COVID-19 linked to increase in biomarkers for abnormal brain proteins
Researchers have uncovered a link between COVID-19 and blood markers linked to faulty proteins in the brain.
Researchers have found that people who had previously had COVID-19 were more likely to have increased levels of biomarkers linked to faulty amyloid – a protein that builds up in the brain in Alzheimer's disease – according to an analysis led by team at Imperial College London and the UK Dementia Research Institute.
Amyloid is a common protein with a range of functions in the body. But the buildup of an abnormal form of the protein, called beta amyloid (Aβ), is a key component of many diseases, including Alzheimer's disease.
The study is published in the journal Nature Medicine and is supported by the National Institute of Health and Care Research (NIHR) Imperial Biomedical Research Centre's (BRC) Multiple Long-term Conditions Theme.
Using data from the UK Biobank, the team analysed over 1,000 participants for known protein biomarkers associated with Alzheimer’s disease which can be detected in the blood, both before and after confirmed SARS-CoV-2 infections.
The team then compared these biomarkers to those in participants with similar characteristics, but without evidence of any prior infection. On average, the effects were comparable to four years of ageing with the greatest effects seen in those hospitalised with severe COVID-19 or with underlying risk factors for dementia such as smoking or high blood pressure.
According to the researchers, the findings suggest that mild or moderate COVID-19 may accelerate biological processes that contribute to the buildup of disease-promoting amyloid in the brain. The new results raise the possibility that COVID-19 might contribute to an increase in later risks of developing Alzheimer’s disease.
Alzheimer’s disease is the most common form of dementia, affecting over half a million people in the UK. Although most people with Alzheimer’s disease develop it after the age of 65, people under this age can develop it too.
Dr Eugene Duff, advanced research fellow at Imperial College London, said: “Our findings suggest COVID-19 may drive changes which contribute to neurodegenerative disease. We think this may be due to the inflammation triggered by the disease, although how this inflammation might impact the brain and changes to amyloid is not yet fully clear."
However, the team urges caution with the findings. They explain their observational study is unable to prove any causal links between COVID-19 and dementia. They also stress it is still unclear whether the effect is specific to SARS-CoV-2 infection, or if a similar effect could be associated with other common infections such as influenza or pneumonia.
The researchers highlight several limitations to the study, including limited information on the severity of infections in the cohort, as well as other factors not captured by the data contributing to changes in blood biomarker levels. They also caution that the blood biomarkers for amyloid and tau are still a relatively new tool and their clinical utility is still being assessed.
Professor Paul Matthews, group leader in the UK Dementia Research Institute at Imperial College London, said: “More studies now are needed to prove any causal links. Ultimately, the more we know about factors that contribute to dementia risk – whether they are directly under our control, like lifestyle or diet, or modifiable by vaccines or early treatment for infectious diseases – the more opportunities we may have to intervene for the prevention of dementia.”
This research is supported by the NIHR Imperial BRC, a translational research partnership between Imperial College Healthcare NHS Trust and Imperial College London, which was awarded £95m in 2022 to continue developing new experimental treatments and diagnostics for patients.
This article is adapted from a press release by Imperial College London.
