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«It creates a barrier in the brain»

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«It creates a barrier in the brain»

New Research Shows Possible Explanation for Why Not All ApoE4 Carriers Develop Alzheimer’s

A recent study conducted by researchers from Columbia University has shed light on why not all individuals carrying the gene responsible for the production of the protein apolipoprotein E4 (ApoE4) develop Alzheimer’s disease. Published in the journal Acta Neuropathologica, the study analyzed data from 11 thousand people and found that the expression of a protein called fibronectin, produced by a specific gene, was significantly lower in individuals with ApoE4 who did not develop the disease.

The researchers modified zebrafish to validate their findings and discovered that high levels of fibronectin in the animals led to alterations at the glial and vascular levels similar to those observed in patients with Alzheimer’s. Additionally, reducing fibronectin levels in the zebrafish improved the disease.

Fibronectin is typically present in limited quantities in the blood-brain barrier but increases significantly in individuals with Alzheimer’s. The study authors suggest that knocking out fibronectin through genetic mutation could potentially protect ApoE4 carriers from developing the neurodegenerative disease.

The research opens up possibilities for developing new therapies that mimic the protective effect of the gene to prevent or treat Alzheimer’s. However, it may take years to fully understand and implement these potential therapies. In the meantime, following a healthy lifestyle by managing hypertension, avoiding smoking, maintaining a healthy weight, managing diabetes, staying active, limiting alcohol consumption, and pursuing education can reduce the risk of developing Alzheimer’s disease.

This groundbreaking research provides hope for future advancements in the treatment and prevention of Alzheimer’s, offering new insights into the role of genetics in the development of the disease.

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