Russell 

Alzheimer's is a neurodegenerative disease in which patients experience memory loss and cognitive decline. Past research has identified Amyloid Beta Plaques and Tau Protein Tangles as key components that interfere with communication between neurons and ultimately lead to their damage or death. Although genetic factors like the APOE4 allele have been proven to increase the chances of developing Alzheimer's, some individuals with this high genetic risk factor remain healthy. This suggests these people have protective mechanisms against Alzheimer's Disease that allow them to remain healthy. The goal of this paper was to identify a protective gene and study how it influences disease progression. First, they analyzed DNA samples of healthy individuals who had a high risk of Alzheimer's to identify protective genes, then studied human brain tissue and zebrafish models to better understand how these genes clear toxic proteins. They identified a variant of the fibronectin 1 gene (FN1), which may possibly protect against Alzheimer's in high risk patients. This gene is responsible for Fibronectin, a protein that forms the structure of the extracellular matrix and the blood brain barrier. Both of these systems play a role in how effectively amyloid beta is cleared from the brain.This key finding discovered that this variant of the FN1 gene reduces its activity and slows the risk of Alzheimer's by delaying the implication of symptoms. Furthermore, decreased FN1 function was linked to improved clearance of amyloid beta plaques and reduced brain inflammation. Targeting FN1 pathways in the future could be a promising strategy to prevent the disease.