Long COVID in adults is characterized by (protein) markers of:
- inflammation
- blood vessel clotting
However, similar studies in pediatric cohorts are almost non-existent... until now.
This study suggests that pediatric Long COVID is characterized by unique pathophysiology and isn't stress- or anxiety-induced...🧵
\ The Study:
Scientists from the University of Rome and Fondazione Policlinico Universitario discovered that 34 children and adolescents between the ages of 2 and 18 have an abundance of pro-inflammatory cytokines in their blood.
A subset of the cytokines have angiogenic (blood vessel growth-promoting) properties.
\ The Study Continued:
The signature of protein markers was distinct from children with the following:
- Multisystem inflammatory syndrome in children (MIS-C) (27 participants)
- Acute SARS-CoV-2 infection (32 participants)
- Healthy controls (19 participants)
*MIS-C is a rare but serious condition where different body parts can become inflamed, typically following a COVID-19 infection.
Here are the proteins in the blood that were changed.
\ The Results:
The following were high in the pediatric Long COVID cohort:
OSM
CXCL1
CXCL5
CXCL6
CXCL8
CXCL11
TNFSF11
STAMBP1a
These cytokines are pro-inflammatory and pro-angiogenic (promote blood vessel growth).
They represent a unique proteomic profile (yellow dots below).
\ Significance:
This data suggests pediatric Long COVID is characterized by chronic inflammation and is NOT the result of a mental health condition caused by pandemic restrictions.
This proteomic profile identified pediatric Long COVID patients with an accuracy of 93%.
An AI-based blood test is being developed by the same group to diagnose pediatric Long COVID (👇 )
Find out how we are remotely connecting geographically dispersed health professionals with pediatric cohorts.
This is designed to fast-track our understanding of pediatric neuroimmune axis conditions, such as pediatric Long COVID.
Check out our free newsletter (pinned post) to learn more.
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In 2017, Alina Sternberg, a psychiatrist, was hit with crushing fatigue and brain fog.
Neurologists told her the symptoms were caused by depression.
"No, I can enjoy my life, and I know what depression is... I’m a psychiatrist!”
It took 6 years to discover the culprit...🧵
Alina's symptoms became progressively worse.
By 2023, she spent most of her days in bed.
Not only was she hit with soul-crushing fatigue, but her memory deteriorated.
One day,she forgot her way home, a place she had lived for 20 years.
Alina asked a colleague at the hospital where she worked if he would check to see if she had autoantibodies in her blood that might be attacking her brain.
He told her, "That is impossible because you aren't psychotic.”
Patients with atopic dermatitis are at increased risk of having severe depression.
A new study discovered the inflammatory link and new treatment approach...🧵
Proteomic analysis of 353 serum proteins was conducted on healthy controls and patients with either:
- Major depressive disorder (MDD)
- atopic dermatitis
- psoriasis
The inflammatory profile of those with MDD aligned most closely with atopic dermatitis.
(Both showed strong Th2 (T helper type 2) immune activation)
Computational (in silico) simulations were used to predict which drug might reverse this immune signature.
The IL-4/IL-13 inhibitor dupilumab (Dupixent, used for AD) reversed the MDD inflammatory signature more effectively than other agents tested (e.g., cyclosporine).
If this were a healthy brain would light up evenly.
But the brains of Long COVID patients light up in patches...🧵
\ The Discovery:
Researchers from the Department of Nuclear Medicine at Université de Lorraine in Nancy, France, intravenously injected a radioactive tracer into participants with Long COVID and healthy controls.
\ How 18F-FDG Works:
The tracer, 18F fluorodeoxyglucose (18F-FDG), is structurally similar to glucose, a sugar molecule transported into neurons from the bloodstream.
Once 18F-FDG is transported into neurons, it becomes trapped.
Here, the fluorine-18 isotopes decay, emitting light detected by the PET (positron emission tomography) scanner.
Neuropsychiatric symptoms, like OCD, can abruptly occur due to a dysregulated immune response to an infection.
Can depleting the antibody-producing immune cells be an effective form of treatment?
Here are the surprising results...🧵
Brain Inflammation Collaborative and Stanford researcher, Dr. Denise Calaprice, together with others at Stanford’s Immune Behavioral Health team, recently published a paper showing that 16 out of 23 (70%) patients with autoimmune OCD had "an unequivocal recovery following treatment with rituximab" (with and w/o co-administration of immune modulators).