| 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 |
Scientific Rationale
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:
...
Trial Overview
Mermaid diagram (expand to render)
| 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 |
Scientific Rationale
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:
Enhanced electron transport chain complex activity
Skin fibroblasts serve as accessible peripheral biomarkers that reflect mitochondrial dysfunction in PD patients
Study Objectives
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.
Methodology
Study Design
Design: Interventional study
Allocation: To be determined
Intervention: Physical activity program
Primary Outcome: Change in mitochondrial function parameters in skin fibroblasts
Assessment Parameters
Mitochondrial function assessments may include:
Oxygen consumption rate (OCR)
ATP production levels
Mitochondrial membrane potential
Reactive oxygen species (ROS) generation
Mitochondrial DNA copy number
Expected Outcomes Based on Mechanism
Primary Expected Outcomes
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
Mechanistic Rationale
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
Cross-References to NeuroWiki Mechanisms
[Mitochondrial Complex I Dysfunction](/mechanisms/mitochondrial-complex-i-dysfunction) — Target mechanism in PD
[PGC-1α Pathway in Parkinson's](/mechanisms/pgc1alpha-parkinsons-pathway) — Exercise-activated pathway
[AMPK Signaling in Neurodegeneration](/mechanisms/ampk-signaling-neurodegeneration) — Energy sensor pathway
[Mitophagy Pathway](/mechanisms/mitophagy-pathway) — Mitochondrial quality control
[Oxidative Stress in PD](/mechanisms/oxidative-stress-parkinsons) — ROS mechanism target
Therapeutic Implications
Exercise as Disease-Modifying Therapy
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
Implications for PD Treatment
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