In people with neurological long COVID, infection is followed by a significant increase in pTau-181, and in a subset this is accompanied by changes in amyloid markers!
This biomarker pattern is compatible with tau-related pathology and may point to a worse long-term prognosis🧵
This biomarker pattern is compatible with tau-related pathology and may point to a worse long-term prognosis🧵
A new prospective study in eBioMedicine followed 227 individuals with blood samples collected before and after COVID-19.
That matters - this isn’t a cross-sectional snapshot, but a true within-person biological change after infection.
That matters - this isn’t a cross-sectional snapshot, but a true within-person biological change after infection.
The focus was neurological PASC (N-PASC). Persistent symptoms like brain fog, loss of smell/taste, dizziness, balance problems, behavioral changes.
Only this group showed a marked post-COVID rise in pTau-181!
Only this group showed a marked post-COVID rise in pTau-181!
On average, pTau-181 increased by ~59% compared to pre-infection levels (sic)
Controls (no COVID or COVID without N-PASC) did not show this pattern.
Controls (no COVID or COVID without N-PASC) did not show this pattern.
Crucially, the increase was strongest in people whose neurological symptoms persisted longer than 1.5 years.
That argues against a short-lived inflammatory after effect and toward a time dependent biological process.
That argues against a short-lived inflammatory after effect and toward a time dependent biological process.
More than half of N-PASC patients showed ≥20% increases in pTau-181.
Nearly 45% crossed thresholds commonly used in Alzheimer’s disease research (sic)
The study does not say this is Alzheimer’s - but it does signal a concerning biomarker shift.
Nearly 45% crossed thresholds commonly used in Alzheimer’s disease research (sic)
The study does not say this is Alzheimer’s - but it does signal a concerning biomarker shift.
In a subset, elevated pTau-181 coincided with changes in amyloid markers (Aβ40/42).
Together, this combination is typically associated with tau-related neurodegenerative pathways.
Together, this combination is typically associated with tau-related neurodegenerative pathways.
Sum:
Neurological long COVID should not be dismissed as purely functional or transient. Study shows that in a subset of neurological long COVID patients, biology shifts in a direction compatible with tau-pathology, and that the signal grows with time.
Neurological long COVID should not be dismissed as purely functional or transient. Study shows that in a subset of neurological long COVID patients, biology shifts in a direction compatible with tau-pathology, and that the signal grows with time.
Yang at al., Increased phosphorylated tau (pTau-181) is associated with neurological post-acute sequelae of coronavirus disease in essential workers: a prospective cohort study before and after COVID-19 onset. eBioMedicine 2026. thelancet.com/journals/ebiom…
Why this matters for working-age adults?
Brain fog, attention lapses, dizziness and tinnitus directly affect safety, productivity, and employability.
This study suggests these symptoms can have an objective biological correlate, not just subjective distress.
Brain fog, attention lapses, dizziness and tinnitus directly affect safety, productivity, and employability.
This study suggests these symptoms can have an objective biological correlate, not just subjective distress.
Why this matters for children?
Children have decades ahead of them. Even subtle post-infectious neurobiological shifts could compound over time.
This study is in adults - but it raises urgent questions about pediatric long COVID and long-term brain health.
@szupraha @ZdravkoOnline @adamvojtech86
Children have decades ahead of them. Even subtle post-infectious neurobiological shifts could compound over time.
This study is in adults - but it raises urgent questions about pediatric long COVID and long-term brain health.
@szupraha @ZdravkoOnline @adamvojtech86
Why this matters for prevention?
If some post-COVID neurological syndromes involve progressive tau-related processes, then preventing infection isn’t just about avoiding acute illness -
it may also be about preventing long-term neurological risk.
If some post-COVID neurological syndromes involve progressive tau-related processes, then preventing infection isn’t just about avoiding acute illness -
it may also be about preventing long-term neurological risk.
PET studies in long COVID show persistent neuroinflammation and microglial activation.
BBB studies show vascular and barrier dysfunction.
Activated microglia are known to promote tau phosphorylation.
This biomarker signal fits into that broader picture - it doesn’t stand alone.
BBB studies show vascular and barrier dysfunction.
Activated microglia are known to promote tau phosphorylation.
This biomarker signal fits into that broader picture - it doesn’t stand alone.
In HIV-associated neurocognitive disorders (HAND), the role of microglial activation and blood–brain barrier dysfunction in long-term cognitive symptoms has been recognized for years.
In long COVID, a pTau-181/amyloid signal is emerging in a subset of neurological PASC patients. This is not about functional symptoms, but long-term neurobiology.
In long COVID, a pTau-181/amyloid signal is emerging in a subset of neurological PASC patients. This is not about functional symptoms, but long-term neurobiology.
When post-COVID neurological syndromes show signals compatible with long-term neurobiology, minimizing repeated infection becomes a public health responsibility - not a personal preference.
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