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Led by a team from Columbia University, researchers looked closely at a particular group of people: those with another gene variant calledvariant seems to be helping to regulate the amount of fibronectin in the brain.
"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,", a key defense for the brain and an important factor in what gets in and out of it. It's a significant area of interest for scientists studying neurodegenerative diseases like Alzheimer's.
The idea is that too much fibronectin may impair the brain's ability to wash out dangerous substances, particularly the amyloid-beta proteins that"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,"
"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." Tests using a zebrafish model of Alzheimer's backed up this hypothesis, and further tests are planned. They found that reducing fibronectin enhances amyloid clearance, suggesting a direct link to Alzheimer's pathology. Additionally, reducing fibronectin in the fish improved other Alzheimer's-related damage, such as changes toin their blood-brain barrier than people who are healthy, so it's clearly involved somehow.
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