The risk for Alzheimer’s disease (AD) and severe COVID-19 appear to share a common genetic mechanism that is involved with the immune response to viruses. This does not mean that COVID-19 increases the risk for Alzheimer’s disease, only that there appears to be a single genetic variant that increases the risk for both.
Researchers found that one genetic variant in the oligoadenylate synthetase 1 (OAS1) gene increases both the risk for AD of severe COVID-19 outcomes.
Risk for Alzheimer’s disease and susceptibility to severe COVID-19 share a common genetic mechanism involved in the immune response to viruses, according to a peer-reviewed article just published. The findings could lead to new treatment targets to slow the progression and severity of both diseases. If these findings bear out, it could suggest new drugs that could treat both diseases.
COVID-19 and Alzheimer’s disease genetic link
In a paper published online on 7 October 2021 in Brain, researchers at the University College London UK Dementia Research Institute found evidence suggesting a link between the OAS1 gene and AD.
The OAS1 gene is expressed in microglia, which make up around 10-15% of the cells in the central nervous system. They are a type of immune cell that functions as the first line of the active immune response in the brain and spinal cord.
They sequenced the OAS1 gene in 2547 people, approximately 50% with AD and 50% without. The genotyping analysis showed that a single-nucleotide polymorphism (SNP), that is one nucleotide substitution in the gene, was significantly associated with AD.
The same OAS1 SNP was also linked to severe COVID-19 outcomes. And the results indicate that SNPs within OAS1 associated with Alzheimer’s disease also appear to be linked to SNP variants associated with severe illness in COVID-19.
On the surface, this may not seem to mean a lot, but it’s an amazing study that provides us with potential groundbreaking information on a single point mutation in a gene in the central nervous system immune system that has an effect on the risk of both Alzheimer’s disease and severe COVID-19.
As opposed to the approved drug that has little clinical evidence supporting its effectiveness in Alzheimer’s disease, aducanumab, understanding what may actually cause AD may lead to much more effective treatments in the next few years.
Moreover, this data shows why AD patients were more susceptible to severe COVID-19 outcomes across the world.
Understanding how this SNP in the OAS1 gene may allow researchers to find better treatments for both as we understand how this gene impacts the immune system for each disease.
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