In a study that reshapes what we know about COVID19, scientists have discovered that coagulation protein fibrin causes unusual clotting & inflammation that have become hallmarks of the disease, while also suppressing the body's ability to clear virus.
Importantly, the team also identified a new antibody therapy to combat all of these deleterious effects. The study by overturns the prevailing theory that blood clotting is merely a consequence of inflammation in COVID-19.
Through experiments in the lab and with mice, the researchers show that blood clotting is instead a primary effect, driving other problems—including toxic inflammation, impaired viral clearance, and neurological symptoms prevalent in those with COVID-19 and long COVID.
In this study, scientists found that fibrin becomes even more toxic in COVID-19 as it binds to both the virus and immune cells, creating unusual clots that lead to inflammation, fibrosis, and loss of neurons.
Knowing that fibrin is instigator of inflammation & neurological symptoms, we can build a new path forward for treating the disease at the root. In their experiments, neutralizing blood toxicity with fibrin antibody therapy can protect the brain and body after COVID infection.
As fibrinogen plasma levels in acute COVID-19 are a predictive biomarker for cognitive impairment in longCOVID, it could be used to stratify patients as candidates for entry into phase 2 trials.
Fibrin immunotherapy can be tested for its potential to reduce adverse health outcomes due to long COVID as part of a multipronged approach with prevention and vaccination measures.
A small brain-imaging study found that people with #LongCOVID showed slower thinking and reaction times during a cognitive task.
➡️ Advanced MRI scans revealed changes in how important brain networks communicate with each other, especially those involved in attention, language, and decision-making. 1/
Researchers found altered connectivity in key brain networks:
• Salience network
• Language network
• Central executive network
• Sensorimotor and visual networks
➡️ These systems are essential for attention, decision-making, and task control. 2/
The most prominent deficits were seen in the salience network, which helps the brain detect and respond to important stimuli.
➡️ Connectivity problems in this network were more severe with longer illness duration. 3/
➡️ Compared with healthy controls,
✔ Long COVID patients had blunted morning cortisol peaks
✔ Higher evening cortisol
✔ Loss of normal circadian pattern
Blood cortisol alone failed to detect these changes. 2/
Key insight:
➡️ Salivary cortisol profiling may be a more sensitive marker of stress-system dysfunction in LongCOVID than standard blood tests.
➡️ HPA axis disruption could underlie:
• Fatigue
• Brain fog
• Sleep disturbance
• Dysautonomia. 3/
➡️ New review highlights that persistent cognitive symptoms in COVID survivors are strongly linked to pro-inflammatory cytokines and blood–brain barrier (BBB) dysfunction.
➡️ Key culprits include IL-6, TNF-α, IL-1β, IL-8, IL-13 and MCP-1 — many remain elevated months after infection.
🔥 COVID-19 is not just a respiratory disease.
➡️ Evidence suggests cognitive impairment can occur due to:
Post-COVID fatigue isn’t just subjective.
Using advanced MRI, researchers found real changes in brain blood flow and oxygen metabolism in people with Post-COVID-19 Syndrome (PCS) after mild infection.
➡️ Key finding:
PCS patients showed increased oxygen metabolism in the hippocampus (memory hub) but reduced metabolism in the anterior cingulate cortex (ACC) — despite no visible brain atrophy. 1/
Why this matters:
➡️ Higher hippocampal metabolism was linked to better cognitive performance, suggesting a compensatory response to maintain thinking and memory in PCS. 2/
In contrast, lower anterior cingulate cortex (ACC) metabolism correlated with: