A study published in eBioMedicine identified increased phosphorylated Tau-181 (pTau-181) levels in individuals with neurological manifestations of post-acute sequelae of severe acute respiratory syndrome coronavirus 2 (N-PASC), consistent with central nervous system damage.
Researchers, including Xiaohua Yang and Benjamin J. Luft from the World Trade Center Health Program at Stony Brook University, examined whether N-PASC is associated with changes in neurological biomarkers after COVID-19. They analyzed plasma samples retrieved both before and after COVID-19 onset from 227 essential workers who developed COVID-19 with N-PASC. This group was demographically matched with 227 controls, comprising 124 participants who developed COVID-19 without N-PASC and 103 who did not contract COVID-19.
Key findings from the study include:
- N-PASC was associated with a higher total amyloid β burden before the onset of COVID-19.
- In participants who developed N-PASC, plasma pTau-181 levels increased by 59.3 percent following COVID-19 onset. These increases were most pronounced among participants reporting central nervous symptoms that persisted for 1.5 years or longer.
- Post-COVID-19 reductions in glial fibrillary acidic protein and neurofilament light chain were associated with peripheral symptoms of N-PASC, but not with increases in pTau-181.
- Individuals experiencing a 20 percent or greater increase in pTau-181 levels showed increased amyloid β40/42 levels at follow-up and reported central neurological symptoms, such as persistent brain fog and loss of taste or smell.
Senior author Benjamin J. Luft stated that this study is among the first to indicate that a virus may contribute to the development of abnormal tau production over time.