Cited by 16

The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

Association of Apolipoproteins E4 and C1 With Onset Age and Memory: A Study of Sporadic Alzheimer Disease in Taiwan

Chuang, Wen-Li, Hsieh, Yu-Chen, Wang, Chun-Yi, Kuo, Hung-Chou, Huang, Chin-Chang·2010·Journal of Geriatric Psychiatry and Neurology

Abstract

Objective: To identify clinical manifestations and neuropsychological effects of Alzheimer disease (AD) in apolipoprotein (ApoE) e4 carriers and to investigate the relationships between ApoE HhaI polymorphism and apolipoprotein C1 (APOC1) HpaI polymorphism in Taiwanese patients with AD. Participants and methods: A total of 127 patients with AD and 191 elderly individuals were screened for ApoE and APOC1 polymorphism. All patients underwent neuropsychological testing, including a Mini-Mental Status Examination (MMSE), Clinical Dementia Rating (CDR), and/or the Visual Association Memory Test (VAMT) with Cognitive Abilities Screening Instrument. Results: The frequencies of the e4 and A alleles were significantly higher in the AD group. In the patients with AD, the e4 and A allele effects on those with an age-of-onset of 60 to 79 years were stronger than those with an age-of-onset of 80 years or higher. Visual Association Memory Test performance was significantly worse in e4-allele carriers but not in A-allele carriers, in the early AD, particularly in those affected with AD for less than 2 years. Although there was no statistically significant difference in genotypic frequency between patients and controls, the 2 genes were linked. In addition, the presence of the AA genotype concomitant with the e4 allele may be better associated with AD diagnosis than either factor alone. Conclusion: We conclude that the e4 allele affects neuropsychological performance and illness morbidity. Concomitantly, ApoE e4 and APOC1 A alleles have a better association with AD than ApoE e4 alone. In addition, APOC1 may partially contribute to the pathogenesis of AD, but the nature of its relationship with e4 requires further investigation.

Overview

Integrity signals

Registry

Crossref · 10.1177/0891988709351804

Cites

1 of 1 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

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 co-presence of APOE ε4 and APOC1 risk alleles has been reported to be more strongly associated with AD than APOE ε4 alone, indicating that the interaction between these two genes may contribute to the development of AD and cognitive decline.

    “The co-presence of APOE ε4 and APOC1 risk alleles has been reported to be more strongly associated with AD than APOE ε4 alone, indicating that the interaction between these two genes may contribute to the development of AD and cognitive decline [96].”

Citations

Cites

Flagged first, then by citations

Research works printed but not linked: 34

  1. 10.1016/S0021-9258(18)68638-7 · DOI
  2. 10.1007/s100480100122 · DOI
  3. 10.1034/j.1600-0404.2003.00193.x · DOI
  4. 10.1017/S0033291700027914 · DOI
  5. 10.1136/jnnp.73.2.126 · DOI
  6. Chuang WL, 2006, Acta Neurol Taiwan, 15, 98
  7. 10.1007/s00702-005-0424-z · DOI
  8. 10.1093/nar/18.11.3428-a · DOI
  9. 10.1212/WNL.43.8.1467 · DOI · Paper page
  10. 10.1002/ana.410370217 · DOI
  11. 10.1212/WNL.46.6.1749 · DOI
  12. 10.1136/jnnp.57.11.1414 · DOI
  13. 10.1016/S0022-2275(20)33338-1 · DOI
  14. 10.1016/S0304-3940(01)02559-9 · DOI · Paper page
  15. 10.1097/00041444-200109000-00002 · DOI · Paper page
  16. Xu PT, 2006, Neurobiol Dis, 21, 156
  17. 10.1016/j.mcn.2007.06.009 · DOI
  18. 10.1186/1741-7015-4-1 · DOI
  19. 10.1212/WNL.44.8.1513 · DOI
  20. 10.1002/ana.410360429 · DOI
  21. Murman DL, 1996, Dementia, 7, 251
  22. 10.1212/01.WNL.0000137041.86153.42 · DOI
  23. 10.1016/j.neuropsychologia.2008.07.010 · DOI
  24. 10.1038/12137 · DOI
  25. 10.1523/JNEUROSCI.23-17-06748.2003 · DOI
  26. 10.1002/(SICI)1098-1063(1997)7:6<594::AID-HIPO2>3.0.CO;2-F · DOI
  27. 10.1007/s12149-007-0148-2 · DOI
  28. 10.1023/A:1022409617539 · DOI
  29. 10.1212/WNL.51.1.131 · DOI
  30. 10.1097/00041444-200109000-00002 · DOI · Paper page
  31. 10.1074/jbc.M203151200 · DOI
  32. 10.1385/JMN:23:3:225 · DOI
  33. 10.1016/S0021-9258(18)55263-7 · DOI · Paper page
  34. 10.1006/nbdi.2001.0441 · DOI · Paper page

Cited by

Sorted by citations

Metadata

Authors
Chuang, W.-L., Hsieh, Y.-C., Wang, C.-Y., Kuo, H.-C., & Huang, C.-C.
Affiliations
  • Department of Neurology, Chang Gung Memorial Hospital and University, Taipei, Taiwan
  • Department of Neurology, Chang Gung Memorial Hospital and University, Taipei, Taiwan,
Venue
Journal of Geriatric Psychiatry and Neurology
Published
2010-02-09
Volume
23
Issue
1
Pages
42-48
ISSN
  • 0891-9887
  • 1552-5708
Cited by
16
References
1
Language
en

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