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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
Feb 8
This study suggests that in some patients, COVID-19 triggers a long-term process of vascular and cardiac injury that can gradually increase pulmonary pressure, strain the right ventricle, and raise the risk of death in the following years🧵
The study followed 480 hospitalized patients (240 moderate, 240 severe) for one year after discharge. It assessed heart function using echocardiography and measured biomarkers of vascular inflammation.
In severe COVID-19, right-ventricular function was already significantly worse at the first study examination. Over the following year, pulmonary artery pressure increased by 17.8% in severe cases and 7.1% in moderate cases!
Read 14 tweets
Zdenek Vrozina Profile picture
Feb 6
If normal population plasma truly carries more low-grade inflammation, this study hints at a fork in the road.
Either we lower the bar and call it a new normal,
or this is a hidden population burden that will surface later as comorbidities🧵
A new study on the cytokine IL-32 after COVID-19 points directly at this uncomfortable question.
The authors analyzed nearly 1,000 healthy blood donors sampled before and during the pandemic, plus 212 hospitalized COVID-19 patients.
The result is consistent - plasma collected after 2020 shows systematically higher IL-32 levels compared to pre-pandemic plasma.
Read 9 tweets
Zdenek Vrozina Profile picture
Feb 6
Neurocognitive Long COVID doesn’t disappear.
Not with Omicron.
Not in a highly vaccinated population.
Even when most other organ-level signals fade🧵
A new population-level study from Singapore looked at 1.4 million COVID cases in a setting with >90% booster coverage.
Result - multi-organ Long COVID largely attenuates.
But the brain remains an exception.
The study tracked new medical diagnoses 31–300 days after infection across Delta and multiple Omicron waves (BA.1/2, BA.4/5, XBB).
Across variants, most organ systems normalize.
Neurocognitive diagnoses do not.
Read 10 tweets
Zdenek Vrozina Profile picture
Feb 5
This study does not tell us what exactly causes long COVID or ME/CFS, nor does it test clinical symptoms like PEM.
But it may tell us something just as important - what type of biological problem this likely is..🧵
The authors isolated immunoglobulins (IgG) from people with post-infectious ME/CFS, including post-COVID ME/CFS, and tested what these antibodies do to healthy cells.
In a subset of patients, these IgG alter the behavior of endothelial cells and their mitochondria.
Not by killing the cells or shutting down ATP production.
Read 17 tweets
Zdenek Vrozina Profile picture
Feb 2
This isn’t a new comparison.
For years, parallels between NeuroHIV and neuro-COVID/Long COVID have been discussed across fields.
What’s new is that they are now formally described as shared CNS mechanisms, not just analogy!🧵
Just a few years ago, parallels like
HIV - SARS-CoV-2
HAND - brain fog/neuro-LC
microglia - chronic inflammation
vasculature - cognition
were treated mainly as interesting analogies. With caution not to overstate them.
This new review formalizes the shift. These parallels are not Twitter pattern recognition, but convergent CNS phenotypes following viral insults.
A new review shows they are biologically grounded similarities.
Read 15 tweets
Zdenek Vrozina Profile picture
Feb 1
A new review links Alzheimer’s disease, Parkinson’s disease, and COVID-19 through a shared core - neuroinflammation + oxidative stress.
The same pathways, the same immune nodes, the same vulnerabilities of the brain🧵
Key players.
Microglia (the brain’s innate immune cells) and neutrophils (peripheral rapid responders).
When the blood–brain barrier (BBB) is disrupted, neutrophils enter the CNS and inflammation becomes self-amplifying.
Neutrophils can form NETs (neutrophil extracellular traps - DNA + histones + enzymes like MPO/elastase).
In the brain, NETs mean oxidative damage, mitochondrial stress, neuronal injury - and further microglial activation. A vicious cycle.
Read 19 tweets

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