A novel FN1 gene variant slashes Alzheimer’s risk by 70%, offering hope for improved treatments. Columbia University researchers, scrutinizing individuals with the APOEe4 gene, identified a protective FN1 variant, suggesting a counterbalance to APOEe4’s Alzheimer’s risk. Genome sequencing of 10,763 subjects unveiled FN1’s role in regulating brain fibronectin levels, vital for the blood-brain barrier’s integrity.
Neurologist Richard Mayeux proposes targeting fibronectin for Alzheimer’s defense, as excessive fibronectin might hinder brain waste clearance, particularly amyloid-beta removal. Zebrafish trials corroborate this, showing enhanced amyloid clearance upon fibronectin reduction.
Hundreds of thousands with APOEe4 in the US alone may harbor this protective FN1 variant, potentially staving off Alzheimer’s. Although the mechanism remains unclear, the FN1 variant could shield against Alzheimer’s in other APOE variants.
Mayeux underscores the need for early amyloid clearance, possibly through bloodstream interventions, highlighting FN1 as a promising drug target. Understanding fibronectin’s role could pave the way for innovative treatments.
In essence, the FN1 variant’s discovery unveils a potential breakthrough in Alzheimer’s therapy, emphasizing fibronectin’s pivotal role in disease progression.