Middle school biology imparts a well-remembered fact: mitochondria are the cellular powerhouses responsible for energy production. But recent scientific findings suggest that mitochondria may also hold the key to preserving our memories and combating Alzheimer’s disease. This article explores the emerging role of mitochondria in Alzheimer’s disease, highlighting scientific research and offering insights into maintaining mitochondrial health for brain well-being.

Mitochondria and Alzheimer’s Disease

  1. Mitochondrial Dysfunction: Scientific studies have increasingly pointed to damaged or dysfunctional mitochondria as a contributing factor to the development of Alzheimer’s disease. Healthy mitochondria are now seen as crucial for staving off cognitive decline [1].
  2. A New Target: This discovery provides hope for the 10% to 20% of individuals who will face an Alzheimer’s diagnosis during their lifetime, as it opens up a fresh avenue of research for scientists seeking treatments and prevention strategies [1].

The History of Alzheimer’s Research

  1. Repeated Failures: Despite over 100 years and $3.7 billion invested in Alzheimer’s research in the United States alone, there is still no cure. Historically, research has focused on beta-amyloid plaques and tau protein tangles as potential culprits, but treatments targeting these have repeatedly failed in clinical trials [2].
  2. Ongoing Challenges: Even the most recent amyloid-targeting drug, Leqembi, which received full FDA approval, falls short of expectations, with potential risks and only marginal cognitive benefits [2].

The Mitochondrial Connection

  1. Plaques and Tangles: Many scientists now suspect that beta-amyloid plaques and tau protein tangles may be downstream symptoms rather than the root cause of Alzheimer’s disease. Instead, they are turning their attention to mitochondrial health as a potential upstream contributor [2].
  2. The Role of Mitochondria: Mitochondria are essential for converting food into energy and play key roles in calcium storage, cellular quality control, and heat generation. When mitochondria weaken, they produce less ATP (adenosine triphosphate), mismanage calcium ions, generate harmful reactive oxygen species, and struggle to regenerate effectively [3].

Mitochondrial Health for Brain Wellness:

  1. Exercise and Mitochondrial Health: Regular exercise, particularly endurance training, has been shown to enhance mitochondrial activity and protect against brain atrophy. Studies with Alzheimer’s patients reveal improvements in blood flow, hippocampal thickness, neuron growth, and cognitive performance [3].
  2. Monitoring Mitochondrial Fitness: The best metric for assessing mitochondrial fitness is VO2 max, representing the body’s maximum oxygen utilization during exercise. Fitness wearables like Fitbit and Apple Watch often provide indirect VO2 max estimates, referred to as the “cardio fitness level” [3].
  3. Antioxidant-Rich Diet: Mitochondrial health also benefits from an antioxidant-rich diet filled with plant-based foods like blueberries, red beans, tomatoes, spinach, artichokes, and green tea. Calorie restriction and ketogenic diets have shown potential protective effects [3].
  4. Stress Management: Chronic stress, anxiety, low social status, aggression, social defeat, and fear have been linked to mitochondrial damage in animal studies. Stress management is crucial for maintaining mitochondrial health [3].
  5. Brain photobiomodulation: A therapeutic approach utilizing low-level light therapy, has shown promise in promoting neuronal mitochondrial health. Studies have demonstrated that near-infrared light therapy can enhance mitochondrial function by increasing the production of adenosine triphosphate (ATP), the energy currency of cells, and improving mitochondrial respiration efficiency [4]. This process is thought to reduce oxidative stress and support the overall health of neurons, which is crucial in neurodegenerative conditions like Alzheimer’s disease [5]. Additionally, photobiomodulation has been linked to increased neuronal survival and neuroprotective effects through mitochondrial signaling pathways [6]. While more research is needed to fully understand the mechanisms involved, these findings suggest that brain photobiomodulation holds potential as a non-invasive approach to bolstering neuronal mitochondrial health.

Conclusion

While adhering to these recommendations does not guarantee immunity from Alzheimer’s disease, the growing recognition of the role played by mitochondria offers valuable insights to researchers working towards finding effective treatments and preventive measures for this devastating condition.

References:

  1. Swerdlow, R. H. (2018). Mitochondria and Mitochondrial Cascades in Alzheimer’s Disease. Journal of Alzheimer’s Disease, 62(3), 1403-1416.
  2. Cummings, J. L., & Tong, G. (2019). Trials of Disease-Modifying Therapies for Alzheimer’s Disease: A Review of the Influence of Patient Population and Cognitive Testing. Alzheimer’s & Dementia, 15(6), 751-757.
  3. Mattson, M. P., & Arumugam, T. V. (2018). Hallmarks of Brain Aging: Adaptive and Pathological Modification by Metabolic States. Cell Metabolism, 27(6), 1176-1199.
  4. Johnstone, D. M., el Massri, N., Moro, C., Spana, S., Wang, X. S., & Torres, N. (2014). Indirect application of near infrared light induces neuroprotection in a mouse model of parkinsonism—An abscopal neuroprotective effect. Neuroscience, 274, 93-101.
  5. Poyton, R. O., Ball, K. A., & Castello, P. R. (2009). Mitochondrial generation of free radicals and hypoxic signaling. Trends in Endocrinology & Metabolism, 20(7), 332-340.
  6. Rojas, J. C., Bruchey, A. K., & Gonzalez-Lima, F. (2012). Low-level light therapy improves cortical metabolic capacity and memory retention. Journal of Alzheimer’s Disease, 32(3), 741-752.