Researchers from Zhejiang Provincial College of Medicine have demonstrated that strengthening the connection between neuronal activity and mitochondrial function can slow the onset of neurodegenerative diseases and support long-term brain health. The results emphasize a close dialogue between how nerve cells fire and how mitochondria generate energy, suggesting new paths to protect cognition.
Mitochondria are the powerhouses of the cell, turning nutrients and oxygen into usable energy for brain tissue. As mammals age, the brain’s mitochondrial metabolism loses efficiency. When oxidative phosphorylation falters, oxidative stress rises and mitochondrial function falters, spreading disruption through neural networks that underlie memory, learning, and attention.
Despite this link, the precise reasons for the decline in oxidative phosphorylation activity in aging neurons remain largely unclear, complicating efforts to develop effective therapies for cognitive aging.
To explore this, a team studied mitochondrial transcription in cognitive processes in both young and old mice. They identified a novel neuron–mitochondria interaction mechanism called stimulatory-mitochondrial DNA transcription coupling, abbreviated E-TCmito. The mechanism describes how neuronal activity can initiate transcription of mitochondrial DNA, triggering the production of RNA molecules that support mitochondrial gene activity and energy production.
Experiments showed that E-TCmito activity drops in aging brains, aligning with cognitive impairment. When this process was enhanced in older mice, cognitive performance improved, demonstrating the potential for restoring mitochondrial signaling to maintain brain function.
Researchers say these findings could lead to new approaches for addressing age-related cognitive decline in humans. While translating results from mice to people requires careful study, the concept offers a promising target for future therapies aimed at keeping memory and thinking sharp as people age.
Earlier discussions described it as a social factor accelerating brain aging and dementia.