Exploratory analysis shows IL-10 and IL-17A genetic variants influence risk and severity in Parkinson’s disease patients, suggesting a role in inflammation.
Background/Objective: Parkinson’s disease (PD) is the most common neurodegenerative movement disorder, in which the inflammatory hypothesis posits that dysregulation of the immune system is an important factor in its etiology. Based on our previous findings, we aimed to explore if promoter functional genetic variants in cytokines encoded by IL-10 and IL-17A, and a coding variant in the IL-13 gene, confer risk to the inflammatory profile of PD patients. Methods: For population genetic purposes, DNA samples from 239 patients with sporadic PD and 84 healthy controls were included and genotyped for IL-10_rs1800896, IL-10_rs1800872, IL-13_rs20541, IL-17A_rs2275913, and IL-17_rs8193036 variants by allelic discrimination in real-time PCR. All participants were Mexican Mestizos (MMs). Gene frequencies and haplotype association analyses were assessed. Then, a subgroup of 26 untreated PD patients and 21 controls were selected from this cohort for detailed biochemical and clinical data and evaluated by multivariate correlation analysis at the baseline and one year post-dopaminergic replacement treatment. Results and Conclusions: IL-17A_rs8193036 was found to be associated with increased PD risk (p < 0.010, OR = 1.91, CI95% = 1.22–2.98). The genetic variants IL-10_rs1800896, IL-10_rs1800872, and IL_17A_rs8193036 were related to the inflammatory process in sporadic MM PD patients, suggesting that they may play potential roles in the development and severity of the disease.
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Monroy‐Jaramillo et al. (2025) studied this question.
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