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Molecular Neurobiology

, Volume 54, Issue 2, pp 977–982 | Cite as

A Missense Variant in TREML2 Reduces Risk of Alzheimer’s Disease in a Han Chinese Population

  • Teng Jiang
  • Yu Wan
  • Jun-Shan Zhou
  • Meng-Shan Tan
  • Qing Huang
  • Xi-Chen Zhu
  • Huan Lu
  • Hui-Fu Wang
  • Qi Chen
  • Lin Tan
  • Ying-Dong ZhangEmail author
  • Lan TanEmail author
  • Jin-Tai YuEmail author
Article

Abstract

Recently, Benitez and colleagues re-analyzed whole-exome sequencing data and revealed that a coding missense variant (rs3747742-C) in triggering receptor expressed on myeloid cells-like 2 (TREML2) gene reduced late-onset Alzheimer’s disease (LOAD) risk in Caucasians. To date, no study was carried out to test this association in other ethnic groups and populations, including Han Chinese. Therefore, the aim of the current study was to validate the relation between rs3747742 and LOAD susceptibility in a large Han Chinese population including 992 LOAD patients and 1358 healthy controls. In the total sample, the minor (C) allele of rs3747742 was associated with a reduced LOAD risk under the recessive genetic model after Bonferroni correction (odds ratio (OR) = 0.713; 95 % confidence interval (CI): 0.546–0.932; P = 0.013, Bonferroni-corrected P = 0.039). Interestingly, after stratifying data according to apolipoprotein E (APOE) ε4 status, we revealed that this protection only exists in APOE ε4 carriers (recessive genetic model, OR = 0.448; 95 % CI: 0.262–0.765; P = 0.003, Bonferroni-corrected P = 0.009) in our cohort. Taken together, our findings support rs3747742-C as a protective factor for LOAD, especially in APOE ε4 carriers.

Keywords

TREML2 Alzheimer’s disease Han Chinese Variant 

Notes

Compliance with Ethical Standards

Ethics Statement

The protocol for this study was approved by the Ethical Committee of Qingdao Municipal Hospital, and a written informed consent was obtained from each participant or the legal guardian.

Funding

This work was supported by National Natural Science Foundation of China to T.J. (81501092), J.T.Y. (81471309), and L.T. (81571245); Natural Science Foundation of Jiangsu Province to T.J. (BK20150091) and Y.D.Z. (BK20151084); China Postdoctoral Science Foundation to T.J. (2015 M580448); Qingdao Key Health Discipline Development Fund; Qingdao Outstanding Health Professional Development Fund; and Shandong Provincial Collaborative Innovation Center for Neurodegenerative Disorders.

Conflict of Interest

The authors declare that they have no competing interests.

Supplementary material

12035_2016_9706_MOESM1_ESM.docx (14 kb)
ESM 1 (DOCX 14 kb)
12035_2016_9706_MOESM2_ESM.docx (14 kb)
ESM 2 (DOCX 14 kb)

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Copyright information

© Springer Science+Business Media New York 2016

Authors and Affiliations

  • Teng Jiang
    • 1
    • 2
  • Yu Wan
    • 3
  • Jun-Shan Zhou
    • 1
  • Meng-Shan Tan
    • 3
  • Qing Huang
    • 1
  • Xi-Chen Zhu
    • 4
  • Huan Lu
    • 4
  • Hui-Fu Wang
    • 4
  • Qi Chen
    • 5
  • Lin Tan
    • 3
  • Ying-Dong Zhang
    • 1
    Email author
  • Lan Tan
    • 3
    • 4
    Email author
  • Jin-Tai Yu
    • 2
    Email author
  1. 1.Department of Neurology, Nanjing First HospitalNanjing Medical UniversityNanjingChina
  2. 2.Memory and Aging Center, Department of NeurologyUniversity of CaliforniaSan FranciscoUSA
  3. 3.Department of Neurology, Qingdao Municipal Hospital, School of MedicineQingdao UniversityQingdaoChina
  4. 4.Department of Neurology, Qingdao Municipal HospitalNanjing Medical UniversityNanjingChina
  5. 5.Key Laboratory of Cardiovascular Disease and Molecular Intervention, Department of PathophysiologyNanjing Medical UniversityNanjingChina

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