NYC Gazette

Caghan Kizil, PhD, a co-leader of the study at Columbia University Vagelos College of Physicians and Surgeons, highlighted the significance of the discovery of a genetic variant that reduces the odds of developing Alzheimer’s disease by up to 70%. According to Kizil, the protective variant identified in the fibronectin gene seems to prevent the buildup of excess fibronectin at the blood-brain barrier, which could lead to a new direction in therapeutic development for Alzheimer's disease.

Richard Mayeux, MD, chair of neurology at Columbia University, emphasized the potential of targeting fibronectin as a therapy for Alzheimer’s disease. Mayeux stated, "We may need to start clearing amyloid much earlier and we think that can be done through the bloodstream. That's why we are excited about the discovery of this variant in fibronectin, which may be a good target for drug development."

Badri N. Vardarajan, PhD, assistant professor of neurological science at Columbia University, discussed the process of identifying the protective variant by sequencing the genomes of APOEe4 carriers over the age of 70. Vardarajan mentioned that the fibronectin variant reduces the odds of developing Alzheimer’s in APOE4 carriers by 71% and delays the disease by approximately four years.

The research, published in the journal Acta Neuropathologica, was supported by various institutions and foundations, including the Carol and Gene Ludwig Family Foundation, the U.S. National Institutes of Health, and the Alzheimer’s Association. The study's findings provide hope for the development of new therapies for Alzheimer’s disease by targeting the fibronectin gene.

The discovery of this genetic variant offers a promising avenue for future research and treatment of Alzheimer's disease, potentially benefiting a significant number of individuals at risk of developing the condition.