Can Researchers Fix Mitochondria to Treat Alzheimer’s Disease?

Researchers are exploring methods to combat mitochondrial dysfunction, which could serve as a potential indicator of Alzheimer's, in an effort to discover novel treatments for the condition.

New research suggests that boosting mitochondria could be beneficial in treating Alzheimer’s disease.

Researchers analyzing data

Image credit: Westend61/Getty Images.

Did you know that your brain is the most metabolically demanding organ in your body? It consumes a whopping 20% of your body’s energy! This energy is crucial for cell signaling and cognitive processes. However, disruptions to energy metabolism in the brain can lead to cognitive problems and even diseases like Alzheimer’s. And guess what? Researchers have recently made a breakthrough in understanding how mitochondria, the powerhouses of our cells, play a role in Alzheimer’s disease. In this article, we’ll explore the fascinating connection between mitochondrial dysfunction and neurological health, the complexities of energy metabolism in Alzheimer’s, and the exciting possibilities of repairing mitochondria to treat this degenerative disease.

Mitochondrial Dysfunction as a Neurological Health Disruptor

Dr. Clifford Segil, a neurologist at Providence Saint John’s Health Center, explains that mitochondrial dysfunction is not only involved in muscle disorders but also potentially plays a role in neurodegenerative diseases like Alzheimer’s. Mitochondria, known as the powerhouses of cells, produce the energy needed for cells to function correctly. When mitochondria malfunction, cells don’t work properly, which can lead to decreased synapses or connections between brain cells.

Energy Metabolism in Alzheimer’s Disease

Recent studies have shown that mitochondrial activity increases in the neurons of mouse models of Alzheimer’s disease before the disease even manifests. This increased mitochondrial activity is directly associated with oxidative phosphorylation, a process that occurs inside mitochondria to produce energy. Surprisingly, these hyperactive neurons also exhibit increased excitatory and decreased inhibitory activity, affecting the signaling between brain cells.

One study led by Prof. Stuart Lipton contributes significantly to our understanding of Alzheimer’s disease. The study created neuron models from induced pluripotent stem cells taken from individuals with Alzheimer’s. These models showed increased electronic signaling in synapses, leading to the development of the Alzheimer’s drug Namenda. Namenda reduces abnormal brain activity, slowing down the progression of the disease.

Can We Repair Mitochondria in Alzheimer’s?

Drumroll, please! Researchers at the Scripps Research Institute have made a groundbreaking discovery. They have successfully used neuron models derived from skin biopsies to identify the mechanism behind mitochondrial dysfunction in Alzheimer’s disease. By analyzing glycolysis and oxidative phosphorylation in these models, they found that a key molecule called succinate in the Krebs cycle, responsible for energy production, was disrupted.

Excitingly, the researchers were able to restore energy production in a significant number of synapses by introducing a succinate analog that passed through cell membranes. This discovery could have profound implications for treatment options and offers a potential pathway to combat mitochondrial dysfunction in the fight against Alzheimer’s.

Opportunities for Future Drug Development

While the molecule used in the study and succinate itself cannot be administered as drugs, the research team is now focusing on developing a drug target for this mechanism. Prof. Lipton’s team is currently working on improved drugs that can regulate excessive electrical activity in the brain associated with Alzheimer’s disease. These drugs are undergoing the regulatory process and show immense promise. The team is also exploring other routes and inflammatory pathways that contribute to nerve cell damage in Alzheimer’s.

With this groundbreaking research, the future looks brighter in the battle against Alzheimer’s disease. By understanding the critical role mitochondria play in the disease’s progression, researchers are paving the way for innovative treatments and potentially even a cure.


Q: Can mitochondrial dysfunction contribute to diseases other than Alzheimer’s?

A: Absolutely! Mitochondrial dysfunction has been implicated in various conditions, including muscle disorders or myopathies. Specific mitochondrial diseases, such as MELAS (mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes), are also closely associated with mitochondrial dysfunction. These discoveries indicate the far-reaching impact of mitochondrial dysfunction on both neurological and muscular health.

Q: Are there any lifestyle factors that can help prevent mitochondrial dysfunction?

A: While mitochondrial dysfunction is primarily linked to genetic factors, lifestyle choices can play a role in maintaining mitochondrial health. A diet rich in antioxidants and essential nutrients, regular exercise, stress management, and adequate sleep can all support overall mitochondrial function. Additionally, avoiding smoking and excessive alcohol consumption can help protect against mitochondrial damage and dysfunction.

Q: What are some ongoing debates in the scientific community surrounding Alzheimer’s disease and mitochondrial dysfunction?

A: One ongoing debate centers around the chicken-and-egg question: Does mitochondrial dysfunction cause Alzheimer’s disease, or is it a consequence of the disease? While the research discussed in this article suggests a causal relationship, further studies are needed to fully understand this complex relationship. Additionally, researchers are actively investigating the potential of targeted therapies that specifically address mitochondrial dysfunction as a standalone treatment for Alzheimer’s.

Q: Are there any non-pharmacological interventions that can support mitochondrial health?

A: Yes! Emerging research suggests that certain dietary interventions, such as intermittent fasting and ketogenic diets, may have potential benefits in supporting mitochondrial health. These interventions promote metabolic flexibility, enhance cellular stress resistance, and stimulate mitochondrial biogenesis. However, it’s essential to consult with a healthcare professional before making any significant dietary changes.


The connection between mitochondrial dysfunction and Alzheimer’s disease is a fascinating area of research. With each new discovery, we inch closer to unraveling the mysteries of this degenerative disease. The breakthroughs in repairing mitochondria offer hope for innovative treatments and potential therapeutic breakthroughs. As we continue to explore the link between energy metabolism and neurodegenerative diseases, we move one step closer to improving the lives of countless individuals affected by Alzheimer’s. Stay tuned for more exciting advancements in the field, and remember, together we can make a difference!


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