In a recent study published in Nature Communications, researchers at the Buck Institute for Research on Aging have uncovered a mechanism explaining how dietary restriction slows brain aging and increases lifespan, providing potential therapeutic targets for age-related neurodegenerative diseases. The focus was on a gene called OXR1, crucial for the lifespan extension associated with calorie restriction and vital for healthy brain aging.
Contrary to the common belief that dietary restriction primarily impacts the digestive tract and fat buildup, the study reveals OXR1’s importance in the brain. The research, conducted on fruit flies and human cells, elucidated a neuron-specific response that mediates neuroprotection through dietary restriction, offering insights into potential therapeutic strategies such as intermittent fasting.
The team identified the retromer, a protein complex crucial for recycling cellular proteins and lipids, as a key player affected by OXR1. Dysfunctions in the retromer have been linked to age-related neurodegenerative diseases like Alzheimer’s and Parkinson’s, conditions protected by dietary restriction. The study demonstrated that OXR1 preserves retromer function, influencing neuronal health, brain aging, and the lifespan extension associated with calorie restriction.
The findings emphasize the impact of diet on gene expression, with calorie restriction enhancing the sorting of proteins in cells by upregulating OXR1. The researchers also noted that increasing the expression of a related gene in fruit flies extended their lifespan, suggesting that excess OXR1 expression might have similar effects in humans. The next steps involve identifying compounds that elevate OXR1 levels to potentially delay brain aging and gain insights into the degeneration of the brain. Overall, the study underscores the broader influence of diet on various bodily processes, supporting the notion that dietary choices play a crucial role in overall health.
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