Abstract
Saitohin (STH) Q7R polymorphism has been reported to influence the individual's susceptibility to Alzheimer's disease (AD); however, conclusions remain controversial. Therefore, we performed this meta‐analysis to explore the association between STH Q7R polymorphism and AD risk. Systematic literature searches were performed in the PubMed, Embase, Cochrane Library and Web of Science for studies published before 31 August 2016. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated to assess the strength of the association using a fixed‐ or random‐effects model. Subgroup analyses, Galbraith plot and sensitivity analyses were also performed. All statistical analyses were performed with STATA Version 12.0. A total of 19 case–control studies from 17 publications with 4387 cases and 3972 controls were included in our meta‐analysis. The results showed that the Q7R polymorphism was significantly associated with an increased risk of AD in a recessive model (RR versus QQ+QR, OR = 1.27, 95% CI = 1.01–1.60, P = 0.040). After excluding the four studies not carried out in caucasians, the overall association was unchanged in all comparison models. Further subgroup analyses stratified by the time of AD onset, and the quality of included studies provided statistical evidence of significant increased risk of AD in RR versus QQ+QR model only in late‐onset subjects (OR = 1.56, 95% CI = 1.07–2.26, P = 0.021) and in studies with high quality (OR = 1.37, 95% CI = 1.01–1.86, P = 0.043). This meta‐analysis suggests that the RR genotype in saitohin Q7R polymorphism may be a human‐specific risk factor for AD, especially among late‐onset AD subjects and caucasian populations.
Highlights
Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine
19 case–control studies from 17 articles with 4387 cases and 3972 controls were included in our meta-analysis to determine the association between STH Q7R polymorphism and Alzheimer’s disease (AD) [3, 5,6,7,8,9,10,11,12,13,14,15,16, 21,22,23,24] (Table 1)
Many researchers have reported the association of AD with gene polymorphism, among which amyloid precursor protein (APP), PSEN1, PSEN2 and apolipoprotein E (APOE) gene are widely accepted as important risk factors in AD
Summary
The processes of AD could be triggered by many environmental factors, previous studies suggested that genetic polymorphisms play an important role in AD, among which mutations in amyloid precursor protein (APP), presenilin-1 (PSEN1), presenilin-2 (PSEN2) and STH, an intronless gene, was first discovered between exons 9 and 10 of the human microtubule-associated protein tau (MAPT) gene on chromosome 17q21.1 and rediscovered in MAPT 50 intron 11 [3, 4]. It encodes a 128-amino acid protein with no clear homologues [3].
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