One of the strongest - and most concerning - studies so far. A true before/after design, a clear tau signal in persistent neurological symptoms, and nearly half exceeding Alzheimer’s research pTau-181 thresholds🧵
Related evidence. A large UK Biobank longitudinal analysis in Nature Medicine - Duff et al., 2025 -compared plasma Alzheimer’s-related biomarkers before vs after SARS-CoV-2 infection (with matched controls).
They found that SARS-CoV-2 infection was associated with a shift toward an AD-like biomarker profile - notably a reduced plasma Aβ42:Aβ40 ratio, and in more vulnerable participants lower Aβ42 and higher pTau-181.
Taken together with the new N-PASC pTau-181 findings, the message is consistent - across different cohorts and designs, SARS-CoV-2 can be followed by measurable changes in biomarkers linked to neurodegenerative pathways.
Lancet eBioMedicine shows a pTau-181 signal in neurological long COVID.
Nature Medicine shows post–SARS-CoV-2 shifts in AD-related biomarkers, including pTau-181, in vulnerable groups.
Different cohorts. Same warning signal.
Ignoring converging tau and amyloid signals reported by Lancet and Nature is not caution - it risks becoming the public health error of the century. @szupraha @ZdravkoOnline @adamvojtech86
Duff at al., Plasma proteomic evidence for increased β-amyloid pathology after SARS-CoV-2 infection. nature.com/articles/s4159…
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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🧵
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.
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!
For years, Epstein–Barr virus (EBV) has been linked to multiple sclerosis.
The association was strong.
But the mechanism remained frustratingly abstract - until now.🧵
This new paper in Cell (2026) finally does what’s been missing.
It doesn’t just connect EBV and MS statistically -
it shows how the immune system gets it wrong.
Instead of focusing on antibodies, the authors look at CD4+ T cells.
Long-lived memory cells.
The ones that shape immune behavior over decades.
People with Long COVID often describe brain fog, mental fatigue, slowed thinking.
For a long time, we lacked direct biological evidence that something measurable was wrong in the brain.
Now we have one🧵
This new study used 31P magnetic resonance spectroscopy.
Unlike standard MRI, it doesn’t look at brain structure - it looks at cellular energy metabolism.
Specifically, it measures the balance between
ATP, the cell’s immediate energy currency
phosphocreatine (PCr), a fast energy reserve - basically a buffer/backup battery
A new preprint study followed the same individuals before and after SARS-CoV-2 infection and asked a simple question -
What happens to immune memory after COVID?
Not during acute illness.
Not only in long COVID.
But months later, in people considered recovered.
The researchers focused on memory T cells - the cells that allow us to respond quickly when we encounter familiar pathogens again.
They tested responses to common, everyday threats
Influenza A
Varicella-zoster virus (VZV)
Staphylococcus aureus
Prenatal COVID can shift the trajectory of brain development.
The differences are measurable - and they appear before diagnoses exist.
It’s based on neonatal brain MRI and standardized developmental testing🧵
What study is this?
A prospective study (Brain, Behavior, and Immunity, 2025)
children exposed to SARS-CoV-2 in utero
brain MRI ~2 weeks after birth
developmental testing at 2 years (Bayley-III, ITSEA)
compared to a pre-pandemic control cohort
The study asks whether the exposed group as a whole shows a shifted developmental pattern.
This is about a population-level shift, not a few extreme cases.
The authors show that COVID-19 can disrupt the heart’s electrical wiring (the cardiac conduction system) -causing bradycardia, pauses, and AV block...🧵
... even when they can’t detect viral proteins in the heart, pointing instead to innate immune signaling (IFN/JAK–STAT) plus mitochondrial oxidative stress (ROS) as the likely drivers.
What they did.
Syrian golden hamsters infected intranasally with SARS-CoV-2 (Delta), followed for 4 weeks.
Continuous telemetry in freely moving animals. ECG + breathing + body temperature.
Interferon-stimulated genes, cytokines, macrophages in the conduction system, and gap-junction proteins.