Research conducted at Imperial College London has revealed a significant correlation between COVID-19 infection and elevated levels of biomarkers associated with faulty amyloid proteins in the brain. The observed effects were substantial, equivalent to approximately four years of aging, with more pronounced changes in patients hospitalized with severe COVID-19 and individuals with underlying risk factors such as smoking or high blood pressure12. While these findings suggest a potential acceleration of biological processes contributing to amyloid buildup in the brain, researchers emphasize caution in interpretation due to the observational nature of the studies1.

Research has identified several key biomarkers associated with COVID-19 and potential brain damage. Analysis of 1,252 UK Biobank participants found that SARS-CoV-2 infection was linked to changes in blood proteins associated with beta-amyloid (Aβ) pathology, a hallmark of Alzheimer's disease1. Specifically, researchers observed a reduced plasma Aβ42:Aβ40 ratio, and in more vulnerable participants, lower plasma Aβ42 and higher plasma pTau-181 levels1. These changes were more pronounced in older individuals, those hospitalized with COVID-19, and those with a history of hypertension1.

The magnitude of these biomarker changes was comparable to that associated with the APOE4 genetic variant, a known risk factor for Alzheimer's disease1. Importantly, these alterations correlated with poorer cognitive test scores, reduced overall health evaluations, and subtle changes in brain imaging patterns associated with neurodegeneration1. These findings suggest that COVID-19 may have significant neurological implications, potentially accelerating processes linked to cognitive decline and brain aging.

While the observed biomarker changes suggest potential neurological impacts of COVID-19, researchers emphasize caution in interpreting these findings. The studies' observational nature precludes establishing definitive causal links between COVID-19 and dementia1. It remains unclear whether these effects are specific to SARS-CoV-2 infection or could be associated with other common infections1. Nevertheless, the presence of these biomarkers underscores the importance of monitoring COVID-19 patients for potential neurological complications, particularly in severe cases23. Some biomarkers, such as NSE, show significant decreases 21 days post-infection, indicating potential recovery from acute neurological effects4. These findings highlight the need for further research to fully understand the long-term neurological implications of COVID-19 and to develop targeted interventions for affected individuals.