Newly discovered subspecies FN1 genes responsible for making fibronectin protein, reduces the chance of developing Alzheimer’s disease by up to 70 percent. This discovery could lead to more effective treatments for the disease.
Researchers led by a team from Columbia University took a closer look at a specific group of people. It’s people with another genetic mutation called. APOEe4 People who have never developed Alzheimer’s disease.under consideration APOEe4 increase significantly They thought it might reduce the risk of contracting the disease.
As expected, genome sequencing The protective effects of specific substances were determined in 10,763 individuals across two groups. FN1 mutants of people with APOEe4.of FN1 This variant appears to help regulate the amount of fibronectin in the brain.
“These results give rise to the idea that treatments that target fibronectin and mimic protective mutants may provide powerful protection against disease in people.” To tell Richard Mayeux, a neurologist at Columbia University.
Fibronectin exists in small amounts in nature. blood brain barrier, an important defense of the brain and a key factor in what enters and leaves the brain. This is an important area of interest for scientists studying neurodegenerative diseases like Alzheimer’s disease.
The idea is that too much fibronectin can impair the brain’s ability to flush out dangerous substances, especially amyloid beta protein, which accumulates prominently in the brains of people who develop Alzheimer’s disease.
“This is a classic case of too much of a good thing. It got us thinking that excess fibronectin might be preventing the removal of amyloid deposits from the brain.” To tell Kagan Kizil, a neurologist at Columbia University.
“Anything that reduces excess fibronectin should provide some protection, and drugs that do this could be an important step forward in the fight against this debilitating condition.”
Testing using a zebrafish model of Alzheimer’s disease supports this hypothesis, and further testing is planned. They found that reducing fibronectin enhanced amyloid clearance, suggesting a direct relationship with Alzheimer’s disease. Furthermore, reducing fibronectin in fish also ameliorated other Alzheimer’s disease-related damage. glial cells.
Researchers estimate that hundreds of thousands of people suffer from this condition. APOEe4 Only the US allele has this protective function FN1 This gene mutation may prevent the development of Alzheimer’s disease, but more research will be needed to understand exactly how this gene mutation helps.
Fibronectin variants have been found in people with the following diseases: APOEe4but may also protect people with other variants. Apoe From getting Alzheimer’s disease.
We know that Alzheimer’s patients have the following symptoms: Much more fibronectin They have more abnormalities in the blood-brain barrier than healthy people, and it’s clear that they are involved in some way. Once that is established, treatment may be able to be based on that.
“We may need to start clearing amyloid much earlier, but we think it can be done through the bloodstream.” To tell Mayu. “That’s why we’re excited about the discovery of this variant in fibronectin, which could be a good target for drug development.”
This study acta neuropathologica.
