Persistent parainfectious brain injury in COVID-19 follow-up despite reduced cytokine and autoantibody response – A prospective cohort study

Don’t miss the fantastic article by Michael, B.D., Dunai, C., Needham, E.J. et al. which has been published in Nature Communications in December 2023.

The researchers measured markers of brain injury, inflammatory mediators, and autoantibodies in 203 hospitalised participants; 111 with acute sera (1–11 days post-admission) and 92 convalescent sera (56 with COVID-19-associated neurological diagnoses).
They analysed markers such as GFAP (glial fibrillary acidic protein, marker of astrocyte injury), UCH-L1 (a marker of neuronal cell body injury), and NfL (neurofilament light) and Tau (both markers of axonal and dendritic injury) and compared them with samples from 60 uninfected healthy controls.

Here we show that compared to 60 uninfected controls, tTau, GFAP, NfL, and UCH-L1 are increased with COVID-19 infection at acute timepoints and NfL and GFAP are significantly higher in participants with neurological complications. Inflammatory mediators (IL-6, IL-12p40, HGF, M-CSF, CCL2, and IL-1RA) are associated with both altered consciousness and markers of brain injury. Autoantibodies are more common in COVID-19 than controls and some (including against MYL7, UCH-L1, and GRIN3B) are more frequent with altered consciousness. Additionally, convalescent participants with neurological complications show elevated GFAP and NfL, unrelated to attenuated systemic inflammatory mediators and to autoantibody responses.“
(Michael, B.D., Dunai, C., Needham, E.J. et al. , 2023).

Para-infectious brain injury in COVID-19 persists at follow-up despite attenuated cytokine and autoantibody responses | Nature Communications

Michael, B.D., Dunai, C., Needham, E.J. et al. Para-infectious brain injury in COVID-19 persists at follow-up despite attenuated cytokine and autoantibody responses. Nat Commun 14, 8487 (2023). https://doi.org/10.1038/s41467-023-42320-4