Your browser doesn't support javascript.
loading
Longitudinal Changes in Mitochondrial DNA Copy Number and Telomere Length in Patients with Parkinson's Disease.
Ortega-Vázquez, Alberto; Sánchez-Badajos, Salvador; Ramírez-García, Miguel Ángel; Alvarez-Luquín, Diana; López-López, Marisol; Adalid-Peralta, Laura Virginia; Monroy-Jaramillo, Nancy.
Afiliación
  • Ortega-Vázquez A; Departamento de Sistemas Biológicos, Universidad Autónoma Metropolitana, Unidad Xochimilco, Mexico City 04960, Mexico.
  • Sánchez-Badajos S; Doctorado en Ciencias Biológicas y de la Salud, Universidad Autónoma Metropolitana, Unidad Xochimilco, Mexico City 04960, Mexico.
  • Ramírez-García MÁ; Departamento de Genética, Instituto Nacional de Neurología y Neurocirugía, Mexico City 14269, Mexico.
  • Alvarez-Luquín D; Laboratorio de Reprogramación Celular del Instituto de Fisiología Celular UNAM en el Instituto Nacional de Neurología y Neurocirugía, Mexico City 14269, Mexico.
  • López-López M; Departamento de Sistemas Biológicos, Universidad Autónoma Metropolitana, Unidad Xochimilco, Mexico City 04960, Mexico.
  • Adalid-Peralta LV; Laboratorio de Reprogramación Celular del Instituto de Fisiología Celular UNAM en el Instituto Nacional de Neurología y Neurocirugía, Mexico City 14269, Mexico.
  • Monroy-Jaramillo N; Departamento de Genética, Instituto Nacional de Neurología y Neurocirugía, Mexico City 14269, Mexico.
Genes (Basel) ; 14(10)2023 10 07.
Article en En | MEDLINE | ID: mdl-37895262
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.
Asunto(s)
Palabras clave
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Enfermedad de Parkinson / ADN Mitocondrial Límite: Humans Idioma: En Revista: Genes (Basel) Año: 2023 Tipo del documento: Article País de afiliación: México Pais de publicación: Suiza
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Enfermedad de Parkinson / ADN Mitocondrial Límite: Humans Idioma: En Revista: Genes (Basel) Año: 2023 Tipo del documento: Article País de afiliación: México Pais de publicación: Suiza