- Archives of Neurology
- Publisher
- American Medical Association (AMA)
- Published
- 2010-08-01
- Volume
- 67
- Issue
- 8
- Pages
- 961-4
- ISSN
- 0003-9942 (ISSN-L)
- PMC
- PMC2919638
- OpenAlex
- W2065929647
- Cited by
- 208
- References
- 24
- Citations by year
- 2025: 2 · 2024: 4 · 2023: 1 · 2022: 7 · 2021: 6 · 2020: 11 · 2019: 5 · 2018: 15 · 2017: 8 · 2016: 17 · 2015: 13 · 2014: 23 · 2013: 23 · 2012: 29
- FWCI
- 20.80
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Archives of Neurology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (U01 AG 06576, P50‐AG16574, AG03949, R01AG018023, U01AG006786, P01AG003949, AG 25711, R01-AG18023, AG 17216, U24 AG21886, P50AG025711, P01AG017216, U24AG021886, P50AG016574)
- 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
- Alzheimer's disease, late-onset Alzheimer's disease, CLU gene, genetic association, single nucleotide polymorphisms, genetic risk factors, replication study
- MeSH terms
- Alzheimer Disease, Follow-Up Studies, Gene Frequency, Genotype, Humans, Residence Characteristics, Odds Ratio, Case-Control Studies, Receptors, Complement 3b, Genetic Predisposition to Disease, Polymorphism, Single Nucleotide, Monomeric Clathrin Assembly Proteins, White People, Clusterin, Genome-Wide Association Study
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