COVID-19 May Increase Alzheimer's Risk, Study Suggests
A groundbreaking study by researchers at Imperial College London and the UK Dementia Research Institute has uncovered a concerning link between COVID-19 and increased levels of biomarkers tied to abnormal brain proteins. These biomarkers, including beta amyloid, are known to play a key role in the development of Alzheimer’s disease.
The analysis of over 1,200 participants revealed that those who had previously contracted COVID-19 showed significant changes in blood proteins associated with brain health. The changes, similar to those caused by four years of natural aging, were most pronounced in individuals who were hospitalized with severe COVID-19 or had pre-existing risk factors for dementia, such as hypertension or smoking.
Potential Long-Term Risks
The researchers explained that the inflammation triggered by SARS-CoV-2 infection might be driving these changes. However, it remains unclear whether these effects are specific to COVID-19 or could be linked to other common infections like influenza or pneumonia.
“This research highlights how COVID-19 may trigger changes that could increase the risk of neurodegenerative diseases like Alzheimer’s,” said Dr. Eugene Duff, lead author from the Department of Brain Sciences at Imperial. “However, more studies are needed to establish whether a single episode of COVID-19 increases the long-term risk and to what extent.”
The study also compared the impact of COVID-19 on biomarkers to the effects of APOE4, a genetic variant associated with a higher risk of Alzheimer’s. The magnitude of changes in participants' blood proteins following infection was comparable to those observed in individuals with this genetic risk factor.
Amyloid and Neurodegeneration
Amyloid proteins, particularly beta amyloid, play a central role in Alzheimer’s disease. Abnormal accumulations of beta amyloid in the brain lead to the formation of toxic clumps that damage neurons, resulting in cognitive decline and behavioral changes.
Using data from the UK Biobank, researchers analyzed participants' blood samples before and after confirmed SARS-CoV-2 infections. They found significant increases in markers of beta amyloid buildup, especially among older participants or those with severe cases of COVID-19. These changes were associated with poorer cognitive performance and brain imaging patterns indicative of early neurodegeneration.
Study Limitations and Future Directions
Despite the compelling findings, the researchers caution against drawing definitive conclusions. Limitations include limited data on the severity of COVID-19 infections and other factors that may influence biomarker levels. Moreover, blood tests for amyloid and tau proteins, while promising, are still relatively new and require further validation.
Professor Paul Matthews, senior author and Group Leader at the UK Dementia Research Institute, emphasized the broader implications of the study: “Infectious diseases have long been suspected of influencing neurodegeneration. This study suggests COVID-19 may be another driver of brain disease, particularly among those with underlying health risks. However, more work is needed to confirm this.”
He added, “Understanding the factors that contribute to dementia risk – whether infections, genetics, or lifestyle – is crucial. The more we learn, the better equipped we’ll be to develop prevention strategies, from vaccines to early treatments.”
A Call for Further Research
This study opens new avenues for understanding how infections like COVID-19 could impact brain health and contribute to dementia. The researchers urge additional studies to explore causal links and determine whether interventions, such as vaccines or anti-inflammatory treatments, could mitigate the risks.
The research was supported by the UK Dementia Research Institute, the NIHR Imperial Biomedical Research Centre, and funding from the Edmond J. Safra Foundation and Lily Safra.
For more information, read the full study titled “Plasma proteomic evidence for increased β-amyloid pathology after SARS-CoV-2 infection” in Nature Medicine (DOI: 10.1038/s41591-024-03426-4).
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