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Genetic association of an apolipoprotein C-I (APOC1) gene polymorphism with late-onset Alzheimer's disease

Ki, Chang-Seok, Na, Duk Lyul, Kim, Doh Kwan, Kim, Hye Jin, Kim, Jong-Won·2002·Neuroscience Letters
DOI 10.1016/s0304-3940(01)02559-9
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Abstract

Since a deletion/insertion polymorphism in the promoter region of the apolipoprotein C-I (APOC1) gene has been reported to be associated with late-onset Alzheimer's disease (LOAD), we examined the hypothesis in a Korean population with 120 LOAD cases and 132 age-matched controls. The frequency of APOC1 insertion allele (H2) was significantly increased in LOAD than in controls, giving an odds ratio of 3.3 (95% CI 2.0-5.5, P<0.0001). Logistic regression analysis revealed that the interaction model between APOE epsilon4 and APOC1 H2 yielded larger odds ratio than other models including either APOE epsilon4 or APOC1 H2 alone. In addition, the association between APOC1 H2 and LOAD remained significant after adjustment of the effect of APOE epsilon4 (P=0.036). These results support previous observations that the APOC1 might be an additional susceptibility gene for LOAD.

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  • APOC1 insertion allele (H2) is significantly associated with an increased risk of late-onset AD, especially when interacting with APOE ε4.

    “Furthermore, APOC1 insertion allele (H2) is significantly associated with an increased risk of late-onset AD, especially when interacting with APOE ε4, indicating that APOC1 could be considered as a target for AD pathology [15].”

    From Association of APOC1 with cortical atrophy during conversion to Alzheimer’s disease (2025) · cites this paper as [15]

  • A study found that the association of APOC1 H2 with AD remained significant even after adjusting for APOE ε4 status, suggesting that the APOC1 allele may act as an independent risk factor.

    “For example, a study found that the association of APOC1 H2 with AD remained significant even after adjusting for APOE ε4 status, suggesting that the APOC1 allele may act as an independent risk factor [15].”

    From Association of APOC1 with cortical atrophy during conversion to Alzheimer’s disease (2025) · cites this paper as [15]

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Research works printed but not linked: 13

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  3. Kamino, 1996, Genetic association study between senile dementia of Alzheimer's type and APOE/C1/C2 gene cluster, Gerontology, 42, 12, 10.1159/000213820 · DOI
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  6. Poduslo, 1998, The apolipoprotein CI A allele as a risk factor for Alzheimer's disease, Neurochem. Res., 23, 361, 10.1023/A:1022409617539 · DOI
  7. Poduslo, 1995, A closely linked gene to apolipoprotein E may serve as an additional risk factor for Alzheimer's disease, Neurosci. Lett., 201, 81, 10.1016/0304-3940(95)12158-Z · DOI
  8. Quandt, 1995, MatInd and MatInspector: new fast and versatile tools for detection of consensus matches in nucleotide sequence data, Nucleic Acids Res., 23, 4878, 10.1093/nar/23.23.4878 · DOI
  9. Scacchi, 1999, Plasma levels of apolipoprotein E and genetic markers in elderly patients with Alzheimer's disease, Neurosci. Lett., 259, 33, 10.1016/S0304-3940(98)00889-1 · DOI · Paper page
  10. Smit, 1988, Apolipoprotein gene cluster on chromosome 19, Hum. Genet., 78, 90, 10.1007/BF00291243 · DOI
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  12. Tysoe, 1998, Apo E and Apo CI loci are associated with dementia in younger but not older late-onset cases, Dement. Geriatr. Cogn. Disord., 9, 191, 10.1159/000017046 · DOI
  13. Xu, 1999, A common HpaI RFLP of apolipoprotein C-I increases gene transcription and exhibits an ethnically distinct pattern of linkage disequilibrium with the alleles of apolipoprotein E, J. Lipid Res., 40, 50, 10.1016/S0022-2275(20)33338-1 · DOI

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Metadata

Authors
Ki, C.-S., Na, D. L., Kim, D. K., Kim, H. J., & Kim, J.-W.
Venue
Neuroscience Letters
Publisher
Elsevier BV
Published
2002-02
Volume
319
Issue
2
Pages
75-78
ISSN
0304-3940
DOI
10.1016/s0304-3940(01)02559-9
Cited by
37
References
0
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)

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