Association of paraoxonase 1 gene polymorphisms with risk of Parkinson’s disease: a meta-analysis

Zintzaras, Elias; Hadjigeorgiou, Georgios M.

doi:10.1007/s10038-004-0176-x

Cited by 105 publications

(82 citation statements)

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“…Recently, a number of meta-analyses investigating the association between gene polymorphisms and PD have been published. These meta-analyses involved: alpha-synuclein (Mellick et al 2005), the tau gene (Zhang et al 2005), the paraoxonase 1 gene (Zintzaras and Hadjigeorgiou 2004), APOE-[varepsilon2] (Huang et al 2004), the CYP2D6 polymorphism (Persad et al 2003), and the catechol-O-methyltransferase gene (Mizuta et al 2000).…”

Section: Discussionmentioning

confidence: 99%

“…Analyses were performed using Meta-Analyst (Joseph Lau, Boston, MA, 1998), SAS software, and CVF90 with IMLS library (Whitehead 2002;Zintzaras and Hadjigeorgiou 2004;.…”

Section: Meta-analysismentioning

confidence: 99%

“…In two studies (Momose et al 2002;Parsian et al 2004), the distribution of genotypes in the control group was not in HWE (P=0.03 and <0.01, respectively), indicating genotyping errors and/or population stratification (Xu et al 2002;Zintzaras and Hadjigeorgiou 2004). Therefore, a sensitivity analysis was carried out for these studies; however, the results produced should be interpreted with caution.…”

Section: Summary Statisticsmentioning

confidence: 99%

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The role of G196A polymorphism in the brain-derived neurotrophic factor gene in the cause of Parkinson’s disease: a meta-analysis

Ζιντζαράς

Hadjigeorgiou

2005

J Hum Genet

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The association between Parkinson's disease (PD) and the G196A polymorphism in the brain-derived neurotrophic factor (BDNF) gene has been investigated in several case-control studies, producing contradictory results: one study indicated that homozygocity of AA is associated with PD, another study produced the opposite result, whereas other studies found no association. To investigate these contradictory findings, a metaanalysis of all available association studies between the G196A polymorphism and the risk of developing PD was conducted. Four out of six identified studies included populations of East Asian descent, and two included populations of European descent (Whites). Overall, the meta-analysis of the allele contrast (A vs G) suggested large heterogeneity between studies (P=0.07, I 2 =51%) and no association between G196A and the risk of developing PD: random effects odds ratio (OR)=1.00 [95% CI (0.85, 1.18)]. The sensitivity analysis (exclusion of two studies: one East Asian and one White) with the controls not in Hardy-Weinberg equilibrium showed large heterogeneity (P=0.10, I 2 =52%) and no significant association: random effects OR=0.94 [95% CI (0.77, 1.15)]. The subgroup analyses for East Asians and Whites produced no significant association. In addition, the contrast of homozygotes, and the dominant and recessive models for allele A did not support a major role for this polymorphism in the pathogenesis of PD. There were no sources of bias in the selected studies, and the differential magnitude of effect in large vs small studies was not significant. The metaanalysis results suggest that the involvement of the BDNF gene in susceptibility to PD merits further exploration with larger and more rigorous population association studies.

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Section: Discussionmentioning

confidence: 99%

“…Analyses were performed using Meta-Analyst (Joseph Lau, Boston, MA, 1998), SAS software, and CVF90 with IMLS library (Whitehead 2002;Zintzaras and Hadjigeorgiou 2004;.…”

Section: Meta-analysismentioning

confidence: 99%

Section: Summary Statisticsmentioning

confidence: 99%

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The role of G196A polymorphism in the brain-derived neurotrophic factor gene in the cause of Parkinson’s disease: a meta-analysis

Ζιντζαράς

Hadjigeorgiou

2005

J Hum Genet

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“…Only studies that used validated genotyping methods were considered, and the distribution of the genotypes in the control group was tested for Hardy-Weinberg equilibrium (HWE) (P Ն .05). [16][17][18] Finally, studies based on pedigree data were excluded because they investigate linkage and not association. 19 Data Abstraction.…”

Section: Selection Of Studiesmentioning

confidence: 99%

“…Studies with controls not in HWE were subjected to a sensitivity analysis. 17,18 In sensitivity analysis, the effect of excluding specific studies was examined. Analyses were performed using Meta-Analyst (Lau, Boston, MA), and CVF90.…”

Section: Selection Of Studiesmentioning

confidence: 99%

Do alcohol-metabolizing enzyme gene polymorphisms increase the risk of alcoholism and alcoholic liver disease?

et al. 2006

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Case-control studies that have investigated the association between alcoholism and alcoholinduced liver damage and the ADH2, ADH3, CYP2E1, and ADLH2 polymorphisms have reported controversial or inconclusive results. Thus, we conducted a meta-analysis of 50 association studies of the above polymorphisms. We explored potential sources of heterogeneity and bias, performed subgroup analyses by racial background and sex, performed sensitivity analyses for studies not in Hardy-Weinberg equilibrium, and performed a subgroup analysis for cases that met strict criteria for alcoholism. The present meta-analysis underscores significant associations of ADH2*1, ADH3*2, and ALDH2* . When strict criteria were imposed, the pattern of results remained unaltered. For liver disease, there were no significant associations for ADH2*1, ADH3*2, or ALDH2*1 in all subpopulations. The CYP2E1 polymorphism showed no association whatsoever. There is evidence that alleles are mainly dominant. In conclusion, there was heterogeneity between studies in alcoholism for ADH2, ADH3, and ALDH2, and lack of bias in all polymorphisms. The above findings reinforce the need for more rigorous studies, and for regular synthesis of studies' results. O ver the last few years, an increasing number of studies have provided compelling evidence for the involvement of genetically defined predisposing factors in alcoholism and alcohol-induced cirrhosis. The strongest support comes from the fact that not all subjects with a high daily intake of alcohol develop alcohol-induced liver disease. Mostly metabolized in the liver by the successive action of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH), the rate of conversion of ingested ethanol to acetaldehyde, and of acetaldehyde to acetate, is influenced by genetic polymorphisms at both loci. ALDH2 is the most important gene that affects predisposition to alcoholism in Asian populations. Thus, the prevalence in these populations of the inactive ALDH enzymatic form encoded by the ALDH2*2 allele appears to protect against alcoholism. 1 Furthermore, alcoholics with this inactive allele may be at great risk for advanced alcoholic liver disease. [2][3][4] Regarding the ADH gene cluster, polymorphisms are also detected at the ADH2 and ADH3 loci with two alleles (referred to as *1 and *2) each. Alleles ADH2*2 and ADH3*1 encode, respectively, for the highly active ␤ 2 and ␥ 1 allozymes, 5 and a low prevalence of both alleles has been reported in alcoholic Asians-although some studies did not detect associations between ADH3 polymor-

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Angiotensin-Converting Enzyme Insertion/Deletion Gene Polymorphic Variant as a Marker of Coronary Artery Disease<subtitle>A Meta-analysis</subtitle>

Ζιντζαράς¹

2008

Arch Intern Med

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114

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Background: Many studies have investigated the association between the angiotensin-converting enzyme (ACE) gene insertion (I)/deletion (D) polymorphic variant and coronary artery disease (CAD). However, the evidence is inadequate to draw robust conclusions because most studies were generally small and conducted in heterogeneous samples. To shed light on these inconclusive findings, we conducted a meta-analysis of studies relating the ACE I/D polymorphic variant to the risk of CAD.Methods: We searched the PubMed database for Englishlanguage articles on CAD in humans. We estimated summary odds ratios and explored potential sources of heterogeneity and bias. Results:The 118 studies chosen for the analysis involved 43 733 cases with CAD and 82 606 controls. The heterogeneity between studies was significant. When we compared homozygotes with the D and I alterations, the ACE I/D polymorphic variant was associated with a 25% increased risk of CAD (odds ratio, 1.25; 95% confidence interval, 1.16-1.35). Subgroup analyses for myocardial infarction, diabetes mellitus, male sex, white race, East Asian subjects, and Turkish subjects showed significant associations. No association was found in other racial/ethnic groups, in women, in premature cases, or in cases with low levels of risk factors. The major sources of heterogeneity were due to racial/ethnic diversity, genotyping procedure, and age matching. Cumulative meta-analysis for the allelic contrast showed a trend of association as information accumulated. There was a differential magnitude of effect in large vs small studies. Conclusions:The meta-analysis demonstrated evidence of a modest positive association between ACE I/D polymorphic variant and CAD. The meta-analysis also highlights the heterogeneity of reported results, considerable gaps in research, and the need for future studies focused on certain high-risk patient populations.

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Association of paraoxonase 1 gene polymorphisms with risk of Parkinson’s disease: a meta-analysis

Cited by 105 publications

References 24 publications

The role of G196A polymorphism in the brain-derived neurotrophic factor gene in the cause of Parkinson’s disease: a meta-analysis

The role of G196A polymorphism in the brain-derived neurotrophic factor gene in the cause of Parkinson’s disease: a meta-analysis

Do alcohol-metabolizing enzyme gene polymorphisms increase the risk of alcoholism and alcoholic liver disease?

Angiotensin-Converting Enzyme Insertion/Deletion Gene Polymorphic Variant as a Marker of Coronary Artery Disease<subtitle>A Meta-analysis</subtitle>

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