Association of tripartite motif family-like 2 (TRIML2) polymorphisms with late-onset Alzheimer's disease risk in a Korean population

Won Sub Kang, Jin Kyung Park, Young Jong Kim, Ah Rang Cho, Hae Jeong Park, Su Kang Kim, Jong Woo Paik, Kang Joon Lee, Hae Ri Na, Young Youl Kim, Hyun Kook Lim, Hyun-Ghang Jeong, Jong Woo Kim

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Abstract

Apoptosis is a prominent feature in the progression of Alzheimer's disease (AD), regulated in part by the activity of p53. As tripartite motif family-like 2 (TRIML2), a member of the TRIM family of proteins, has been implicated in the regulation of p53-mediated apoptosis, we hypothesized that TRIML2 polymorphisms may result in an increased AD susceptibility. Here, we investigated the association between coding region single nucleotide polymorphisms (cSNPs) in TRIML2 and AD in a Korean population. Two cSNPs (rs79698746 and rs2279551) were genotyped using the Sequenom iPLEX® Gold assay and direct sequencing in 162 AD patients and 191 controls. Multiple logistic regression models were used to determine the odds ratios, 95% confidence intervals, and p-values. Significant associations were observed between AD and the allelic frequencies of two SNPs (rs79698746, p = 0.007; rs2279551, p = 0.01); genotype frequencies were also significantly different between the two groups [rs79698746: p = 0.003 in the codominant 2 model (CC vs. TT), p = 0.01 in the dominant model (TC/CC vs. TT), p = 0.016 in the recessive model (CC vs. TT/TC), and p = 0.0025 in the log-additive model (TC vs. CC vs. TT); rs2279551: p = 0.003 in the codominant 2 model (CC vs. TT), p = 0.011 in the dominant model (TC/CC vs. TT), p = 0.019 in the recessive model (CC vs. TT/TC), and p = 0.0028 in the log-additive model (TC vs. CC vs. TT)]. In the haplotype analyses, CC haplotypes containing two cSNPs were significantly associated with AD (p = 0.013). Taken together, these findings indicate that the C allele of both SNPs was associated with an increased risk of AD. These results suggest that TRIML2 may contribute to AD susceptibility.

Original languageEnglish
Pages (from-to)127-131
Number of pages5
JournalNeuroscience Letters
Volume630
DOIs
Publication statusPublished - 2016 Sep 6

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Alzheimer Disease
Single Nucleotide Polymorphism
Population
Disease Susceptibility
Haplotypes
Logistic Models
Apoptosis
Gold
Alleles
Odds Ratio
Genotype
Confidence Intervals

Keywords

  • Alzheimer's disease
  • Apoptosis
  • Tripartite motif family-like 2 (TRIML2) gene

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Association of tripartite motif family-like 2 (TRIML2) polymorphisms with late-onset Alzheimer's disease risk in a Korean population. / Kang, Won Sub; Park, Jin Kyung; Kim, Young Jong; Cho, Ah Rang; Park, Hae Jeong; Kim, Su Kang; Paik, Jong Woo; Lee, Kang Joon; Na, Hae Ri; Kim, Young Youl; Lim, Hyun Kook; Jeong, Hyun-Ghang; Kim, Jong Woo.

In: Neuroscience Letters, Vol. 630, 06.09.2016, p. 127-131.

Research output: Contribution to journalArticle

Kang, WS, Park, JK, Kim, YJ, Cho, AR, Park, HJ, Kim, SK, Paik, JW, Lee, KJ, Na, HR, Kim, YY, Lim, HK, Jeong, H-G & Kim, JW 2016, 'Association of tripartite motif family-like 2 (TRIML2) polymorphisms with late-onset Alzheimer's disease risk in a Korean population', Neuroscience Letters, vol. 630, pp. 127-131. https://doi.org/10.1016/j.neulet.2016.07.046
Kang, Won Sub ; Park, Jin Kyung ; Kim, Young Jong ; Cho, Ah Rang ; Park, Hae Jeong ; Kim, Su Kang ; Paik, Jong Woo ; Lee, Kang Joon ; Na, Hae Ri ; Kim, Young Youl ; Lim, Hyun Kook ; Jeong, Hyun-Ghang ; Kim, Jong Woo. / Association of tripartite motif family-like 2 (TRIML2) polymorphisms with late-onset Alzheimer's disease risk in a Korean population. In: Neuroscience Letters. 2016 ; Vol. 630. pp. 127-131.
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abstract = "Apoptosis is a prominent feature in the progression of Alzheimer's disease (AD), regulated in part by the activity of p53. As tripartite motif family-like 2 (TRIML2), a member of the TRIM family of proteins, has been implicated in the regulation of p53-mediated apoptosis, we hypothesized that TRIML2 polymorphisms may result in an increased AD susceptibility. Here, we investigated the association between coding region single nucleotide polymorphisms (cSNPs) in TRIML2 and AD in a Korean population. Two cSNPs (rs79698746 and rs2279551) were genotyped using the Sequenom iPLEX{\circledR} Gold assay and direct sequencing in 162 AD patients and 191 controls. Multiple logistic regression models were used to determine the odds ratios, 95{\%} confidence intervals, and p-values. Significant associations were observed between AD and the allelic frequencies of two SNPs (rs79698746, p = 0.007; rs2279551, p = 0.01); genotype frequencies were also significantly different between the two groups [rs79698746: p = 0.003 in the codominant 2 model (CC vs. TT), p = 0.01 in the dominant model (TC/CC vs. TT), p = 0.016 in the recessive model (CC vs. TT/TC), and p = 0.0025 in the log-additive model (TC vs. CC vs. TT); rs2279551: p = 0.003 in the codominant 2 model (CC vs. TT), p = 0.011 in the dominant model (TC/CC vs. TT), p = 0.019 in the recessive model (CC vs. TT/TC), and p = 0.0028 in the log-additive model (TC vs. CC vs. TT)]. In the haplotype analyses, CC haplotypes containing two cSNPs were significantly associated with AD (p = 0.013). Taken together, these findings indicate that the C allele of both SNPs was associated with an increased risk of AD. These results suggest that TRIML2 may contribute to AD susceptibility.",
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AU - Kim, Young Jong

AU - Cho, Ah Rang

AU - Park, Hae Jeong

AU - Kim, Su Kang

AU - Paik, Jong Woo

AU - Lee, Kang Joon

AU - Na, Hae Ri

AU - Kim, Young Youl

AU - Lim, Hyun Kook

AU - Jeong, Hyun-Ghang

AU - Kim, Jong Woo

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N2 - Apoptosis is a prominent feature in the progression of Alzheimer's disease (AD), regulated in part by the activity of p53. As tripartite motif family-like 2 (TRIML2), a member of the TRIM family of proteins, has been implicated in the regulation of p53-mediated apoptosis, we hypothesized that TRIML2 polymorphisms may result in an increased AD susceptibility. Here, we investigated the association between coding region single nucleotide polymorphisms (cSNPs) in TRIML2 and AD in a Korean population. Two cSNPs (rs79698746 and rs2279551) were genotyped using the Sequenom iPLEX® Gold assay and direct sequencing in 162 AD patients and 191 controls. Multiple logistic regression models were used to determine the odds ratios, 95% confidence intervals, and p-values. Significant associations were observed between AD and the allelic frequencies of two SNPs (rs79698746, p = 0.007; rs2279551, p = 0.01); genotype frequencies were also significantly different between the two groups [rs79698746: p = 0.003 in the codominant 2 model (CC vs. TT), p = 0.01 in the dominant model (TC/CC vs. TT), p = 0.016 in the recessive model (CC vs. TT/TC), and p = 0.0025 in the log-additive model (TC vs. CC vs. TT); rs2279551: p = 0.003 in the codominant 2 model (CC vs. TT), p = 0.011 in the dominant model (TC/CC vs. TT), p = 0.019 in the recessive model (CC vs. TT/TC), and p = 0.0028 in the log-additive model (TC vs. CC vs. TT)]. In the haplotype analyses, CC haplotypes containing two cSNPs were significantly associated with AD (p = 0.013). Taken together, these findings indicate that the C allele of both SNPs was associated with an increased risk of AD. These results suggest that TRIML2 may contribute to AD susceptibility.

AB - Apoptosis is a prominent feature in the progression of Alzheimer's disease (AD), regulated in part by the activity of p53. As tripartite motif family-like 2 (TRIML2), a member of the TRIM family of proteins, has been implicated in the regulation of p53-mediated apoptosis, we hypothesized that TRIML2 polymorphisms may result in an increased AD susceptibility. Here, we investigated the association between coding region single nucleotide polymorphisms (cSNPs) in TRIML2 and AD in a Korean population. Two cSNPs (rs79698746 and rs2279551) were genotyped using the Sequenom iPLEX® Gold assay and direct sequencing in 162 AD patients and 191 controls. Multiple logistic regression models were used to determine the odds ratios, 95% confidence intervals, and p-values. Significant associations were observed between AD and the allelic frequencies of two SNPs (rs79698746, p = 0.007; rs2279551, p = 0.01); genotype frequencies were also significantly different between the two groups [rs79698746: p = 0.003 in the codominant 2 model (CC vs. TT), p = 0.01 in the dominant model (TC/CC vs. TT), p = 0.016 in the recessive model (CC vs. TT/TC), and p = 0.0025 in the log-additive model (TC vs. CC vs. TT); rs2279551: p = 0.003 in the codominant 2 model (CC vs. TT), p = 0.011 in the dominant model (TC/CC vs. TT), p = 0.019 in the recessive model (CC vs. TT/TC), and p = 0.0028 in the log-additive model (TC vs. CC vs. TT)]. In the haplotype analyses, CC haplotypes containing two cSNPs were significantly associated with AD (p = 0.013). Taken together, these findings indicate that the C allele of both SNPs was associated with an increased risk of AD. These results suggest that TRIML2 may contribute to AD susceptibility.

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