Increased pTau-181 Levels Linked to Neurologic Long COVID

TUESDAY, Jan. 20, 2026 (HealthDay News) — Increased phosphorylated Tau-181 (pTau-181) levels are seen in association with neurological manifestations of post-acute sequelae of severe acute respiratory syndrome coronavirus 2 (Neurological PASC [N-PASC]) consistent with central damage, according to a study published in the January issue of eBioMedicine.

Xiaohua Yang, from the World Trade Center Health Program at Stony Brook University in New York, and colleagues examined whether N-PASC is associated with changes in neurological biomarkers after COVID-19. Plasma samples were retrieved before and after COVID-19 onset among 227 essential workers who developed COVID-19 with N-PASC and were demographically matched with data from 227 controls who developed COVID-19 without N-PASC or who did not develop COVID-19 (124 and 103 participants, respectively).

The researchers found that N-PASC was only associated with higher total amyloid β burden before onset of COVID-19 (area under receiver operating characteristic curve, 0.77). In participants who developed N-PASC, plasma pTau-181 levels increased by 59.3 percent following COVID-19 onset, and were worst among participants reporting central nervous symptoms persisting ≥1.5 years. 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. There was an association seen for having ≥20 percent increases in pTau-181 with increased amyloid β40/42 levels at follow-up and with central neurological symptoms such as persistent brain fog and loss of taste/smell.

“This is one of the first studies to show that a virus may contribute to the development of abnormal tau production over time,” senior author Benjamin J. Luft, M.D., also with the World Trade Center Health Program, said in a statement.

Abstract/Full Text