Alzheimer's disease is a debilitating condition that not only steals away memories but also affects a person's ability to communicate and respond to their surroundings. Recent controversy has arisen in the world of Alzheimer's research, revolving around the Food and Drug Administration's (FDA) accelerated approval of two drugs, aducanumab and lecanemab. These drugs, designed to clear beta-amyloid plaques in the brains of Alzheimer's patients, have sparked debates among researchers about their effectiveness. According to experts, the clinical trials have not conclusively shown that these drugs improve Alzheimer's symptoms, leading to questions about whether we should explore different approaches to treating this complex disease.
Luckily, at PIH, we're all about science-backed different approaches.
The Mitochondria-Alzheimer's Connection
To identify fresh avenues for Alzheimer's research, scientists are delving into alternative mechanisms underlying the disease's development. One promising area of investigation is energy metabolism. The human brain consumes approximately 25% of the body's energy, and disruptions in this process can impair its normal functioning.
A recent study by researchers at the Karolinska Institutet in Sweden shed light on the connection between changes in mitochondria and neuronal damage in mouse models of Alzheimer's disease.
Our Medical Director, Dr. Vinny, elaborated on this discovery: "The role of mitochondria in Alzheimer's is a significant breakthrough. These findings support the idea that Alzheimer's is a 'multi-hit' disorder caused by numerous changes in the brain."
Previous research suggests that Alzheimer's disease is linked to alterations in the brain's energy metabolism. One study using induced pluripotent stem cells revealed age-related changes in how brain cells use glucose to produce energy. These findings suggest that such changes might predispose individuals to Alzheimer's in later life.
Energy metabolism in the brain occurs in mitochondria, small subcellular structures that convert glucose from our food into energy through a process called oxidative phosphorylation, resulting in the creation of adenosine triphosphate (ATP), a crucial molecule used for cellular energy. Any disruption in these mechanisms can significantly impact energy metabolism.
The Karolinska Institutet researchers used genetically modified mouse models to explore changes in energy metabolism in the brain. They examined the genes being transcribed in neurons in the hippocampus, measured ATP levels, and analyzed oxygen levels in cells. Surprisingly, they discovered that mitochondrial activity increased before the mice displayed Alzheimer's pathology, challenging previous beliefs that a decrease in oxidative phosphorylation predicts the disease.
The team also found that once amyloid beta plaques began forming in the mouse brains, mitochondrial activity reversed, potentially as a compensatory response. Simultaneously, a robust inflammatory reaction occurred, suggesting that the initial increase in oxidative phosphorylation made neurons vulnerable to oxidative damage, triggering inflammation.
The researchers further investigated changes in synapses, the spaces between neurons in the brain. They observed the accumulation of vesicles designed to degrade proteins, which disrupted signaling and access to essential proteins. This disruption could potentially explain some of the symptoms seen in Alzheimer's patients.
The PIH Perspective
At PIH, we believe in using the mitochondria to leverage health. After all, they're the powerhouse of the cell!
Here are a couple of our services that we offer to boost mitochondrial, and therefore cognitive health.
Hyperbaric Oxygen Therapy (HBOT) involves breathing pure oxygen in a pressurized environment, which increases the oxygen levels in the body. This therapy has demonstrated positive effects on cognitive health. HBOT may improve cognitive function by increasing oxygen delivery to the brain, helping repair damaged neural tissues, and reducing inflammation.
Moreover, studies suggest that HBOT may enhance mitochondrial function. Mitochondria are the powerhouses of our cells, producing energy in the form of ATP. Increased oxygen levels can optimize the energy production within these mitochondria, which is crucial for maintaining healthy cognitive function.
Low-Level Light Laser Therapy, also known as photobiomodulation, utilizes specific wavelengths of light to stimulate cellular processes. This non-invasive treatment has shown potential in enhancing cognitive health. It works by promoting the release of nitric oxide, which increases blood flow and oxygen delivery to the brain. This can improve cognition and may have a positive impact on mitochondria.
Research has suggested that photobiomodulation can enhance mitochondrial function by increasing ATP production and reducing oxidative stress. This therapy provides an exciting avenue for optimizing brain health and mitochondrial performance.
BrainTap is a meditative device that combines guided meditation with light and sound therapy. It aims to help users reach a state of deep relaxation, reduce stress, and enhance cognitive function. Stress reduction is paramount for maintaining cognitive health, as chronic stress can negatively affect brain function and mitochondrial health.
By promoting relaxation and stress reduction, BrainTap can indirectly benefit mitochondria. High stress levels can lead to increased inflammation, oxidative stress, and cellular damage, all of which can be detrimental to mitochondria. Thus, using BrainTap as a tool for relaxation can support overall cognitive health and potentially protect mitochondrial function.
- Nutritional Counseling with Certified Nutrition Specialist Lee
Nutrition plays a pivotal role in cognitive health and mitochondrial function. Certified Nutrition Specialist Lee can provide personalized guidance on dietary choices and nutritional strategies to optimize brain health and energy production. A well-balanced diet rich in antioxidants, omega-3 fatty acids, and other essential nutrients can support mitochondrial function and cognitive well-being.
Additionally, Lee can offer dietary recommendations that focus on reducing inflammation and oxidative stress, both of which are linked to mitochondrial health and cognitive function. Proper nutrition can provide the foundation for maintaining cognitive health and supporting mitochondrial efficiency.
Conclusion
Alzheimer's disease remains a formidable challenge for both researchers and those affected by it. The controversy surrounding recent drug approvals has driven scientists to explore new paths in understanding and potentially treating this condition. As we uncover the intricate relationship between energy metabolism, mitochondria, and Alzheimer's, we move one step closer to unlocking the mysteries of this devastating disease.
Questions? Call PIH at 609.512.1468 for more information.