Abstract
Folate metabolism plays quite a critical role in Parkinson’s disease (PD). Previous published research works have studied the link existing between the folate metabolism genetic polymorphisms and PD susceptibility; nevertheless, the results continue having controversies and inconclusiveness. Accordingly, we carried out the present meta-analysis for the assessment of the potential link between the folate metabolism genetic polymorphisms and the susceptibility to PD. In addition we carried out a literature search in the PubMed, EMBASE, Cochrane Library, and WanFang databases till November 10, 2018. The odds ratios (ORs) with corresponding 95% credible interval (95%CI) were put to use for evaluating the strength of the association of three folate metabolism genetic polymorphism ( C677T, A1298C, and A2756G) with the susceptibility to PD. Each statistical analysis was carried out with the use of STATA 15.0. An aggregate of twenty-one case-control investigations were retrieved, which involved 3,944 PD patients and 4,412 controls. We discovered the existence of no substantial link between the C677T and A1298C polymorphism and PD risk in any genetic framework comparisons. With regard to A2756G polymorphism, we discovered that there was an association between the A2756G genetic polymorphism and an augmented threat of PD in the co-dominant genetic framework (GG vs. AA: OR=1.86, 95%CI=1.02-3.37, P=0.042) and the recessive genetic model (GG vs. GA+AA: OR=1.90, 95%CI=1.06-3.41, P=0.031). To summarize, our research work indicates that the A2756G polymorphism of the folate metabolism gene had an association with an augmented threat of PD. Also, A1298C polymorphisms is unlikely to significantly contribute towards the susceptibility to PD. Further large-scale case-control studies are still required.
Highlights
Parkinson’s disease (PD) is termed as the second most frequently prevalent neurodegenerative disorder following the Alzheimer’s disease, which impacts approximately 1% of the individuals aged more than 60 across the globe and 4-5% of people aged more than 85 years [1, 2]
Despite the fact that the reason leading to the neuronal loss is not clear, more and more evidence has suggested that mitochondrial impairment, endothelial damage, inflammatory process, and oxidative stress are considered as playing key roles when it comes to the selective dopaminergic cell death in the brain of those patients, who have PD [4, 5]
In terms of Methylenetetrahydrofolate reductase (MTHFR) A2756G polymorphism, there was statistically significant association discovered in the co-dominant genetic model (GG vs. AA: Odds ratio (OR)=1.86, 95%confidence interval (CI)=1.02-3.37, P=0.042) and recessive genetic model (GG vs. AA+AG: OR=1.90, 95% credible interval (95%CI)=1.06-3.41, P=0.031) in the overall population (Figure 4A and 4B)
Summary
Parkinson’s disease (PD) is termed as the second most frequently prevalent neurodegenerative disorder following the Alzheimer’s disease, which impacts approximately 1% of the individuals aged more than 60 across the globe and 4-5% of people aged more than 85 years [1, 2]. PD is manifested by the classical motor symptoms, which include the tremor, and the rigidity, bradykinesia, and postural instability, significantly impacting the patients’ quality of life [2, 3]. These medicinal presentations constitute the results of dopaminergic neuron loss in the substantia nigra, leading the lowered degrees of dopamine in the striatum and disrupted motor control. Homocysteine (Hcy) has been observed as enhancing mitochondrial dysfunction, apoptosis, and oxidative stress, together with being a contributing determinant in the pathophysiological process to a number of neurodegenerative diseases that include PD [6, 7]. Methylenetetrahydrofolate reductase (MTHFR) is a folate-reliant enzyme that cata-
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