Preprint Article Version 2 Preserved in Portico This version is not peer-reviewed

Single Nucleotide Polymorphisms of Indoleamine 2,3-Dioxygenase Influenced the Age Onset of Parkinson’s Disease

Version 1 : Received: 7 October 2020 / Approved: 8 October 2020 / Online: 8 October 2020 (10:25:43 CEST)
Version 2 : Received: 3 June 2021 / Approved: 4 June 2021 / Online: 4 June 2021 (09:41:35 CEST)

A peer-reviewed article of this Preprint also exists.

Nóra Török, Rita Maszlag-Török, Kinga Molnár, Zoltán Szolnoki, Ferenc Somogyvári, Krisztina Boda, Masaru Tanaka, Péter Klivényi, László Vécsei. Single Nucleotide Polymorphisms of Indoleamine 2,3-Dioxygenase 1 Influenced the Age Onset of Parkinson's Disease. Front. Biosci. (Landmark Ed) 2022, 27(9), 265. https://doi.org/10.31083/j.fbl2709265 Nóra Török, Rita Maszlag-Török, Kinga Molnár, Zoltán Szolnoki, Ferenc Somogyvári, Krisztina Boda, Masaru Tanaka, Péter Klivényi, László Vécsei. Single Nucleotide Polymorphisms of Indoleamine 2,3-Dioxygenase 1 Influenced the Age Onset of Parkinson's Disease. Front. Biosci. (Landmark Ed) 2022, 27(9), 265. https://doi.org/10.31083/j.fbl2709265

Abstract

Aims 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) has 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. Main methods 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. Key findings 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. Significance 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.

Keywords

kynurenines; tryptophan; indoleamine 2,3-dioxygenase; single nucleotide polymorphisms; Parkinson’s diseases; neurodegenerative diseases

Subject

Medicine and Pharmacology, Neuroscience and Neurology

Comments (1)

Comment 1
Received: 4 June 2021
Commenter: Masaru Tanaka
Commenter's Conflict of Interests: Author
Comment: The manuscript was revised to the format of Life Sciences.
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