the team investigated four variants of oas1 and found that in addition to dampening the activity of the gene and increasing the risk of alzheimer’s, the variants were linked — or inherited together — and raised the risk of severe covid by as much as 20 per cent.
they also found that the oas1 gene exerts control over amount of pro-inflammatory proteins the immune system releases. microglia cells that expressed the gene more weakly were more likely to overreact to tissue damage and create a cytokine storm that caused the body’s immune system to attack itself. because the activity of this gene accelerates with age, subsequent research may be able to unlock why older individuals are more prone to alzheimer’s, severe covid and other similar diseases.
“our findings suggest that some people may have increased susceptibility to both alzheimer’s disease and severe covid-19, irrespective of their age, as some of our immune cells appear to engage a common molecular mechanism in both diseases,” said naciye magusali, a phd student at uk dementia research institute at ucl.
the researchers, who normally study dementia, have turned their attention to the long-term neurological effects of covid, tracking neuroinflammation and neuron damage in the hopes of shedding new light on both diseases. “if we could develop a simple way of testing for these genetic variants when someone tests positive for covid -19, then it might be possible to identify who is at greater risk of needing critical care but there is plenty more work to be done to get us there,” salih said. “similarly, we hope that our research could feed into the development of a blood test to identify whether someone is at risk of developing alzheimer’s before they show memory problems.