Alzheimer’s and Covid share genetic risk factor
Researchers have identified an anti-viral gene that impacts the risk of both Alzheimer’s disease and severe Covid-19.
A team from the University College London (UCL) estimated that one genetic variant of the OAS1 gene increases the risk of Alzheimer’s disease by about 3-6 per cent in the population as a whole, while related variants on the same gene increase the likelihood of severe Covid-19 outcomes.
“While Alzheimer’s is primarily characterised by harmful build-up of amyloid protein and tangles in the brain, there is also extensive inflammation in the brain that highlights the importance of the immune system in Alzheimer’s. We have found that some of the same immune system changes can occur in both Alzheimer’s disease and Covid-19,” said lead author Dr Dervis Salih, from UCL’s Queen Square Institute of Neurology and UK Dementia Research Institute.
“In patients with severe Covid-19 infection, there can also be inflammatory changes in the brain. Here we have identified a gene that can contribute to an exaggerated immune response to increase risks of both Alzheimer’s and Covid-19,” Salih added, in the paper published in the journal Brain.
To understand the gene’s link to Alzheimer’s, the team sequenced genetic data from 2,547 people, half of whom had the brain disorder.
They found that people with a particular variation, called rs1131454, of the OAS1 gene were more likely to have Alzheimer’s disease, increasing carriers’ baseline risk of Alzheimer’s by an estimated 11-22 per cent.
The new variant identified is common, and it has a bigger impact on Alzheimer’s risk than several known risk genes, the researchers said.
Further, the researchers investigated four variants on the OAS1 gene, all of which dampen its expression (activity).
They found that the variants increasing the risk of Alzheimer’s are linked (inherited together) with OAS1 variants recently found to increase the baseline risk of needing intensive care for Covid-19 by as much as 20 per cent.
That is, the microglia cells where OAS1 gene was expressed more weakly had an exaggerated response to tissue damage, unleashing what they call a ‘cytokine storm,’ which leads to an autoimmune state where the body attacks itself, the team said.
OAS1 activity changes with age, so further research into the genetic network could help to understand why older people are more vulnerable to Alzheimer’s, Covid-19, and other related diseases, they added.
