Version 1
: Received: 18 September 2020 / Approved: 20 September 2020 / Online: 20 September 2020 (14:27:12 CEST)
How to cite:
Török, N.; Maszlag-Török, R.; Molnár, K.; Szolnoki, Z.; Somogyvári, F.; Boda, K.; Tanaka, M.; Klivényi, P.; Vécsei, L. Single Nucleotide Polymorphisms of Indoleamine 2,3-Dioxygenase 1 Influenced the Age Onset of Parkinson’s Disease. Preprints2020, 2020090470. https://doi.org/10.20944/preprints202009.0470.v1
Török, N.; Maszlag-Török, R.; Molnár, K.; Szolnoki, Z.; Somogyvári, F.; Boda, K.; Tanaka, M.; Klivényi, P.; Vécsei, L. Single Nucleotide Polymorphisms of Indoleamine 2,3-Dioxygenase 1 Influenced the Age Onset of Parkinson’s Disease. Preprints 2020, 2020090470. https://doi.org/10.20944/preprints202009.0470.v1
Török, N.; Maszlag-Török, R.; Molnár, K.; Szolnoki, Z.; Somogyvári, F.; Boda, K.; Tanaka, M.; Klivényi, P.; Vécsei, L. Single Nucleotide Polymorphisms of Indoleamine 2,3-Dioxygenase 1 Influenced the Age Onset of Parkinson’s Disease. Preprints2020, 2020090470. https://doi.org/10.20944/preprints202009.0470.v1
APA Style
Török, N., Maszlag-Török, R., Molnár, K., Szolnoki, Z., Somogyvári, F., Boda, K., Tanaka, M., Klivényi, P., & Vécsei, L. (2020). Single Nucleotide Polymorphisms of Indoleamine 2,3-Dioxygenase 1 Influenced the Age Onset of Parkinson’s Disease. Preprints. https://doi.org/10.20944/preprints202009.0470.v1
Chicago/Turabian Style
Török, N., Péter Klivényi and László Vécsei. 2020 "Single Nucleotide Polymorphisms of Indoleamine 2,3-Dioxygenase 1 Influenced the Age Onset of Parkinson’s Disease" Preprints. https://doi.org/10.20944/preprints202009.0470.v1
Abstract
Earlier studies reported alterations of the kynurenine (KYN) pathway of tryptophan (TRP) metabolism in Parkinson’s disease (PD). The first rate-limiting enzymes indoleamine 2,3-dioxygenase (IDO) and tryptophan dioxygenase were observed upregulated, resulting elevated KYN/TRP ratios in the serum and cerebrospinal fluid samples of patients with PD. An increasing number of single nucleotide polymorphisms (SNPs) have been identified in a population of PD. However, little is known if genetic variations of the IDO contribute to disturbance of the KYN metabolism in and the pathogenesis of PD. SNP analysis of IDO1 was performed by allelic discrimination assay with fluorescently labelled TaqMan probes and a subgroup analysis was conducted according to the age of PD onset. The frame shifts variant rs34155785, intronic variant rs7820268, and promotor region variant rs9657182 SNPs of 105 PD patients without comorbidity were analyzed and compared to 129 healthy controls. No significant correlation was found in three SNPs between PD patients and healthy controls. However, the subgroup analysis revealed that A alleles of rs7820268 SNP or rs9657182 SNP carriers contribute to later onset of PD than non-carriers. The study suggested that SNPs of IDO1 influenced the age onset of PD and genotyping of SNPs in certain alleles potentially serves as a risk biomarker of PD.
Medicine and Pharmacology, Neuroscience and Neurology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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