Science

Fierce mitochondria is important for favorable brain aging

As we grow older, our brain has undergone major changes, which will affect memory, thinking, and overall cognitive functions. Recent research shows the culprit behind these changes: our mitochondria, small power rooms in cells. This study shows that the decline in mitochondrial function will trigger a series of negative effects, which will cause brain health to deteriorate. Understanding the connection between mitochondrial health and brain aging may release new strategies to retain cognitive functions with age.

A new study found the important role of mitochondria dysfunction in brain aging, which emphasizes its impact on the three vital biological processes. The study was the first to be published in the magazine of “Biomers” by Professor Stephen Bondy of the University of California.

Professor Bondi deepened how mitochondrial defects gradually affected brain aging, emphasizing three key areas: immune response, oxidation stress and neurological transmission. Based on this study, these adverse changes began in middle age. As they grow, they reflect the decline in the critical process of the health of the brain.

Studies have shown that with the increase of age, the efficiency of the immune system decreases, resulting in the transition from targeted immune response to chronic and unsteady inflammatory state. Professor Bondi said: “This chronic inflammation is neither effective and harmful, which has led to a variety of diseases related to age.” These diseases include Alzheimer’s, Parkinson’s disease, Hentington and muscle atrophy. Sclerosis.

Oxidation stress is another key aspect of exploration in this study. Researchers have discovered that with aging, the balance between the production and neutralization of active oxygen (ROS) is damaged, resulting in cell damage. Professor Bondi explained: “Failure to maintain oxidation and restoration of the damage caused by free radicals is the main factor of neurodegenerative diseases.”

In addition, the study involves the emergence of chronic low -level excitement in aging brain, which is related to mitochondrial dysfunction. This continuous excessive stimulation is caused by excessive level of calcium in the cell, and the mitochondria cannot be fully isolated. This may lead to excitement toxicity, where the activation of prolonged glutamic acid receptor can cause neuronal damage.

Researchers suggested that with age, the decline in mitochondrial quality will trigger these harmful changes. They emphasized that the aging mitochondrial DNA (MTDNA) shows greater free radical leakage, leading to damage to phosphoric acidization. Professor Bondi pointed out: “The accumulation of mitochondrial dysfunction has made a significant contribution to the low metabolic status observed in the elderly brain.”

Professor Bondi emphasizes the importance of mitochondria, that is, the process of eliminating defective mitochondria, and decreased with age. The reduction of mitochondrial efficiency leads to the accumulation of mitochondria damage, which further exacerbates cell dysfunction. Professor Bonda asserts: “Effective mitochondria is essential for maintaining mitochondrial quality and overall brain health.”

When solving potential treatment methods, research pointed out that catering and lifestyle intervention measures that can enhance mitochondrial function and reduce brain aging. A resveratrol, sperm, and curcumin compounds are used through the SIRT1 pathway. Professor Bondi added: “Human tests are currently undergoing human tests to evaluate the effects of these drugs in promoting brain health and extending their life.”

The results of this study emphasize the core role of mitochondria in brain aging and nervous degeneration. Professor Bondi concluded: “By aimed at mitochondrial dysfunction, we can develop new treatment strategies to slow down brain aging and crack down on neurodegenerative diseases.”

Journal reference

Bondy, SC “mitochondrial dysfunction is the main foundation of brain aging.” Biomolecular 2024, 14,402. DOI:

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