An analysis led by Prof Paul Matthews and Dr Eugene Duff at the UK DRI at Imperial found that people who had previously had Covid-19 were more likely to have increased levels of blood biomarkers linked to faulty amyloid proteins – a known hallmark for Alzheimer’s disease. The findings are published in the journal Nature Medicine.
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.
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 infection with SARS-CoV-2, the virus that causes Covid-19, or if a similar effect could be associated with other common infections such as influenza or pneumonia.
We’ve long suspected a link between infectious diseases and the progression of neurodegenerative disease – both with viral diseases, like herpes and influenza, and with some chronic bacterial infections. This latest analysis suggests that SARS-CoV-2 infection could potentially be another of these drivers of disease, particularly among those with underlying risk factors.
Group Leader
First author Dr Eugene Duff, from the UK DRI and Department of Brain Sciences at Imperial, 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.
We can’t say that catching the SARS-CoV-2 virus directly causes these changes, or if it does, by how much a single episode of infection increases someone’s risk. But our findings do suggest that Covid-19 may increase the risk of Alzheimer’s in future - as has been suggested in the past for other kinds of infections - especially among people with pre-existing risk factors.”
The team analysed biomarkers in 1,252 participants from the UK Biobank, aged 46 to 80 years of age, both before and after confirmed Covid-19 infections. The team then compared these biomarkers to those in participants with similar characteristics, but without evidence of any prior infection.
They found Covid-19 infection was associated with changes in several blood proteins previously linked to brain amyloid pathology. The magnitude of the changes was similar to that associated with APOE4, a well-known genetic risk factor for Alzheimer’s.
Greater changes were found in older participants and those that had been hospitalised with Covid-19 or had a history of hypertension. These correlated with poorer cognitive test scores and measures of overall health, as well as subtle changes in brain imaging patterns associated with neurodegeneration.
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 blood biomarkers for amyloid and tau are still a relatively new tool, and their clinical utility is still being assessed.
Senior author Professor Paul Matthews, Group Leader at the UK DRI at Imperial, said:
“We’ve long suspected a link between infectious diseases and the progression of neurodegenerative disease – both with viral diseases, like herpes and influenza, and with some chronic bacterial infections. This latest analysis suggests that SARS-CoV-2 infection could potentially be another of these drivers of disease, particularly among those with underlying risk factors.”
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.”
The research was funded by the UK DRI and by the NIHR Imperial Biomedical Research Centre Multiple Long-Term Conditions theme, as well as by an endowment to Imperial College London from the Edmond J Safra Foundation and Lily Safra to support Professor Matthews’ chair.
Source: Imperial College London
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