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New Genetic Variant Found To Protect Against Alzheimer's Disease

Tests for patients suffering from Alzheimer's disease are displayed at the Memory Centre in Geneva

A recent study conducted by researchers at Columbia University has revealed a new genetic variant that may offer protection against Alzheimer’s disease. This gene has been found to reduce the risk of developing the disease by up to 70%, providing hope for individuals at high risk.

While Alzheimer's disease does not have a single responsible gene, genetic factors play a significant role in determining one's susceptibility to the disease. The apolipoprotein E (APOE) gene has long been identified as a major genetic risk factor for Alzheimer's, with certain variants of this gene associated with increased risk of developing the disease.

Individuals carrying the APOEe4 allele, particularly in non-Hispanic white populations, are at a higher risk of cognitive decline and dementia, especially if they inherit two copies of the allele. However, the age at onset and severity of symptoms can vary among carriers, with some individuals never displaying symptoms at all.

Apolipoprotein E (APOE) gene is a major risk factor for Alzheimer's disease.
Recent study at Columbia University identifies gene variant reducing Alzheimer's risk by 70%.
Carrying APOEe4 allele increases risk of cognitive decline and dementia.

The recent study identified a gene called fibronectin 1 that appears to protect against Alzheimer's disease by maintaining the extracellular matrix, a network of proteins that support cell structure. Individuals with a unique variant in this gene were found to be resilient to Alzheimer's, showing lower levels of protein accumulation associated with the disease.

Further research confirmed these findings in zebrafish models, suggesting that reducing fibronectin levels in the blood-brain barrier could potentially delay the onset of Alzheimer's and prevent cognitive decline. It is estimated that around 620,000 individuals carrying the APOEe4 allele may also possess the Alzheimer’s-resistant fibronectin variant.

This discovery opens up new possibilities for developing therapeutic interventions that target fibronectin production to protect against neurodegeneration in Alzheimer’s disease. While more studies are needed to explore the broader implications of this genetic variant, the potential for a novel treatment approach is promising.

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