Intermittent Fasting May Help Slow Brain Ageing and Boost Longevity

Written By :  Niveditha Subramani
Medically Reviewed By :  Dr. Kamal Kant Kohli
Published On 2024-01-18 06:00 GMT   |   Update On 2024-01-18 11:14 GMT

Fasting has been traditionally followed in India since ages, and the effects of fasting has been evaluated since long. Intermittent fasting is proven beneficial for several diseases.OXR1 gene is an important brain resilience factor protecting against ageing and neurological diseases, said the researchers in the study, published in the journal Nature Communications.A study led by...

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Fasting has been traditionally followed in India since ages, and the effects of fasting has been evaluated since long. Intermittent fasting is proven beneficial for several diseases.

OXR1 gene is an important brain resilience factor protecting against ageing and neurological diseases, said the researchers in the study, published in the journal Nature Communications.

A study led by Indian-origin researchers at the Buck Institute for Research on Ageing reveals that intermittent fasting and calorie restriction can slow brain ageing and extend lifespan. The OXR1 gene plays a vital role in this process, protecting against ageing and neurodegenerative diseases. The study identifies potential therapeutic targets for age-related conditions.

If you want to help slow down your brain from ageing and increase your lifespan than follow diet patterns like intermittent fasting or restrict your calorie intake, suggests a study, led by researchers one of Indian-origin.

A team of scientists at the Buck Institute for ‘Research on Ageing’ in California have found a role for a gene called OXR1 that is necessary for the lifespan extension seen with dietary restriction and is essential for healthy brain ageing.

“When people restrict the amount of food that they eat, they typically think it might affect their digestive tract or fat buildup, but not necessarily about how it affects the brain,” said Kenneth Wilson, postdoctoral student at the Institute.

“As it turns out, this is a gene that is important in the brain.” The team additionally demonstrated a detailed cellular mechanism of how dietary restriction can delay ageing and slow the progression of neurodegenerative diseases.

The study, done in fruit flies and human cells, also identifies potential therapeutic targets to slow ageing and age-related neurodegenerative diseases.

“We found a neuron-specific response that mediates the neuroprotection of dietary restriction,” said Professor Pankaj Kapahi from Buck Institute.

“Strategies such as intermittent fasting or caloric restriction, which limit nutrients, may enhance levels of this gene to mediate its protective effects,” he added.

The team began by scanning about 200 strains of flies with different genetic backgrounds. The flies were raised with two different diets, either with a normal diet or with dietary restriction, which was only 10 per cent of normal nutrition.

They found the loss of OXR1 in humans results in severe neurological defects and premature death. In mice, extra OXR1 improves survival in a model of amyotrophic lateral sclerosis (ALS).

Further, a series of in-depth tests found that OXR1 affects a complex called the retromer, which is a set of proteins necessary for recycling cellular proteins and lipids.

Retromer dysfunction has been associated with age-related neurodegenerative diseases that are protected by dietary restriction, specifically Alzheimer's and Parkinson's diseases.

The team found that OXR1 preserves retromer function and is necessary for neuronal function, healthy brain ageing, and lifespan extension seen with dietary restriction.

“Diet is influencing this gene. By eating less, you are actually enhancing this mechanism of proteins being sorted properly in your cells, because your cells are enhancing the expression of OXR1,” said Wilson.

Reference:Wilson, K.A., Bar, S., Dammer, E.B. et al. OXR1 maintains the retromer to delay brain aging under dietary restriction. Nat Commun 15, 467 (2024). https://doi.org/10.1038/s41467-023-44343-3

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Article Source : Nature Communications

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