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

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–...

Full description

Saved in:
Bibliographic Details
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
Cell division
Copy number
Cytokines
Development and progression
Disease
Dopamine
Dopamine receptors
Enzyme-linked immunosorbent assay
Ethnicity
Genetic testing
Inflammation
Longitudinal studies
Mathematical models
Mitochondrial DNA
Movement disorders
Neurodegeneration
Neurodegenerative diseases
Oxidative stress
Parkinson's disease
Patients
Pramipexole
Risk factors
Telomerase
Telomeres
Type 2 diabetes
Variance analysis
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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.
ISSN:2073-4425
2073-4425
DOI:10.3390/genes14101913