| Field |
Value |
| NCT Number |
NCT05963425 |
| Status |
ACTIVE_NOT_RECRUITING |
| Phase |
Not Applicable |
| Sponsor |
To be verified |
| Study Type |
Interventional |
| Intervention |
Physical Activity |
| Conditions |
Parkinson's Disease |
| Outcome Measures |
Mitochondrial function in skin fibroblasts |
¶ Physical Activity and Mitochondrial Health
Physical exercise has emerged as a potential disease-modifying intervention in Parkinson's disease. This study focuses on understanding the molecular mechanisms underlying exercise-induced neuroprotection, specifically through mitochondrial function modulation.
Key Rationale:
-
Mitochondrial dysfunction is a central hallmark of Parkinson's disease, involving impaired Complex I activity, reduced ATP production, and increased oxidative stress
-
Exercise activates multiple pathways that enhance mitochondrial biogenesis and function:
- PGC-1α (Peroxisome proliferator-activated receptor gamma coactivator 1-alpha) upregulation
- AMPK (AMP-activated protein kinase) activation
- Increased mitochondrial DNA copy number
- Enhanced electron transport chain complex activity
-
Skin fibroblasts serve as accessible peripheral biomarkers that reflect mitochondrial dysfunction in PD patients
The primary objective is to determine whether physical activity interventions can improve mitochondrial function in Parkinson's disease patients, as measured in skin fibroblast cultures.
- Design: Interventional study
- Allocation: To be determined
- Intervention: Physical activity program
- Primary Outcome: Change in mitochondrial function parameters in skin fibroblasts
Mitochondrial function assessments may include:
- Oxygen consumption rate (OCR)
- ATP production levels
- Mitochondrial membrane potential
- Reactive oxygen species (ROS) generation
- Mitochondrial DNA copy number
Based on the exercise-induced mitochondrial pathways, the study aims to demonstrate:
- Improved OCR: Increased oxygen consumption rate in skin fibroblasts
- Enhanced ATP Production: Restored cellular energy levels
- Reduced ROS: Decreased reactive oxygen species generation
- Mitochondrial Biogenesis: Increased mitochondrial DNA copy number
The expected outcomes are derived from known exercise pathways:
- PGC-1α Activation: Master regulator of mitochondrial biogenesis is activated by exercise
- AMPK Activation: Energy sensor activates catabolic pathways
- SIRT1 Activation: NAD+-dependent deacetylase enhances mitochondrial function
This trial addresses the critical question of whether exercise can genuinely modify disease progression in PD through mitochondrial mechanisms.
Potential Benefits:
- Non-pharmacological intervention with minimal side effects
- May enhance dopaminergic neuron survival
- Could improve motor and non-motor symptoms
- Accessible and cost-effective therapeutic approach
Positive results would support:
- Integration of structured exercise programs in PD care
- Development of exercise-mimetic compounds
- Personalized exercise prescriptions based on mitochondrial biomarkers
- Combination approaches with existing pharmacological treatments