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Zdenek Vrozina Profile picture
@ZdenekVrozina
Jan 16 • 7 tweets • 2 min read • Read on X
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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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More from @ZdenekVrozina

Zdenek Vrozina Profile picture
Apr 14
Very small study, but a genuinely interesting one on long COVID.
After reinfection, the biology did not simply replay the first infection - and in this cohort, the booster did not worsen the measured inflammatory/neurology protein profile🧵
The authors measured 182 inflammatory and neurology related proteins in plasma -
6-9 months after primary infection
after a booster
after breakthrough infection.
In a subset, they had longitudinal samples at 3 timepoints, which makes the paper much more interesting than a simple one time comparison.
It’s small, exploratory, and more hypothesis generating study.
But it asks a very good question.
Read 24 tweets
Zdenek Vrozina Profile picture
Apr 12
COVID-19 is not just a story of inflammation. This review argues that it is also a story about what SARS2 does to mitochondria - and how that can turn infection into energy failure, cell injury, and worse oxygenation. This is an important mechanistic review🧵
Mitochondria are not framed here as passive bystanders damaged late in severe illness. In this model, they are active participants in disease - they shape ATP production, ROS, apoptosis, and oxygen sensing.
The review describes two main routes of damage -
very early changes in expression of mito-related genes (hours)
direct interactions between viral proteins and host mito proteins.
So not just the cell is stressed, but a more specific viral rewiring of core cell machinery.
Read 23 tweets
Zdenek Vrozina Profile picture
Apr 11
This interesting paper lays out a very specific idea for how severe COVID-19 may be driven not only by the virus itself, but by the way the immune system handles what the virus leaves behind🧵
The starting point is simple.
SARS2 can leave behind viral RNA and nucleocapsid protein (N). N naturally binds viral RNA, and during infection people also make antibodies against N.
The authors build the story from there.
Viral RNA + nucleocapsid (N) + anti-N IgG
= an immune complex carrying viral genetic material.
Read 18 tweets
Zdenek Vrozina Profile picture
Apr 10
Can Long COVID show up in a blood sample?
A new preprint @resiapretorius suggests it might. Researchers found much higher platelet-monocyte aggregates in people with Long COVID than in healthy controls - about 29% vs 4.6%🧵
That is a striking signal, and it hints that Long COVID may leave a measurable trace in blood.
In healthy controls, a monocyte was more likely to have just one platelet attached. In Long COVID, researchers more often saw multiple platelets attached to a single monocyte.
Why does that matter?
Because platelet-monocyte aggregates sit right at the intersection of clotting and inflammation. When they rise, it can point to ongoing thromboinflammatory activity - in simple words, blood clotting biology and immune signaling feeding into each other.
Read 7 tweets
Zdenek Vrozina Profile picture
Apr 9
Long COVID research badly needs studies that move beyond description and toward intervention. This is why this preprint is worth attention. It starts to sketch a possible treatment path.🧵
A new preprint is interesting because it points to something important
a potentially treatable biological mechanism.
Not a clinical breakthrough. More like a promising preclinical proof of concept.
This study is a strong mechanistic signal that at least some of the neurological problems after COVID may be driven by persistent neuroinflammation - and that shifting immune regulation can improve that state in mice.
Read 16 tweets
Zdenek Vrozina Profile picture
Apr 9
Do you have hypertension?
This study in Nature suggests that for people who already had hypertension before getting COVID, the infection was linked to a higher long-term risk of serious cardiovascular events.🧵
In people with hypertension, an infection can leave behind - or speed up - processes that raise the risk of cardiovascular disease over the months and years that follow.
The excess risk was more pronounced in people with poorer blood pressure control at baseline, and that signs of a stronger acute inflammatory response during infection predicted worse long-term outcomes.
Read 12 tweets

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