scholarly journals Glutamate ionotropic receptor NMDA type subunit 2A ( GRIN 2A ) gene polymorphism (rs4998386) and Parkinson's disease susceptibility: A meta‐analysis

2019 ◽  
Vol 2 (3) ◽  
pp. 174-183
Author(s):  
Gaurav Nepal ◽  
Jessica Holly Rehrig ◽  
Rajeev Ojha
Open Medicine ◽  
2016 ◽  
Vol 11 (1) ◽  
pp. 578-583 ◽  
Author(s):  
Chen Weikang ◽  
Li Jie ◽  
Lan Likang ◽  
Qiu Weiwen ◽  
Lu Liping

AbstractThe aim of this meta-analysis was to evaluate whether there was an association between glutathione S-transferase M1(GSTM1)gene polymorphism and Parkinson’s disease (PD) susceptibility by pooling published data.We performed comprehensive electronic database search for articles published between February12,2015 and April30 2016. The published case-control or cohort studies related to GSTM1 gene polymorphism and Parkinson’s disease susceptibility were screened, reviewed, and included in this meta-analysis. The correlation between GSTM1 gene polymorphism and PD susceptibility was expressed by odds ratio (OR) and its corresponding 95% confidence interval (95%CI). Publication bias was evaluated by Begg’s funnel plot and Egger’s line regression test. All analysis was done by stata11.0 software.After searching the PubMed, EMBASE, and CNKI databases, seventeen case-control studies with 3,538 PD and 5,180 controls were included in the final meta-analysis. The data was pooled by a fixed-effect model for lack of statistical heterogeneity across the studies; the results showed GSTM1 null expression can significant increase the susceptibility of PD (OR=1.11, 95% CI:1.01-1.21, P<0.05). Subgroup analysis indicated GSTM1 gene polymorphism was associated with PD susceptibility in the Caucasian ethnic group (OR=1.15, 95% CI:1.05-1.27, P<0.05) but not in the Asian ethnic group (OR=0.89, 95% CI:0.70-1.12, P>0.05). Begg’s funnel plot and Egger’s line regression test showed no significant publication bias.Based on the present evidence, GSTM1 null expression can significant increase the susceptibility of PD in persons of Caucasian ethnicity.


2016 ◽  
Vol 37 (7) ◽  
pp. 1119-1126 ◽  
Author(s):  
Xianjing Zhao ◽  
Yanfeng Wu ◽  
Can Zhao ◽  
Meijiang Feng

Author(s):  
Lucinda Rawlings ◽  
Laura Turton ◽  
Stephen C. Mitchell ◽  
Glyn B. Steventon

Abstract Background The S-oxidation of S-carboxymethyl-L-cysteine has been reported previously to be a biomarker of disease susceptibility in Parkinson’s disease and amyotrophic lateral sclerosis. In the present investigation, the original observations have been extended and confirmed. Methods Meta-analysis of previously published investigations into the S-oxidation polymorphism together with new subject data was evaluated. Results The incidence of the poor metaboliser phenotype (no urinary recovery of S-oxide metabolites) was found to be 3%–7% within healthy and non-neurological disease populations, whereas 38% of the Parkinson’s disease subjects and 39% of the amyotrophic lateral sclerosis group were phenotyped as poor metabolisers. The consequent odds risk ratio of developing Parkinson’s disease was calculated to be 33.8 [95% confidence interval (CI), 13.3–86.1] and for amyotrophic lateral sclerosis was 35.2 (95% CI, 13.0–85.1). Conclusions The possible involvement of the enzyme responsible for this S-oxidation biotransformation reaction, phenylalanine hydroxylase, should be further investigated to elucidate its potential role in the mechanism(s) of toxicity in susceptible individuals displaying these diseases. The “Janus hypothesis,” possibly explaining why phenylalanine hydroxylase is a biomarker of neurodegenerative disease susceptibility, together with the general theme that this concept may apply to many other hitherto unsuspected enzyme systems, is presented.


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