Gene Variant Reduces Alzheimer’s Risks By 70%

Gene Variant Reduces Alzheimer’s Risks By 70%

It has been just reported that there is a gene variant that can reduce the risks of developing Alzheimer’s by 70%. Check out the latest reports about this below.

Reducing the risks of developing Alzheimer’s

A team of researchers from Columbia University has discovered a new variant in the FN1 gene, responsible for producing the fibronectin protein, which significantly reduces the chances of developing Alzheimer’s disease by up to 70%.

This discovery can potentially lead to more effective treatments for the disease.

To investigate further, the team focused on a group of individuals who have never developed Alzheimer’s but carry the APOEe4 gene variant, which significantly increases the risk of getting the disease.

The researchers suspected that there might be a counterbalance to the APOEe4 gene variant.

After conducting genome sequencing of 10,763 individuals from two groups of people, researchers discovered that a specific variant of FN1 provides protection to individuals with APOEe4.

The FN1 variant appears to regulate the levels of fibronectin in the brain, thus providing protective effects.

“These results gave us the idea that a therapy targeting fibronectin and mimicking the protective variant could provide a strong defense against the disease in people,” says neurologist Richard Mayeux from Columbia University.

Fibronectin is a protein that is found naturally in small quantities in the blood-brain barrier.

The blood-brain barrier is a crucial defense mechanism for the brain and plays a significant role in controlling the substances that enter and exit the brain.

Researchers who are investigating neurodegenerative diseases such as Alzheimer’s disease are particularly interested in this protein.

They believe that excessive amounts of fibronectin in the brain may hinder its ability to eliminate harmful substances, especially amyloid-beta proteins, which tend to accumulate in the brains of individuals who develop Alzheimer’s disease.

“It’s a classic case of too much of a good thing. It made us think that excess fibronectin could be preventing the clearance of amyloid deposits from the brain,” says neurologist Caghan Kizil from Columbia University.

“Anything that reduces excess fibronectin should provide some protection, and a drug that does this could be a significant step forward in the fight against this debilitating condition.”

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