Aside from the potential curse of long COVID, people who’ve had the SARS-CoV-2 virus may be more likely to develop high levels of biomarkers for brain proteins linked to Alzheimer’s disease, scientists report in a new study.
The average estimated effect of the virus on beta amyloid proteins was comparable to the effect from four years of aging, researchers found.
The difference was most pronounced in patients who’d been hospitalized with severe COVID-19, the study found, or in those with underlying risk factors for dementia, like high blood pressure.
These results hint at yet another insidious effect of COVID, the researchers write, suggesting even mild or moderate cases might speed up biological processes promoting the accumulation of beta amyloid proteins, which previous research has linked with Alzheimer’s.
There are important caveats to note, however. For one, this was an observational study, so it can establish correlation but not causation.
And even if COVID does raise the risk for these biomarkers, we don’t know if that effect would be unique to SARS-CoV-2, or if it could be similarly triggered by other pathogens like influenza.
The blood biomarkers used in this study are also fairly new, the authors acknowledge, and debatably reliable as clinical tools.
Nonetheless, given the devastating effects of Alzheimer’s and its uncertain origins, clues like this could be valuable pieces of an urgent puzzle.
This does fit with past research suggesting some types of infections might increase Alzheimer’s risk for some people, says neuroscientist Eugene Duff from Imperial College London.
“Our findings suggest COVID-19 may drive changes which contribute to neurodegenerative disease,” Duff says. “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,” he notes.
“But our findings do suggest that COVID-19 may increase the risk of Alzheimer’s in the future – as has been suggested in the past for other kinds of infections – especially among people with pre-existing risk factors,” he says.
Alzheimer’s is a cruel and mysterious neurodegenerative disease that can gradually destroy a person’s memory and cognitive abilities. It’s the most common form of dementia, a group of brain disorders that afflict more than 55 million people globally.
About 10 million new cases of dementia are diagnosed each year, according to the World Health Organization, which estimates Alzheimer’s may account for two-thirds of all cases.
Despite its prevalence, Alzheimer’s is still shrouded in mystery. Much attention has focused on beta amyloid plaques, although it’s unclear what role those play, and whether they cause the disease or vice versa.
Beta amyloid proteins are common in the body, serving an array of purposes. Their accumulation into clumps, or plaques, is what’s troubling.
These plaques are strongly associated with Alzheimer’s, and while their role remains murky, they might trigger symptoms of the disease by damaging neurons in the brain, the study’s authors note.
Given the uncertainty, it seems wise to at least pay attention if something correlates with suspected Alzheimer’s biomarkers – in this case, ratios of different forms of beta amyloid.
Duff and his colleagues looked at data from 1,252 participants in the UK Biobank, ranging from 46 to 80 years old. This included data collected both before and after confirmed SARS-CoV-2 infections.
They compared biomarkers from former COVID patients with those from participants who have similar traits but no evidence of past infections.
People with a COVID history were likelier to have specific changes in blood proteins that previous research has linked to beta-amyloid pathology in the brain, the study found.
The magnitude of change recalled that of a genetic variant known as APOE4, which is an established risk factor for Alzheimer’s disease, the researchers note.
The change was also more dramatic among people who’d been hospitalized for COVID – and for those with known Alzheimer’s risk factors, like hypertension.
“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,” says senior author Paul Matthews, a neurologist in the UK Dementia Research Institute at Imperial College London.
“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,” he says.
​​”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,” he adds.
The study was published in Nature Medicine.
