Apolipoprotein E, angiotensin-converting enzyme and kallikrein gene polymorphisms and the risk of Alzheimer’s disease and vascular dementia

Wang, H. K.; Fung, Hon-Chung; Hsu, Wen‐Chuin; Wu, Yih Ru; Jian, Lin; Ro, Long Sun; Chang, Kuo Hsuan; Hwu, F. J.; Hsu, Yu-Wei; Huang, Shiang-Yu; Lee‐Chen, Guey‐Jen; Chen, C. M.

doi:10.1007/s00702-005-0424-z

Cited by 42 publications

(18 citation statements)

References 54 publications

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“…Other results were that ACE D-allele might affect cognitive function and serum ACE level, implying a possible role for the development of a MCI to Alzheimer's disease (Zhang et al 2012). Thus, the results from this study support the hypothesis that the D-allele may be a genetic risk factor for the development of AD, consistent with the research results in Taiwanese people (Wang et al 2006). Thus, D-allele is speculated to increase the ACE activity level in human body, thereby increasing the onset risk of AD (Zhang et al 2012).…”

Section: Discussionsupporting

confidence: 86%

Association between ACE polymorphism, cognitive phenotype and APOE E4 allele in a Tunisian population with Alzheimer disease

et al. 2015

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Angiotensin-converting enzyme (ACE) has shown altered activity in patients with neurological diseases. An insertion/deletion (I/D) polymorphism of the ACE gene encoding angiotensin-converting enzyme has been reported to be associated with the risk for Alzheimer's disease (AD), and is generally considered to be a disorder primarily affecting memory. We conducted a case-control study in a sample composed of 85 sporadic AD patients and 90 age- and sex-matched controls to investigate the possible effect of the polymorphism and cognitive profile. Our data revealed an association between the ACE polymorphism and AD risk. There was a significant difference in the ACE allele or genotype frequencies between cases and controls. The D/D genotype showed an increased risk for AD and in the amnestic group and the effect was independent on ApoE genotypes.

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Section: Discussionsupporting

confidence: 86%

Association between ACE polymorphism, cognitive phenotype and APOE E4 allele in a Tunisian population with Alzheimer disease

et al. 2015

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“…Of the 20 reports focusing on the relationship between ApoE polymorphism and AD, 18 were from mainland171819202122232425262728293031323334, two were from Taiwan3536. The distribution of the genotypes in the control group was consistent with Hardy-Weinberg equilibrium (HWE).…”

Section: Resultsmentioning

confidence: 89%

Apolipoprotein E gene polymorphism and Alzheimer's disease in Chinese population: a meta-analysis

Liu

Bian

Zhang

et al. 2014

Sci Rep

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The relationship between Apolipoprotein E (ApoE) genotype and the risk of Alzheimer's disease (AD) is relatively well established in Caucasians, but less established in other ethnicities. To examine the association between ApoE polymorphism and the onset of AD in Chinese population, we searched the commonly used electronic databases between January 2000 and November 2013 for relevant studies. Total 20 studies, including 1576 cases and 1741 controls, were retrieved. The results showed statistically significant positive association between risk factor ε4 allele carriers and AD in Chinese population (OR = 3.93, 95% CI = 3.37–4.58, P < 0.00001). Genotype ApoE ε4/ε4 and ε4/ε3 have statistically significant association with AD as well (ε4/ε4: OR = 11.76, 95% CI = 6.38–21.47, P < 0.00001; ε4/ε3: OR = 3.08, 95% CI = 2.57–3.69, P < 0.00001). Furthermore, the frequency of the ApoE ε3 is lower in AD than that in the health controls, and the difference of ε3 allele is also statistically significant (OR = 0.42, 95% CI = 0.37–0.47, P < 0.00001). No significant heterogeneity was observed among all studies. This meta-analysis suggests that the subject with at least one ApoE ε4 allele has higher risk suffering from AD than controls in Chinese population. The results also provide a support for the protection effect of ApoE ε3 allele in developing AD.

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“…Otherwise, HWE, language, geographic location, quality of studies, sample size, publication time, source of controls and genotyping methods did not contribute the heterogeneity across the overall studies under other genetic comparisons (P>0.05) (Table S2 in File S1). Galbraith plots spotted at least fourteen studies (studies were spotted as the outliers in at least two genetic models) [11], [45], [47], [50], [56], [64], [65], [71], [72], [77], [80]–[82] as the outliers and the possible major sources of heterogeneity in the analyses of total studies (Figure S2a–e). It was noted that 9 [45], [50], [56], [64], [71], [72], [77], [81], [82] of these 14 studies belonged to Asian subgroup.…”

Section: Resultsmentioning

confidence: 99%

Angiotensin-Converting Enzyme Insertion/Deletion Polymorphism Is Not a Major Determining Factor in the Development of Sporadic Alzheimer Disease: Evidence from an Updated Meta-Analysis

et al. 2014

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Angiotensin-converting enzyme gene (ACE) insertion/deletion (I/D) polymorphism have long been linked to sporadic Alzheimer disease (SAD), but the established data remained controversial. To clarify this inconsistency, a comprehensive meta-analysis was conducted. Through searching of Pubmed, Embase, Alzgene, China National Knowledge Infrastructure (CNKI) and manually searching relevant references, 53 independent studies from 48 articles were included, involving a total of 8153 cases and 14932 controls. The strength of association was assessed by using odds ratios (ORs) with 95% confidence intervals (CIs). Further stratified analyses and heterogeneity analyses were tested, as was publication bias. Overall, significant associations were revealed between I/D polymorphism and SAD risk using allelic comparison (OR = 1.09, 95%CI = 1.01–1.17, p = 0.030), homozygote comparison (OR = 1.17, 95%CI = 1.01–1.34, p = 0.030) and the dominant model (OR = 1.16, 95%CI = 1.04–1.29, p = 0.008), but they were not sufficiently robust to withstand the false-positive report probability (FPRP) analyses. Otherwise, in subgroup analyses restricted to the high quality studies, the large sample size studies and studies with population-based controls, no significant association was observed in any genetic models. In summary, the current meta-analysis suggested that the ACE I/D polymorphism is unlikely to be a major determining factor in the development of SAD.

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Apolipoprotein E, angiotensin-converting enzyme and kallikrein gene polymorphisms and the risk of Alzheimer’s disease and vascular dementia

Cited by 42 publications

References 54 publications

Association between ACE polymorphism, cognitive phenotype and APOE E4 allele in a Tunisian population with Alzheimer disease

Association between ACE polymorphism, cognitive phenotype and APOE E4 allele in a Tunisian population with Alzheimer disease

Apolipoprotein E gene polymorphism and Alzheimer's disease in Chinese population: a meta-analysis

Angiotensin-Converting Enzyme Insertion/Deletion Polymorphism Is Not a Major Determining Factor in the Development of Sporadic Alzheimer Disease: Evidence from an Updated Meta-Analysis

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