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1.
Effect of dietary vitamins C and E on the risk of Parkinson's disease: A meta-analysis.
Chang, MC, Kwak, SG, Kwak, S
Clinical nutrition (Edinburgh, Scotland). 2021;(6):3922-3930
Abstract
BACKGROUND & AIMS A neuroprotective effect of dietary vitamins C and E on Parkinson's disease (PD) has been suggested, however, several human studies have reported controversial results. Therefore, we conducted a meta-analysis on the effect of vitamins C and E on the risk of Parkinson's disease. METHODS A comprehensive literature search was conducted using the PubMed, EMBASE, Cochrane Library, and SCOPUS databases for studies published up to January 23, 2021. We included studies that reported (1) intake of vitamins C and E using validated methods; (2) assessment of odds ratio (OR), relative risk (RR), or hazard ratio (HR); and (3) patients with PD identified by a neurologist, hospital records, or death certificates. The Comprehensive Meta-Analysis Software 2 program was used for statistical analyses of the pooled data. RESULTS A total of 12 studies (four prospective cohort and eight case-control studies) were included in our meta-analysis. No significant risk reduction was observed in the high vitamin C intake group compared to low intake group. On the other hand, the high vitamin E intake group showed a significantly lower risk of development of PD than the low intake group (pooled OR = 0.799. 95% CI = 0.721 to 0.885). CONCLUSIONS We conclude that vitamin E might have a protective effect against PD, while vitamin C does not seem to have such an effect. However, the exact mechanism of the transport and regulation of vitamin E in the CNS remains elusive, and further studies would be necessary in this field.
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2.
Diet Quality and Risk of Parkinson's Disease: A Prospective Study and Meta-Analysis.
Liu, YH, Jensen, GL, Na, M, Mitchell, DC, Wood, GC, Still, CD, Gao, X
Journal of Parkinson's disease. 2021;(1):337-347
Abstract
BACKGROUND Several dietary components have been shown to be neuroprotective against risk of neurodegeneration. However, limited observational studies have examined the role of overall diet quality on risk of Parkinson's disease. OBJECTIVES We examined the associations between diet quality and risk of Parkinson's disease in a prospective cohort study and meta-analysis. METHODS Included in the cohort study were 3,653 participants (1,519 men and 2,134 women; mean age: 81.5 years) in the Geisinger Rural Aging Study longitudinal cohort in Pennsylvania. Diet quality was assessed using a validated dietary screening tool containing 25 food- and behavior-specific questions in 2009. Potential Parkinson's cases were identified using electronic health records based on ICD9 (332.*), ICD10 (G20), and Parkinson-related treatments. Hazard ratios (HRs) and 95% confidence intervals (CIs) across diet quality tertiles were calculated using Cox proportional hazards models after adjusting for potential confounders. We further performed a meta-analysis by pooling our study with four published papers on this topic. Random-effects model was utilized to calculate the pooled risk ratios and 95% CIs. RESULTS During a mean of 6.94 years of follow-up, 47 incident Parkinson's cases were documented. Having high diet quality at baseline was associated with lower Parkinson's disease risk (adjusted HR for the highest vs the lowest diet quality tertile = 0.39; 95% CI: 0.17, 0.89; p-trend = 0.02). The meta-analysis including 140,617 individuals also showed that adherence to high diet quality or a healthy dietary pattern was associated with lower risk of Parkinson's disease (pooled risk ratio = 0.64; 95% CI: 0.49, 0.83). CONCLUSION Having high diet quality or a healthy dietary pattern was associated with lower future risk of Parkinson's disease.
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3.
Causal Association between Periodontitis and Parkinson's Disease: A Bidirectional Mendelian Randomization Study.
Botelho, J, Machado, V, Mendes, JJ, Mascarenhas, P
Genes. 2021;(5)
Abstract
The latest evidence revealed a possible association between periodontitis and Parkinson's disease (PD). We explored the causal relationship of this bidirectional association through two-sample Mendelian randomization (MR) in European ancestry populations. To this end, we used openly accessible data of genome-wide association studies (GWAS) on periodontitis and PD. As instrumental variables for periodontitis, seventeen single-nucleotide polymorphisms (SNPs) from a GWAS of periodontitis (1817 periodontitis cases vs. 2215 controls) and eight non-overlapping SNPs of periodontitis from an additional GWAS for validation purposes. Instrumental variables to explore for the reverse causation included forty-five SNPs from a GWAS of PD (20,184 cases and 397,324 controls). Multiple approaches of MR were carried-out. There was no evidence of genetic liability of periodontitis being associated with a higher risk of PD (B = -0.0003, Standard Error [SE] 0.0003, p = 0.26). The eight independent SNPs (B = -0.0000, SE 0.0001, p = 0.99) validated this outcome. We also found no association of genetically primed PD towards periodontitis (B = -0.0001, SE 0.0001, p = 0.19). These MR study findings do not support a bidirectional causal genetic liability between periodontitis and PD. Further GWAS studies are needed to confirm the consistency of these results.
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4.
Association between vitamin D receptor polymorphisms and susceptibility to Parkinson's disease: An updated meta-analysis.
Gao, J, Teng, J, Liu, Z, Cai, M, Xie, A
Neuroscience letters. 2020;:134778
Abstract
The relationships between vitamin D receptor (VDR) gene polymorphisms, particularly ApaI, BsmI, FokI, and TaqI, and Parkinson's disease (PD) has received increasing attention in the research community. However, as the results yielded by this increased research have hitherto conflicted, we performed an updated meta-analysis of reports on the relationships between VDR polymorphisms and PD published before October 2019 that we collected from the PUBMED, EMBASE, EBSCO, China National Knowledge Infrastructure (CNKI), and Wanfang databases. The ten articles that met our screening criteria included 2782 patients and 3194 healthy controls. All the data that we received were analyzed with Stata 12.0 statistical software. The odds ratio (OR) and 95 % confidence intervals (CIs) were used to determine the relationship between VDR gene diversity and PD. While we did not find a significant correlation between the ApaI, BsmI, and TaqI polymorphisms and the risk of PD in any of the considered genetic models, we found a clear association between the FokI polymorphism and susceptibility to PD (C vs. T: OR = 1.246, 95 % CI: 1.101-1.411, P = 0; CC vs. TT: OR = 1.630, 95 % CI: 1.243-2.139, P = 0; CT vs. TT: OR = 1.382, 95 % CI: 1.059-1.804, P = 0.017; CC + CT vs. TT: OR = 1.491, 95 % CI: 1.159-1.919,P = 0.002; CC vs. CT + TT: OR = 1.261, 95 % CI: 1.062-1.496, P = 0.008). Our subgroup analysis performed according to ethnicity revealed that FokI increased the risk of PD in Asian populations (C vs. T: OR = 1.261, 95 % CI: 1.080-1.472, P = 0.003; CC vs. TT: OR = 1.664, 95 % CI: 1.189-2.330, P = 0.003; CT vs.TT: OR = 1.387, 95 % CI: 1.000-1.925, P = 0.05; CC + CT vs. TT: OR = 1.497, 95 % CI: 1.098-2.042, P = 0.011; CC vs. CT + TT: OR = 1.285, 95 % CI: 1.036-1.593, P = 0.022). Overall, the gene polymorphism of FokI only increases the risk of PD among Asian populations. Given the limited sample size of this study, the findings should be carefully explained.
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5.
Postmenopausal hormone therapy and Alzheimer's disease, dementia, and Parkinson's disease: A systematic review and time-response meta-analysis.
Wu, M, Li, M, Yuan, J, Liang, S, Chen, Z, Ye, M, Ryan, PM, Clark, C, Tan, SC, Rahmani, J, et al
Pharmacological research. 2020;:104693
Abstract
Hormone therapy continues to be a favourable option in the management of menopausal symptomatology, but the associated risk-benefit ratios with respect to neurodegenerative diseases remain controversial. The study aim was to determine the relation between menopausal hormone therapy and Alzheimer's disease, dementia, and Parkinson's disease in human subjects. A literature search was performed in PubMed/Medline, Cochrane collaboration, and Scopus databases from onset of the database to September 2019. Random-effects model was used to estimate pooled odd ratio (OR) and 95 % confidence intervals (CI). Subgroup analysis was performed based on the type and formulation of hormone. In addition, the time-response effect of this relationship was also assessed based on duration of hormone therapy. Associations between hormone therapy and Alzheimer's disease, dementia, and Parkinson's disease in menopausal women were reported in 28 studies. Pooled results with random effect model showed a significant association between hormone therapy and Alzheimer's disease (OR 1.08, 95 % CI 1.03-1.14, I2: 69 %). This relationship was more pronounced in patients receiving the combined estrogen-progestogen formulation. Moreover, a significant non-linear time-response association between hormone therapy and Alzheimer's disease was also identified (Coef1 = 0.0477, p1<0.001; Coef2 = -0.0932, p2<0.001). Similarly, pooled analysis revealed a significant association between hormone therapy and all-cause dementia (OR 1.16, 95 % CI 1.02-1.31, I2: 19 %). Interestingly, no comparable relationship was uncovered between hormone therapy as a whole and Parkinson's disease (OR 1.14, 95 % CI 0.95-1.38, I2: 65 %); however, sub-group analysis revealed a significant relationship between the disease and progestogen (OR 3.41, 95 % CI 1.23-9.46) or combined estrogen-progestogen formulation use (OR 1.49, 95 % CI 1.34-1.65). Indeed, this association was also found to be driven by duration of exposure (Coef1 = 0.0626, p1 = 0.04). This study reveals a significant direct relationship between the use of certain hormonal therapies and Alzheimer's disease, all-cause dementia, and Parkinson's disease in menopausal women. However, the association appears to shift in direct after five years in the context of Alzheimer's disease, adding further weight to the critical window or timing hypothesis of neurodegeneration and neuroprotection.
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6.
Selenium and Other Trace Elements in the Etiology of Parkinson's Disease: A Systematic Review and Meta-Analysis of Case-Control Studies.
Adani, G, Filippini, T, Michalke, B, Vinceti, M
Neuroepidemiology. 2020;(1):1-23
Abstract
BACKGROUND Parkinson's disease (PD) is the most common neurodegenerative disease after Alzheimer's dementia. Whereas the exact etiology of PD remains unknown, risk of developing PD seems to be related to a combination of genetic and environmental factors. This also includes abnormal exposure to trace elements of nutritional and toxicological interest. OBJECTIVES In this systematic review and meta-analysis, we summarized the results of case-control studies comparing levels of selenium, copper, iron, and zinc in PD patients and controls in either blood (whole blood, serum/plasma) or cerebrospinal fluid (CSF). METHODS We performed a systematic PubMed search selecting studies reporting trace element levels in different specimens of patients and controls. We performed a meta-analysis using a random-effect model to compute the weighted mean differences (WMD) and corresponding 95% CI of selenium, copper, iron, and zinc levels in the blood or CSF of patients and their matched controls. RESULTS We retrieved 56 papers reporting data for selenium (cases/controls: 588/721), copper (2,190/2,522), iron (2,956/3,469), and zinc (1,798/1,913) contents in CSF and blood. Cases showed considerably higher levels of selenium in CSF compared with controls (+51.6%; WMD 5.49; 95% CI 2.82 to 8.15), while levels in serum were similar (-0.2%; WMD -0.22; 95% CI -8.05 to 7.62). For copper, cases showed slightly higher levels in CSF and slightly lower concentrations in serum (+4.5%; WMD 1.87; 95% CI -3.59 to 7.33, and -4.5%; WMD -42.79; 95% CI -134.35 to 48.76, respectively). A slight increase was also found for CSF iron -levels (+9.5%; WMD 9.92; 1.23 to 18.61), while levels were -decreased in serum/plasma (-5.7%; WMD -58.19; 95% CI -106.49 to -9.89) and whole blood (-10.8%; WMD -95.69; 95% CI -157.73 to -33.65). Conversely, for zinc cases exhibited lower levels both in CSF (-10.8%; WMD -7.34; 95% CI -14.82 to 0.14) and serum/plasma (-7.5%; WMD -79.93; 95% CI -143.80 to -16.06). A longer duration of the disease tends to be associated with overall lower trace element levels in either CSF or blood. CONCLUSIONS Due to the study findings and the greater relevance of the CSF compartment compared with the circulating peripheral ones, this meta-analysis suggests that overexposure in the central nervous system to selenium, and possibly to copper and iron, may be a risk factor of the disease, while zinc might have a protective -effect.
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7.
A systematic review and meta-analysis of the associations of vitamin D receptor genetic variants with two types of most common neurodegenerative disorders.
Geng, J, Zhang, J, Yao, F, Liu, X, Liu, J, Huang, Y
Aging clinical and experimental research. 2020;(1):21-27
Abstract
BACKGROUND Whether vitamin D receptor (VDR) genetic variants influence individual susceptibility to neurodegenerative disorders remains controversial. AIMS This meta-analysis was conducted to analyze correlations of VDR genetic variants with two types of most common neurodegenerative disorders, Parkinson's disease (PD) and Alzheimer's disease (AD). METHODS Systematic literature research of PubMed and Embase was performed to identify eligible articles. Q test and I2 statistic were employed to decide whether pooled analyses would be performed with random-effect models (REMs) or fixed-effect models (FEMs). All statistical analyses were conducted with Review Manager. RESULTS Totally sixteen studies were enrolled for analyses. Among these eligible studies, ten studies were about PD (2356 cases and 2815 controls) and six studies were about AD (1256 cases and 1205 controls). Pooled overall analyses suggested that VDR rs7975232 (additive model: p = 0.03, OR = 1.19, 95% CI 1.01-1.39) and rs2228570 (recessive model: p < 0.008, OR = 1.26, 95% CI 1.06-1.50; allele model: p < 0.001, OR = 0.80, 95% CI 0.71-0.91) variants were significantly correlated with PD, and VDR rs731236 (dominant model: p = 0.003, OR = 0.70, 95% CI 0.56-0.89; additive model: p = 0.02, OR = 1.32, 95% CI 1.06-1.66; allele model: p = 0.02, OR = 0.82, 95% CI 0.69-0.96) variant was significantly correlated with AD. Further subgroup analyses by ethnicity revealed that the positive results were mainly driven by the Asians, whereas no significant associations were observed in Caucasians. CONCLUSION Our meta-analysis suggested that VDR rs7975232 and rs2228570 variants might serve as genetic biomarkers of PD, whereas VDR rs731236 variant might serve as a genetic biomarker of AD.
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8.
Association between ambient air pollution and Parkinson's disease: Systematic review and meta-analysis.
Hu, CY, Fang, Y, Li, FL, Dong, B, Hua, XG, Jiang, W, Zhang, H, Lyu, Y, Zhang, XJ
Environmental research. 2019;:448-459
Abstract
Air pollution has been evaluated as a possible risk factor for Parkinson's disease (PD), but, the present results are inconsistent and have not been combined. We performed a systematic review and meta-analysis to estimate the association between long-term exposure to ambient air pollution and PD, given the nature of disease etiology. A total of 10 studies were identified by searching Web of Science, Science Direct, and PubMed before October 2017. We found a significantly increased risk of PD with 10 parts per billion (ppb) increase in nitrogen oxides (NOx) exposure (relative risk (RR) = 1.06; 95% confidence interval (CI): 1.04, 1.09). The pooled RR for the association between carbon monoxide (CO) exposure, 1 parts per million (ppm) increment, and the risk of PD was 1.65 (95% CI: 1.10, 2.48). The pooled RRs for the association between nitrogen dioxide (NO2) and ozone (O3) exposure per 1 ppb increment, and the risk of PD were 1.01 (95% CI: 1.00, 1.03) and 1.01 (95% CI: 1.00, 1.02), respectively. There was a significant heterogeneity in the meta-analysis for fine particulate matter (PM2.5), NO2, sulfur dioxide (SO2), and CO. We concluded that NO2, NOx, CO and O3 exposure were associated with an increased risk of PD, although there is high risk of bias. The dose-response effects evaluated by high-quality studies are needed. Researches should be expanded to low- and/or middle- income countries where indoor and outdoor air pollution are high. CAPSULE Long-term exposure to ambient NO2, NOx, CO and O3 can increase the risk of Parkinson's disease.
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9.
Vitamin D receptor polymorphisms and the susceptibility of Parkinson's disease.
Wang, X, Shen, N, Lu, Y, Tan, K
Neuroscience letters. 2019;:206-211
Abstract
Epidemiological evidence concerning the association between vitamin D receptor (VDR) polymorphisms, including rs2228570, rs731236, rs7975232, rs1544410 and Parkinson's disease (PD) risk is inconsistent. A meta-analysis was performed to evaluate these associations via searching PubMed and EMBASE databases up to Jan 4, 2019. Odds ratio (OR) with 95% confidence interval (CI) were applied to assess the strength of these associations. 6 studies with 1391 PD cases and 1570 controls for rs2228570, 7 studies with 1881 PD cases and 2135 controls for rs731236, 5 studies with 1298 PD cases and 1536 controls for rs7975232, and 6 studies with 932 PD cases and 1377 controls for rs1544410 were included in this meta-analysis. Significant associations between rs2228570 and PD risk were found in allelic, dominant, and additive models but not in recessive model. Stratified study revealed that rs2228570 was associated with PD susceptibility in Asian population, while no significant association was observed in Caucasian population. Sensitivity analysis showed stable results for rs2228570 and no publication bias existed. Rs731236 was associated with increased PD risk in dominant model, however, this result was unstable. No significant association was found between rs7975232 or rs1544410 and PD.
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10.
Lee Silverman Voice Treatment (LSVT)-BIG to improve motor function in people with Parkinson's disease: a systematic review and meta-analysis.
McDonnell, MN, Rischbieth, B, Schammer, TT, Seaforth, C, Shaw, AJ, Phillips, AC
Clinical rehabilitation. 2018;(5):607-618
Abstract
OBJECTIVE The technique called Lee Silverman Voice Treatment (LSVT)-LOUD has previously been used to improve voice quality in people with Parkinson's disease. The objective of this study was to assess the effectiveness of an alternate intervention, LSVT-BIG (signifying big movements), to improve functional mobility. DESIGN Systematic review with meta-analysis of randomized trials. DATA SOURCES Medline, Embase, CINAHL, AgeLine, Scopus and Cochrane Library were searched from inception to September 2017 using multiple search terms related to Parkinson's disease and LSVT-BIG. REVIEW METHOD Two researchers searched the literature for studies of the LSVT-BIG intervention of 16 sessions, delivered by a certified instructor over four weeks, to any other intervention. Outcomes related to functional ability were included. Study quality was appraised using the Cochrane Risk of Bias tool. RESULTS Four studies were included, reporting on three randomized trials of 84 participants with mild Parkinson's disease. Compared to physiotherapy exercises, or a shorter training protocol, there was a significant improvement in motor function assessed with the Unified Parkinson's Disease Rating Scale part III (mean difference = -3.20, 95% confidence interval = -5.18 to -1.23) and a trend towards faster Timed Up and Go performance (mean difference = -0.47, 95% confidence interval = -0.99 to 0.06) and 10-metre walk test (mean difference = -0.53, 95% confidence interval = -1.07 to 0.01). CONCLUSION Compared to shorter format LSVT-BIG or general exercise, LSVT-BIG was more effective at improving motor function. This provides preliminary, moderate quality evidence that amplitude-oriented training is effective in reducing motor impairments for people with mild Parkinson's disease.