New Research Suggests Healthy Mitochondria Could Be Key to Fighting Alzheimer’s Disease
Mitochondria, the powerhouse of cells responsible for producing energy, may hold the key to fighting Alzheimer’s disease, according to emerging scientific research. Damaged mitochondria have been linked to the progression of the disease, while healthy mitochondria could potentially prevent cognitive decline.
Currently, there is no effective therapy for Alzheimer’s, despite years of research and billions of dollars spent. Previous research has focused on targeting amyloid, a protein that forms plaques in the brain and is associated with the disease. However, drugs targeting amyloid have shown limited clinical benefits and come with safety risks, including cases of cerebral hemorrhage.
Promising results have also been observed in gene therapy targeting the tau protein, another cause of Alzheimer’s. However, many scientists believe that both amyloid and tau are downstream symptoms, and mitochondrial health is what lies upstream.
Mitochondria, often referred to as the “powerhouse” of the brain, convert food into energy and perform various vital functions. When mitochondria malfunction, they produce less energy, mismanage calcium ions, and have reduced regenerative abilities. This dysfunction is linked to aging and Alzheimer’s, occurring before clinical symptoms appear. Abnormal mitochondrial function has also been associated with an overabundance of tau protein.
Exercise has been shown to be a key way to maintain healthy mitochondria. Resistance training improves mitochondrial activity and protects against brain atrophy in mice. In Alzheimer’s patients, exercise has increased blood flow to the brain, thickened the hippocampus, promoted the growth of new neurons, and improved cognitive performance. Conversely, a sedentary lifestyle has been found to increase brain inflammation, oxygen free radicals, and reduce mitochondrial activity.
Gianfranco Beltrami, vice president of the Italian Sports Medicine Federation, emphasizes the importance of healthy mitochondria in preventing Alzheimer’s. He explains that physical activity reduces insulin resistance, promotes the production of a neuroprotective protein called BDNF, improves vascular function, reduces stress and inflammation, and enhances sleep, all vital for cognitive health.
To assess mitochondrial fitness, measuring maximum aerobic power, known as VO2 max, is the best parameter. VO2 max reflects the body’s ability to use oxygen for energy production and can be estimated using fitness watches or measured with special equipment. Beltrami adds that measuring maximum aerobic power can also provide insight into a person’s biological age, which may differ from their chronological age.
In addition to exercise, a diet rich in antioxidants, including blueberries, red beans, tomatoes, spinach, artichokes, and green tea, can improve mitochondrial health. Calorie restriction and ketogenic diets, under medical supervision, may also be protective. Chronic stress, anxiety, aggression, and fear have been found to damage mitochondria in animal studies.
While further research is needed to fully understand the role of mitochondria in Alzheimer’s, these findings highlight the importance of promoting mitochondrial health through exercise and a healthy diet as potential strategies for preventing cognitive decline and fighting the disease.