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 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 11
A new study in Frontiers in Medicine analyzed 959 hospitalized COVID-19 patients (pre-vaccination).
It shows that T cell counts at admission strongly predict severe outcomes and mortality.
This isn’t just about inflammation - adaptive immunity is central🧵
Patients with CD3 T cells ≤ 666/mm³ had
2.3× higher risk of needing ventilatory support
2.4× higher risk of in-hospital death
CD4 ≤ 359/mm³ was associated with
2.8× higher risk of death
These associations remained independent after adjustment.
The study supports a model in which
T-cell responses (especially CD3/CD4) are weakened
Adaptive immunity fails to adequately control the virus
The body compensates through hyperactivation of innate immunity
The result is severe disease
Read 5 tweets
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
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

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