Thread by @ZdenekVrozina

Long COVID can injure the brain - and persistent autoimmunity could be a major driver.
A study links persistent AT1 receptor autoantibodies (AT1-AA) with neuroaxonal injury and cognitive symptoms.
Here’s what it means🧵

https://twitter.com/bagaidr/status/1945134508841337059

The study focused on post-COVID patients with neurological symptoms like brain fog, memory issues, or fatigue.
They found:
Elevated AT1-AA in serum and cerebrospinal fluid (CSF)
Correlation with neurofilament light chain (NfL), a marker of axonal damage
Signs of a compensatory immune response - often insufficient

What are AT1-AA?
Autoantibodies that act as agonists at the angiotensin II type 1 receptor (AT1R), which mediates pro-inflammatory, pro-thrombotic, and vasoconstrictive signals.
Unlike typical antibodies, these lock the receptor in an “always on” state - driving inflammation and oxidative stress.

NfL is a marker of axonal damage - its elevation in serum reflects ongoing or recent neural injury.
In this study, NfL strongly correlated with AT1-AA levels.
Suggesting that immune activation via RAS isn’t just inflammation - it may physically damage the brain.

The body tries to compensate - but often too late!
In CSF, patients showed increased autoantibodies activating anti-inflammatory RAS receptors (AT2-AA, MasR-AA).
This may reflect a feedback response to chronic AT1R stimulation.
But in many patients, this compensatory axis isn’t enough.

Strikingly, patients with the worst cognitive deficits had the highest levels of MasR-AA.
This suggests the compensatory response may scale with injury - but fail to reverse it.
Post-COVID cognitive issues may reflect measurable CNS damage.

These findings echo what we’ve seen in other diseases:
Pre-eclampsia: AT1-AA drive endothelial damage
Parkinson’s: AT1-AA found in serum & CSF
HIV: chronic neuroinflammation, axonal loss
Alzheimer’s: AT1R overactivity linked to hippocampal atrophy
Long COVID may follow similar patterns.

So what are the implications?
AT1-AA and NfL may serve as biomarkers for CNS-involved Long COVID
Could stratify patients and guide care
AT1 receptor blockers (eg telmisartan) could be repurposed - already studied in neurodegeneration

Big picture: Post-COVID is not a diagnostic trashbin.
In some patients, it’s a biologically defined neuroinflammatory syndrome, with
Persistent autoantibodies
Axonal damage
Failed CNS homeostasis
And we can measure it.

Limitations? Yes - and they matter.
Small cross-sectional study (n = 69).
Subgroups (eg severe cognitive impairment) are even smaller.
Causality can’t be established - yet.
But the signal is real. And it’s consistent with prior research.

This doesn’t reinvent the wheel - it reinforces a signal we’ve seen again and again.
AT1-AA, NfL, hippocampal atrophy, BBB disruption - these threads are converging!
Meanwhile, public health hasn’t moved an inch. No screening. No follow-up. No guidelines.
Just silence.

Bottom line:
Some Long COVID patients may suffer persistent autoimmune RAS activation in the brain - a measurable, actionable form of CNS injury.
We now have biomarkers.
We have mechanisms.
What we don’t have is urgency.

Rodriguez-Perez et al. (2025). Serum angiotensin type‑1 receptor autoantibodies and neurofilament light chain as markers of neuroaxonal damage in post‑COVID patients.
Frontiers in Immunology. frontiersin.org/journals/immun…