Zdenek Vrozina Profile picture
Feb 16 18 tweets 2 min read Read on X
Which brain circuits were most affected in this study - and what might that mean in everyday life?
The study shows something fundamental - reduced regulatory capacity of the brain. The problem is coordination, not character🧵
The most affected system was the salience network
(insula + anterior cingulate cortex).
Think of it as the brain’s regulatory switch.
It evaluates what is important, controls attention, and shifts the brain between rest and performance modes.
When this network becomes dysregulated, the result is reduced capacity to regulate mental load.
Faster overload, lower tolerance to distraction, increased irritability under fatigue, and difficulty sensing internal limits.
In this study, this network showed the strongest disruption - especially after cognitive exertion.
This points to a core difficulty with switching and regulating effort under stress.
The second key system was the central executive network (prefrontal cortex + parietal regions).
This is the brain’s management system - responsible for planning, working memory, and cognitive control.
When its coordination weakens, everyday functioning may subtly change.
Tasks require more effort to organize, decisions become more tiring, multitasking becomes harder, and mental flexibility decreases.
The study also found involvement of basal ganglia circuits.
These structures help initiate actions and maintain smooth cognitive flow.
When dysregulated, responses slow down and starting tasks becomes more difficult.
Some regions showed increased connectivity - especially the angular gyrus.
The authors interpret this as compensation.
When regulatory circuits weaken, the brain recruits alternative pathways to maintain function.
But compensation is not recovery.
It often means higher energy costs, slower processing, and faster exhaustion.
In simple terms -
the brain works harder to achieve lower efficiency.
What may look like a change in personality is usually something else.
Lower cognitive reserve, reduced network coordination, and increased energetic cost of mental activity.
The salience network sits at a unique crossroads.
It connects cognition, autonomic regulation, body awareness, stress responses, and immune signaling.
This makes it especially sensitive to inflammation.
Neuroimmune connection?
Immune signals - including cytokines and microglial activation - can directly disrupt this network.
Even mild chronic inflammation can impair synchronization between brain systems.
Similar network patterns have been reported in
post-sepsis syndromes
Lyme disease
HIV-associated neurocognitive disorders
ME/CFS
What is most concerning in this study is not just the presence of network disruption - but its dynamic nature.
The findings suggest an ongoing process rather than a static injury.
Over time, key regulatory connections - especially those linked to prefrontal control - appear to weaken.
At the same time, compensatory pathways become stronger.
This pattern is consistent with progressive network remodeling.
The brain reorganizes itself to maintain function under chronic physiological stress.
It does suggest a continuing biological process - not merely a transient after-effect of infection.
The biggest unanswered question remains scale.
Long COVID likely exists on a spectrum, and we still do not know how many people experience similar network-level changes.

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More from @ZdenekVrozina

Feb 17
One of the most important recent studies on post-COVID biology delivers a concerning message.
SARS-CoV-2 doesn’t just affect immune cells.
It can leave long-lasting changes directly in the immune proteins circulating in our blood.🧵
Think of the immune system in three layers.
immune cells (T, B, NK…)
signaling molecules
effector proteins - antibodies and complement
This study shows persistent changes in the deepest layer - the effector proteins themselves.
Researchers analyzed blood samples from more than 400 people after COVID-19.
They identified hundreds of chemical alterations in proteins - called ncAA modifications.
It’s about proteins becoming chemically different.
Read 14 tweets
Feb 16
Reinfection during the Omicron era is associated with about twice the risk of a documented long COVID diagnosis in children. Online September 2025, print issue February 2026🧵
This is a large US cohort study using data from 40 pediatric hospitals and including 465,717 children and adolescents (<21 years).
It compares the risk of long COVID (PASC) after
a first SARS-CoV-2 infection
a reinfection during the Omicron era.
Reinfection significantly increases the risk of long COVID in children.
PASC diagnosis rates
~904 cases per million after first infection
~1,884 per million after reinfection
Relative risk
≈ 2× higher after reinfection (RR 2.08).
Read 12 tweets
Feb 16
With longer duration of Long COVID, some key brain connections become weaker - especially those linked to prefrontal regulatory areas.
At the same time, other connections become stronger.
A new fMRI study shows this reflects a progressive reorganization of how brain networks communicate🧵
The study didn’t just look at isolated brain regions.
It examined how entire brain networks coordinate during cognitive effort - because performance depends less on single areas and more on how well networks synchronize
That synchronization was disrupted in Long COVID.
The main problem wasn’t damage to one function, but impaired regulation - the brain’s ability to detect what matters and shift efficiently into task-focused mode.
Read 21 tweets
Feb 13
A new macaque study looked at how immune memory forms after infections with different SARS-CoV-2 variants.
The main pattern is familiar from other viruses -
immune imprinting tends to stay biased toward earlier variants, even after later infections.🧵
The model is useful because it allows sequential infections under controlled conditions (Wuhan - Delta - Omicron), something that’s hard to observe clearly in humans.
Omicron as a primary infection = relatively weak new immune imprint
After first Omicron infection in macaques -
variant-specific anti-Omicron RBD antibodies developed slowly
overall immunogenicity was lower
T-cell responses were also weaker.
Read 10 tweets
Feb 12
A new study in Neuron links nuclear pore breakdown to TDP-43 pathology in ALS and related dementias.
This pathway is especially relevant because SARS-CoV-2 can both cleave TDP-43 and disrupt nuclear transport - potentially hitting the same vulnerability from two directions.🧵
The nuclear pore is a critical cellular gate.
It regulates the movement of RNA and proteins between the nucleus and cytoplasm.
In ALS and some dementias, this gate is known to fail - and TDP-43 leaves the nucleus and accumulates in toxic aggregates.
But why the pore breaks down has been unclear.
The study identifies a key player - VCP.
Normally, it acts as a cellular cleanup system, removing damaged proteins.
The problem arises when it becomes overactive.
Read 16 tweets
Feb 12
This study evaluated participants in the US who received the LP.8.1 mRNA COVID-19 booster between September and November 2025, showing
a shift of antibody boosting toward current variants, consistent with a partial dilution of immune imprinting🧵
The cohort had very high pre-existing immunity (median of 7 prior vaccine doses and a high rate of previous infection). Antibody responses were measured before boosting and again 3–6 weeks afterward.
The good news - the booster partially dilutes immune imprinting.
The largest relative increases in neutralizing antibodies were observed against currently circulating variants rather than the ancestral strain
Read 13 tweets

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