Longitudinal Changes in Mitochondrial DNA Copy Number and Telomere Length in Patients with Parkinson’s Disease

• Published in: Genes 2023-10, Vol.14 (10), p.1913
• Main Authors: Ortega-Vázquez, Alberto, Sánchez-Badajos, Salvador, Ramírez-García, Miguel Ángel, Alvarez-Luquín, Diana, López-López, Marisol, Adalid-Peralta, Laura Virginia, Monroy-Jaramillo, Nancy
• Format: Article
• Language: English
• Subjects: Activities of daily living; Aging; Analysis; Biomarkers; Blood tests; case-control studies; Cell division; Copy number; Cytokines; Development and progression; Disease; Dopamine; Dopamine receptors; Enzyme-linked immunosorbent assay; Ethnicity; Genetic testing; Inflammation; interleukin-17; Longitudinal studies; Mathematical models; mitochondria; Mitochondrial DNA; Movement disorders; Neurodegeneration; Neurodegenerative diseases; Oxidative stress; Parkinson's disease; pathophysiology; Patients; Pramipexole; risk; Risk factors; statistical models; Telomerase; Telomeres; Type 2 diabetes; Variance analysis
• ISSN: 2073-4425; 2073-4425
• DOI: 10.3390/genes14101913

Parkinson’s disease (PD) pathophysiology includes mitochondrial dysfunction, neuroinflammation, and aging as its biggest risk factors. Mitochondrial DNA copy number (mtDNA-CN) and telomere length (TL) are biological aging markers with inconclusive results regarding their association with PD. A case–control study was used to measure TL and mtDNA-CN using qPCR in PBMCs. PD patients were naive at baseline (T0) and followed-up at one (T1) and two (T2) years after the dopaminergic treatment (DRT). Plasmatic cytokines were determined by ELISA in all participants, along with clinical parameters of patients at T0. While TL was shorter in patients vs. controls at all time points evaluated (p < 0.01), mtDNA-CN showed no differences. An increase in mtDNA-CN and TL was observed in treated patients vs. naive ones (p < 0.001). Our statistical model analyzed both aging markers with covariates, showing a strong correlation between them (r = 0.57, p < 0.01), and IL-17A levels positively correlating with mtDNA-CN only in untreated patients (r = 0.45, p < 0.05). TL and mtDNA-CN could be useful markers for monitoring inflammation progression or treatment response in PD. DRT might modulate TL and mtDNA-CN, reflecting a compensatory mechanism to counteract mitochondrial dysfunction in PD, but this needs further investigation.