Alpha 2-Macroglobulin Polymorphisms and Susceptibility to Alzheimer's Disease: A Comprehensive Meta-Analysis Based on 62 Studies.

A2M Alpha 2-macroglobulin Alzheimer’s disease SNPs meta-analysis systematic review

Journal

Journal of Alzheimer's disease reports
ISSN: 2542-4823
Titre abrégé: J Alzheimers Dis Rep
Pays: Netherlands
ID NLM: 101705500

Informations de publication

Date de publication:
2023
Historique:
received: 15 09 2023
accepted: 09 11 2023
medline: 25 12 2023
pubmed: 25 12 2023
entrez: 25 12 2023
Statut: epublish

Résumé

The relationship between alpha 2-macroglobulin (A2M) gene and Alzheimer's disease (AD) has been widely studied across populations; however, the results are inconsistent. This study aimed to evaluate the association of A2M gene with AD by the application of meta-analysis. Relevant studies were identified by comprehensive searches. The quality of each study was assessed using the Newcastle-Ottawa Scale. Allele and genotype frequencies were extracted from each of the included studies. Odds ratio (OR) with corresponding 95% confidence intervals (CI) was calculated using a random-effects or fixed-effects model. The Cochran Q statistic and I A total of 62 studies were identified and included in the current meta-analysis. The G allele of rs226380 reduced AD risk (OR: 0.64, 95% CI: 0.47-0.87, pFDR = 0.012), but carrier with the TT genotype was more likely to develop AD in Asian populations (OR: 1.56, 95% CI: 1.12-2.19, pFDR = 0.0135). The V allele of the A2M-I/V (rs669) increased susceptibility to AD in female population (OR, 95% CI: 2.15, 1.38-3.35, pFDR = 0.0024); however, the II genotype could be a protective factor in these populations (OR, 95% CI: 0.43, 0.26-0.73, pFDR = 0.003). Sensitivity analyses confirmed the reliability of the original results. Existing evidence indicate that A2M single nucleotide polymorphisms (SNPs) may be associated with AD risk in sub-populations. Future studies with larger sample sizes will be necessary to confirm the results.

Sections du résumé

Background UNASSIGNED
The relationship between alpha 2-macroglobulin (A2M) gene and Alzheimer's disease (AD) has been widely studied across populations; however, the results are inconsistent.
Objective UNASSIGNED
This study aimed to evaluate the association of A2M gene with AD by the application of meta-analysis.
Methods UNASSIGNED
Relevant studies were identified by comprehensive searches. The quality of each study was assessed using the Newcastle-Ottawa Scale. Allele and genotype frequencies were extracted from each of the included studies. Odds ratio (OR) with corresponding 95% confidence intervals (CI) was calculated using a random-effects or fixed-effects model. The Cochran Q statistic and I
Results UNASSIGNED
A total of 62 studies were identified and included in the current meta-analysis. The G allele of rs226380 reduced AD risk (OR: 0.64, 95% CI: 0.47-0.87, pFDR = 0.012), but carrier with the TT genotype was more likely to develop AD in Asian populations (OR: 1.56, 95% CI: 1.12-2.19, pFDR = 0.0135). The V allele of the A2M-I/V (rs669) increased susceptibility to AD in female population (OR, 95% CI: 2.15, 1.38-3.35, pFDR = 0.0024); however, the II genotype could be a protective factor in these populations (OR, 95% CI: 0.43, 0.26-0.73, pFDR = 0.003). Sensitivity analyses confirmed the reliability of the original results.
Conclusions UNASSIGNED
Existing evidence indicate that A2M single nucleotide polymorphisms (SNPs) may be associated with AD risk in sub-populations. Future studies with larger sample sizes will be necessary to confirm the results.

Identifiants

pubmed: 38143774
doi: 10.3233/ADR-230131
pii: ADR230131
pmc: PMC10741958
doi:

Types de publication

Systematic Review

Langues

eng

Pagination

1351-1370

Informations de copyright

© 2023 – The authors. Published by IOS Press.

Déclaration de conflit d'intérêts

The authors have no conflict of interest to report.

Auteurs

Hongwei Zhang (H)

Department of Clinical Medicine, North Sichuan Medical College, Nanchong, Sichuan, China.
Department of Neurology, the Third People's Hospital of Chengdu, Chengdu, Sichuan, China.

Da Liu (D)

Department of Clinical Medicine, North Sichuan Medical College, Nanchong, Sichuan, China.
Department of Neurology, the Third People's Hospital of Chengdu, Chengdu, Sichuan, China.

Yuanyuan Duan (Y)

Department of Neurology, the People's Hospital of Mianyang, Mianyang, Sichuan, China.

Yan Liu (Y)

Department of Neurology, the Third People's Hospital of Chengdu, Chengdu, Sichuan, China.

Jianyu Liu (J)

Department of Neurology, the Third People's Hospital of Chengdu, Chengdu, Sichuan, China.

Na Bai (N)

Department of Neurology, the Sixth People's Hospital of Chengdu, Chengdu, Sichuan, China.

Qiang Zhou (Q)

Department of Neurology, the Third People's Hospital of Chengdu, Chengdu, Sichuan, China.

Zhiyao Xu (Z)

Department of Neurology, the Third People's Hospital of Chengdu, Chengdu, Sichuan, China.
Medical College of Southwest Jiaotong University, Chengdu, Sichuan, China.

Linyan Li (L)

Department of Clinical Medicine, North Sichuan Medical College, Nanchong, Sichuan, China.
Department of Neurology, the Third People's Hospital of Chengdu, Chengdu, Sichuan, China.

Hua Liu (H)

Department of Clinical Medicine, North Sichuan Medical College, Nanchong, Sichuan, China.
Department of Neurology, the Third People's Hospital of Chengdu, Chengdu, Sichuan, China.

Classifications MeSH