Zdenek Vrozina Profile picture
Jun 24 17 tweets 3 min read Read on X
New brain MRI study (2025): Post-COVID patients show measurable structural changes - even without hospitalization.
Participants were not selected for having Long COVID!
What was found, why it matters, and how this fits into what we know about hypothalamus-related circuits. 🧵
COVID-19 doesn’t always leave visible scars - but in the brain, it leaves measurable traces.
A new multimodal MRI study (N=76 post-COVID vs N=51 controls) shows focal loss in key subcortical and limbic areas.
That includes:
Right amygdala, hippocampus, thalamus
Right putamen, caudate, pallidum
These aren’t random.
They’re deep grey structures involved in motivation, memory, alertness - all connected with hypothalamus-mediated homeostasis.
The study used:
structural T1 MRI
diffusion MRI (white matter microstructure)
resting-state fMRI (connectivity)
arterial spin labeling (perfusion)

And crucially:
Participants were not selected for having Long COVID!
That’s key.
All 76 had PCR-confirmed COVID-19.
But they weren’t selected based on symptoms.
59 of them later reported post-COVID symptoms.
So any MRI abnormalities were found regardless of symptom status.
Even non-hospitalized post-COVID patients (NHP; N=46) had statistically significant brain changes compared to healthy controls:
Reduced volume in right thalamus, amygdala, caudate
White matter disruption (eg left uncinate fasciculus)
Now let’s be clear:
The study found consistent, localized changes in brain regions linked to fatigue, memory, sleep, and mood regulation.
How big were the changes?
Average group differences were small - a few percent in volume.
But they were statistically significant even after FDR correction.

Which tells us something important
If every non-hospitalized patient had changes, the group differences would be huge.
If none did, there’d be no statistical signal.

So the most likely interpretation?
Somewhere between 30–60% of NHPs had measurable structural or microstructural changes (eg amygdala volume, FA in uncinate).
But here’s the catch.
The study didn’t do subject-level classification.
We can’t say who’s affected and who’s not.
We only know that as a group, post-COVID brains differ - even without severe illness.
That nuance matters:
Some NHPs were clearly affected.
Some were likely not - otherwise, group averages would differ more.

This also means symptoms ≠ required for damage.
And lack of symptoms ≠ guarantee of normal brain structure.
In the hospitalised subgroup, functional changes were more pronounced - particularly in default mode-insula-caudate connectivity.
But even NHPs showed measurable alterations in limbic white matter, consistent with inflammation or axonal stress.
So, to sum up:
No global brain shrinkage
But focal reductions in thalamus, amygdala, hippocampus
White matter injury in uncinate & cingulum
Changes present even in non-hospitalized
Not all affected - but many are
This fits with what we know about hypothalamus-centered systems:
Hypothalamus integrates signals from limbic and subcortical regions
Fatigue, sleep disruption, mood blunting = plausible outcomes
Damage here can dysregulate core homeostasis
Protect your hypothalamus.
Protect your brain.
Mishraa et al., 2025, Multimodal MRI Reveals Consistent Basal Ganglia and Limbic System Alterations in COVID-19 Survivors @szupraha @ZdravkoOnline
.medrxiv.org/content/10.110…
This is a preprint (Mishraa et al., 2025, medRxiv) and has not yet been peer-reviewed.
Still, its methods are solid, and the findings are consistent with prior studies, including UK Biobank (Nature, 2022).

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More from @ZdenekVrozina

Jun 24
Persistent virus = persistent symptoms. New peer-reviewed data confirm - long COVID patients still carry spike protein fragments - and show signs of immune breakdown.
What’s left behind doesn’t stay silent.🧵
This 2025 study analyzed blood samples from 65 patients with post-COVID condition (PCC, aka long COVID).
All had been infected between 2020 and mid-2021, before Omicron.
Using targeted mass spectrometry (MRM/SRM), researchers detected SARS-CoV-2 spike and nucleocapsid (NCAP) proteins in the plasma of symptomatic PCC patients.
These viral proteins persisted even 3–5 years after infection (sic) - but were absent in recovered, asymptomatic individuals.
Read 15 tweets
Jun 23
Aspirin and post-COVID diabetes:
A new large cohort study (35,000+ participants) found that daily low-dose aspirin reduces the risk of developing type 2 diabetes by 52%.

What exactly did they find? And why does this underscore the role of inflammation in COVID aftermaths?🧵
Researchers followed 35,525 adults in Italy from 2018 to 2022.
Main question: does daily low-dose aspirin (100 mg) reduce the incidence of new-onset type 2 diabetes (T2D)?

They used propensity score matching to balance age, BMI, prediabetes, and medications between groups.
Results:
Aspirin reduced the risk of T2D by 52% overall (HR = 0.48)
By 29% pre-pandemic
By 62% during the COVID-19 pandemic

The more systemic inflammation (eg COVID), the greater the benefit.
Read 10 tweets
Jun 22
Lockdowns hurt children.
We hear it all the time.
But this study shows that COVID-19 infection itself - not just pandemic stress - biologically drives serious mental health risks in kids.
Among 180k children, COVID was linked to:
suicidality
self-harm
poisoning🧵
Researchers analyzed Utah health insurance data from 2019-2021.
They compared kids (6-15) with and without confirmed COVID-19.
Children who had COVID showed:
2× higher risk of suicidal ideation
2.05× higher risk of self-harm
2.21× higher risk of poisoning (eg medication overdose)
And for those who had severe COVID:
Suicidal ideation: 2.53× higher
Self-harm: 2.57× higher
Poisoning: 2.68× higher
This wasn't about anxiety or school closure.
This was a dose-response pattern: more severe infection - more serious outcomes.
Read 11 tweets
Jun 21
COVID can damage memory - even months after recovery.
Not just any memory: the precision of memory, tied to the hippocampus.
A new study shows that it doesn’t recover over time!
It actually gets worse.
A short thread on the hippocampus, neurogenesis, and a virus that lingers.🧵
The hippocampus isn’t just - a memory disk.
It’s one of the only brain areas where new neurons grow in adulthood!
It helps us:
learn new things
navigate space and time
distinguish between “same” and “similar”
Exactly what “brain fog” disrupts.
A new study (Meyer & Zaiser, 2025) tested >1400 people using a memory precision task.
People post-COVID showed significantly lower scores (LDI).
The deficit appeared even in those who felt fully recovered!
This wasn’t fatigue or depression.
It was hippocampal dysfunction.
Read 11 tweets
Jun 20
COVID turns common EBV reactivation into a clinically significant event.

A new Czech study (Cell Reports, 2025):
SARS-CoV-2 can trigger Epstein-Barr virus (EBV) reactivation - and in some people, that leads to long-term lung damage in long COVID.🧵
The study analyzed 687 people with long COVID (4–16 weeks after infection).
Tests included:
lung function & chest X-ray
EBV serology (VCA IgM, IgA, EA-D IgG)
EBV DNA in blood
IL1/IL10 genetics
cytokines & immune profiling
Signs of recent EBV reactivation were found in 23% of patients.
Key marker: anti-VCA IgA
This antibody:
indicates a strong, recent EBV reactivation
correlates with lung damage and higher EBV viral load in blood
Read 9 tweets
Jun 19
A major new review from Yale (Moen, Baker, Iwasaki, 2025) offers the most comprehensive picture yet of what SARS-CoV-2 does to the nervous system.
The conclusion is stark:
Long COVID is a chronic neuroimmune disorder affecting brain, spinal cord, and peripheral nerves.🧵
Warning Sign #1: The pandemic didn’t end - it just changed shape.
The virus keeps evolving. The acute symptoms may fade.
But for many, the infection never truly ends.
Even young, previously healthy people experience:
mental fog,
dizziness when standing,
sensory disturbances,
exhaustion after minimal effort,
racing heart.
That’s Long COVID.
Warning Sign #2: The virus leaves behind molecular debris - and the immune system won’t let it go.
Sometimes it’s spike protein fragments in the blood.
Sometimes viral RNA in the olfactory bulb or even the skull.
This triggers persistent immune alarms:
T cells get activated
Inflammation spreads to the brain
Neuronal connections start breaking down
The war continues - long after the virus is gone.
Read 12 tweets

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