Alzheimer’s disease, a type of dementia affecting millions globally, is still poorly understood in terms of its causes. However, researchers have found that genetics play a role in the development of the disease, with certain genetic variants potentially influencing the risk of developing Alzheimer’s. Recent studies have focused on identifying these genetic variants, such as the APOE gene and TREM2 gene, which may be associated with Alzheimer’s disease. A study published in March 2024 identified 17 genetic variants linked to Alzheimer’s disease in five genomic regions. Researchers from Columbia University Vagelos College of Physicians and Surgeons in New York have now identified a new genetic variant that can reduce a person’s odds of developing Alzheimer’s by up to 71%. This variant occurs in the gene that expresses fibronectin, an adhesive glycoprotein found in the blood-brain barrier that helps control the movement of substances in and out of the brain.
The study conducted by researchers at Columbia University focused on analyzing the protective fibronectin gene variant in individuals who carried the APOEe4 gene variant, which significantly increases the risk of developing Alzheimer’s. They found that the fibronectin gene variant reduced the risk of Alzheimer’s disease by 71% in individuals carrying the APOEe4 gene variant. This discovery suggests that targeting fibronectin through therapy could potentially provide a strong defense against Alzheimer’s disease. The researchers believe that clearing amyloid, a protein associated with Alzheimer’s, through the bloodstream may be a potential therapeutic approach, and the fibronectin gene variant could serve as a promising target for drug development in the future. The protective effects of the fibronectin gene variant have been observed in individuals who have not shown symptoms of Alzheimer’s despite carrying the APOEe4 gene variant.
Neuropsychologists and experts in the field of Alzheimer’s disease have expressed excitement about the findings of the study, highlighting the potential of the fibronectin gene variant as a novel therapeutic target for the disease. The discovery opens up new possibilities for developing treatments that could intervene in the early stages of Alzheimer’s by targeting the blood-brain barrier and reducing excess fibronectin levels. By understanding the mechanisms underlying the protective effects of the fibronectin gene variant, researchers hope to develop more effective treatments that can prevent or treat Alzheimer’s disease. Further research is needed to explore how the genetic variant manifests phenotypically and its potential applications in clinical settings.
Dr. Manisha Parulekar, director of the Division of Geriatrics at Hackensack University Medical Center, emphasized the importance of finding new ways to reduce the risk of Alzheimer’s disease, given the complexity of its etiology. While the exact causes of Alzheimer’s remain unknown, factors such as amyloid plaques and tau tangles, as well as vascular dysfunction, are believed to contribute to its development. The study’s focus on the blood-brain barrier’s role in maintaining brain health offers a novel perspective on potential mechanisms for preventing or correcting disruptions that may lead to Alzheimer’s. By exploring multiple pathways in the disease’s etiology, researchers aim to discover effective interventions that could provide relief to individuals at risk of developing this debilitating condition. Confirming these findings and applying them in clinical settings could pave the way for novel therapies for Alzheimer’s disease.
