Parkinson’s Disease and mitochondria are deeply interconnected through the process of energy production. Mitochondria, often called the “powerhouses” of our cells, generate ATP, the essential energy currency that fuels every function in the body. In Parkinson’s Disease, mitochondrial dysfunction has emerged as a core factor in disease progression.

Scientists are now exploring how nutrition, lifestyle strategies, and emerging therapies can support mitochondrial health in Parkinson’s Disease, potentially slowing symptom progression and improving long-term quality of life.

The Role of Mitochondria in Parkinson’s Disease

Neurons have high energy demands, relying on mitochondria to function efficiently. When these energy systems falter, it leads to:

• Energy deficits: Neurons lose their ability to communicate effectively.
• Oxidative stress: Faulty mitochondria release damaging free radicals.
• Protein aggregation: Misfolded proteins accumulate, harming brain cells.
• Inflammation: Damaged mitochondria can trigger immune responses in the brain.

This creates a vicious cycle, mitochondrial dysfunction worsens oxidative stress and protein misfolding, which in turn further impairs mitochondrial function, driving neurodegeneration in Parkinson’s Disease.

Lifestyle Approaches: Supporting Mitochondria from the Top Down

A top-down approach considers the whole person, looking at how daily choices impact mitochondrial resilience.

• Exercise: Regular physical activity promotes mitochondrial biogenesis (the creation of new mitochondria) and improves cellular efficiency. In Parkinson’s, consistent movement supports brain energy metabolism and enhances motor control.
• Diet: A Mediterranean-style diet for Parkinson’s Disease, rich in antioxidants, healthy fats, and plant-based compounds, helps protect mitochondria by reducing oxidative stress and inflammation.
• Sleep and Stress Management: Quality sleep supports mitochondrial repair, while chronic stress accelerates oxidative damage. Mindful practices such as yoga, breathing exercises, or gentle stretching may help regulate mitochondrial balance.

Scientific and Clinical Approaches: Working from the Bottom Up

The bottom-up approach focuses on therapies that directly target mitochondrial energy systems:

• Boosting energy metabolism:
  • Supplements like vitamin B3 (nicotinamide riboside) support mitochondrial energy pathways by replenishing NAD, a key molecule for ATP production.
  • Early clinical trials show promising improvements in energy balance within neurons.
• Direct mitochondrial targeting:
  • Drugs such as UDCA (ursodeoxycholic acid) have been shown to enhance brain mitochondrial activity in early studies. Ongoing trials aim to determine whether this can slow Parkinson’s Disease progression.
• Reducing oxidative damage:
  • Antioxidants and anti-inflammatory compounds help neutralise free radicals and reduce cellular stress.
  • Immunotherapies are also being explored to clear toxic protein aggregates that interfere with mitochondrial function.

Emerging Therapies in Clinical Trials

As of 2024, approximately 7% of all Parkinson’s disease-modifying clinical trials target mitochondria or related metabolic pathways. Among the most promising are:

• UDCA (Ursodeoxycholic acid): Improves mitochondrial function and brain energy efficiency in early human studies.
• Vitamin B3 (Nicotinamide riboside): Enhances mitochondrial energy production; currently in phase 2 and 3 trials.
• GLP-1 receptor agonists: Originally developed for diabetes, these drugs may enhance mitochondrial resilience, reduce inflammation, and slow motor decline in Parkinson’s.

Challenges in Mitochondrial Research

Despite encouraging findings, challenges remain:

• Measuring mitochondrial function in the living brain remains difficult.
• Therapies must cross the blood–brain barrier to reach target neurons effectively.
• Some mitochondrial-targeted drugs cause unintended weight loss, a concern for those already at risk of undernutrition in Parkinson’s.
• Hormonal influences, particularly oestrogen, may play a role but are underexplored due to gender gaps in research.

The Bigger Picture: Prevention and Protection

Mitochondrial decline in Parkinson’s Disease often begins before visible symptoms appear, meaning early prevention may be key. Encouragingly, even later in the disease, it’s possible to support mitochondrial function and protect remaining neurons.

Lifestyle measures such as balanced nutrition, regular exercise, and stress reduction complement clinical interventions, helping sustain mitochondrial activity and support brain energy health.

Key Takeaways

• Mitochondria are central to Parkinson’s Disease, influencing both energy production and oxidative stress.
• Lifestyle matters: Exercise, sleep, and diet are protective.
• Emerging therapies such as UDCA, vitamin B3, and GLP-1 receptor agonists offer hope for slowing disease progression.
• Challenges remain, but research continues to evolve rapidly.
• Supporting mitochondrial health is one of the most promising strategies for protecting neurons and improving quality of life in Parkinson’s.

Summary

Mitochondria sit at the heart of energy production and cellular repair. In Parkinson’s Disease, protecting mitochondrial health may hold the key to slowing progression. Through targeted nutrition, lifestyle strategies, and ongoing clinical research, there is real hope for maintaining energy, movement, and overall well-being.

Get in Touch

If you’re living with Parkinson’s Disease and want to explore how nutrition and lifestyle can support mitochondrial and brain energy health, I can help. I work with clients across the UK and Europe to optimise diet, energy balance, and resilience.