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.
Feb 16 • 21 tweets • 3 min read
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
Feb 13 • 10 tweets • 2 min read
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.
Feb 12 • 16 tweets • 3 min read
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.
Feb 11 • 5 tweets • 1 min read
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.
Feb 8 • 14 tweets • 2 min read
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.
Feb 6 • 9 tweets • 2 min read
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.
Feb 6 • 10 tweets • 2 min read
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.
Feb 5 • 17 tweets • 2 min read
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.
Feb 2 • 15 tweets • 2 min read
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.
Feb 1 • 19 tweets • 3 min read
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.
Jan 31 • 18 tweets • 3 min read
Long COVID in children is often reduced to fatigue.
This study shows something far more concrete - measurable impairment in language skills - speaking, listening, and reading🧵
A new single-cell multiome study helps answer a key long-COVID question.
Where do the pathological monocyte programs seen later actually come from?
This paper maps how classical monocytes change already during the acute phase of COVID-19.
Jan 30 • 18 tweets • 3 min read
The choroid plexus (ChP) has become one of the most consistent findings in post-COVID and long COVID neuroimaging.
It is enlarged.
But larger alone doesn’t yet tell us what is actually happening🧵
A new paper in Alzheimer’s & Dementia moves the ChP story one step further.
It’s no longer just about volume - the authors also measure choroid plexus blood flow (CBF) and link it to cognition and biomarkers.
Jan 29 • 19 tweets • 3 min read
CD14 monocytes as the main pathological driver of long COVID?
A new Nature Immunology paper points to a clear biological signal in long COVID - CD14 monocytes - cells of the innate immune system🧵
The authors combined
single-cell RNA-seq
ATAC-seq (epigenetics)
plasma cytokines
functional stimulation assays
bronchoalveolar lavage (lung immune cells)
Crucially, they stratified patients by acute COVID severity - something many studies fail to do.
Jan 29 • 15 tweets • 2 min read
ME/CFS is sometimes framed as a body locked in stress mode.
The sympathetic nervous system permanently switched on.
Fight-or-flight with no way out.
It made sense.
Almost too much sense🧵
But the data have started telling a different story.
Not of a system that’s too strong -
but of one that’s exhausted.
Jan 28 • 20 tweets • 3 min read
Review paper.
At the center of Long COVID are three processes that reinforce each other -
persistent viral material, damage to the gut barrier, and chronic immune dysregulation. Together, they help explain why neurological and neuropsychiatric symptoms are so common and so persistent🧵
Viral persistence.
In a subset of people, fragments of SARS-CoV-2 - especially spike protein - persist for months or even years after the acute infection.
These viral remnants don’t need to actively replicate. Their continued presence is enough to keep the immune system switched on, similar to what we see in chronic viral infections like HIV.
Jan 27 • 18 tweets • 3 min read
An interesting metabolomic study suggests that one year after severe COVID-19, some people don’t just show altered metabolites in their blood -
they also carry chemically damaged proteins.
That’s not a sign of an ongoing reaction, but a trace of long-lasting biological stress🧵
Researchers followed patients who survived critical COVID-19 (ICU) and examined them 12M after discharge.
They compared those with Long COVID to those who fully recovered.
Using deep metabolomics and machine learning, they looked at cellular energy and molecular damage.
Jan 25 • 24 tweets • 4 min read
1. COVID-19 infection during pregnancy is not a neutral event.
Inflammation, viral proteins, and especially COVID-specific impairment of placental blood flow can affect fetal development - and abnormalities in exposed newborns are being reported with increasing consistency across studies.
That infection during pregnancy increases the risk of neurodevelopmental difficulties - in speech, motor skills, attention, and learning - has been known in public-health and medical circles for years.
Mothers were simply not told.
This wasn’t ignorance.
It was a decision to downplay the risk.
Jan 25 • 23 tweets • 3 min read
Long COVID is often described as fatigue, sleep disruption, and brain fog.
This preprint study asks a concrete question - does SARS-CoV-2 disrupt specific brain control systems that could explain these symptoms?🧵
They used two mouse models of SARS2
K18-hACE2 mice (low dose - survival - follow-up up to 90 days)
Wild-type BALB/c mice infected with mouse-adapted SARS2 (MA10), also followed long-term.
Jan 24 • 16 tweets • 2 min read
The outcome of SARS-CoV-2 infection seems to depend more on the quality of early innate immunity (pDC + NK cells) than on the strength of the antibody response.
A 2026 immunology study helps explain why.🧵
The authors compared two immune profiles:
Hospitalized COVID-19 patients
PCR-confirmed infection, mild to severe disease
Healthcare workers without proof of infection
PCR-negative and seronegative (IgM/IgG), unvaccinated (2020)
