A recent study published in Science has identified a crucial mechanism linking neuronal activity with mitochondrial function, offering new insights into addressing age-related cognitive decline. The research, led by Wenwen Li, found that the excitation-mitochondrial DNA transcription coupling (E-TCmito) pathway is essential for maintaining synaptic and mitochondrial health.
As we age, the efficiency of mitochondrial metabolism in the brain declines, impacting neuronal function. This decline can lead to oxidative stress and mitochondrial dysfunction, exacerbating cognitive decline. However, the mechanisms underlying this decline remain poorly understood, limiting the development of targeted interventions.
Li and colleagues investigated the role of mitochondrial transcription in cognition in the hippocampus of young and aged mice. They identified a novel coupling mechanism that connects neuronal excitation with mitochondrial DNA transcription, which they dubbed E-TCmito.
The researchers found that this coupling is distinct from traditional excitation-transcription coupling and plays a critical role in maintaining synaptic and mitochondrial health. In aging brains, the effectiveness of E-TCmito declines, leading to cognitive deficits. However, by enhancing E-TCmito in aged mice, the authors observed improved cognitive function.
This discovery highlights the potential of E-TCmito as a therapeutic target for counteracting cognitive decline associated with aging. The study’s findings also raise the possibility of identifying targets for age-related neurocognitive disorders, including Alzheimer’s and Parkinson’s diseases.
The research provides key insights into mitochondrial biology in the aging mammalian brain and has significant implications for understanding the mechanisms underlying cognitive decline.
Source: https://scitechdaily.com/can-we-stop-brain-aging-scientists-uncover-mitochondrial-key