People with a faulty gene linked to a greater risk of dementia, may also have increased chances of developing severe COVID-19, according to a large-scale study which may lead to new ideas for treatments against the deadly infectious disease.
The study, published in the Journal of Gerontology, Medical Sciences, found high risk of severe COVID-19 infection among those who carried two faulty copies of the APOE gene termed e4e4.
Researchers, including those from the University of Exeter Medical School in the UK, assessed data from the UK Biobank -- a large long-term study investigating the respective contributions of genetic predisposition and environmental exposure to the development of disease in over 5,00,000 people.
The scientists found that one in 36 people of European ancestry have two faulty copies of the APOE gene, which they said can increase risks of Alzheimer's disease up to 14-fold, and also increase risks of heart disease.
In the current study, the scientists found that carrying these gene mutations doubles the risks of COVID-19 -- even in people who had not developed these diseases.
Previously, they had found that people with dementia are three times more likely to get severe COVID-19.
However, the researchers said dementia patients are not one of the groups advertised to shield -- or shelter in place -- on health grounds.
The scientists speculated that part of the increased risk effect may have been exposure to the high prevalence of the virus in care homes.
But based on the current study's findings, they said a genetic component may also be at play.
According to the researchers, people with the APOE e4e4 genotype were at double the risk of developing severe COVID-19, compared to those with the common e3e3 form of the gene.
They said a majority of people in the population, and in the sample size, have not yet been exposed to the virus.
From the analysis, the scientists said 2.36 per cent of participants with European ancestries had the ApoE e4e4 faulty gene.
But 5.13 per cent of those who tested positive for COVID-19 had this gene variant, indicating that the risk is doubled compared to e3e3.
"This is an exciting result because we might now be able to pinpoint how this faulty gene causes vulnerability to COVID-19. This could lead to new ideas for treatments," said Chia-Ling Kuo, study co-author from the University of Connecticut School of Medicine in the US.
The researchers believe that increasing disease risks that appear inevitable with ageing might actually be due to specific biological differences.
They said this could help scientists understand why some people stay active to age 100 and beyond, while others become disabled and die in their sixties.
While several studies have shown that people with dementia are at high risk of developing severe COVID-19, the authors of the current research believe that this may not simply be due to the effects of dementia, advancing age or frailty, or exposure to the virus in care homes.
The effect, according to study co-author David Melzer, could be partly due to this underlying genetic change, which puts people at risk for both COVID-19 and dementia.
"Further investigation is needed to understand the biological mechanisms linking ApoE genotypes to COVID-19 severity," the scientists concluded in the study.
