The neuroprotective effects of intermittent fasting on brain aging and neurodegenerative diseases via regulating mitochondrial function

Intermittent fasting (IF) has been studied for its effects on lifespan and the prevention or delay of age-related diseases upon the regulation of metabolic pathways. Mitochondria participate in key metabolic pathways and play important roles in maintaining intracellular signaling networks that modulate various cellular functions. Mitochondrial dysfunction has been described as an early feature of brain aging and neurodegeneration. Although IF has been shown to prevent brain aging and neurodegeneration, the mechanism is still unclear. This review focuses on the mechanisms by which IF improves mitochondrial function, which plays a central role in brain aging and neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, and Huntington's disease. The cellular and molecular mechanisms of IF in brain aging and neurodegeneration involve activation of adaptive cellular stress responses and signaling-and transcriptional pathways, thereby enhancing mitochondrial function, by promoting energy metabolism and reducing oxidant production.

Automated summary

This review focuses on the mechanisms by which intermittent fasting (IF) improves mitochondrial function in brain aging and neurodegenerative diseases such as Alzheimer's, Parkinson's, and Huntington's. IF activates adaptive cellular stress responses and signaling pathways, enhancing mitochondrial function by promoting energy metabolism and reducing oxidant production.