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Posted On: 04/08/2024 9:07:00 PM
Post# of 148870
Good find.
Leronlimab downregulates (antagonist) IL-1 and JAK1, 2 and 3. I took a look at the activation pathway for SCG3, It is upregulated by increased intracellular CA2+, by downregulating CA2+ leronlimab would downregulate SCG3. SGC3 is implicated in a host of diseases - Alzheimer's disease, Parkinson's disease, diabetic retinopathy, various cancers, macular degeneration, heart disease, stroke, and type 2 diabetes.
What SCG3 and so many other inflammatory and inflammation disease causing proteins link back to is CCR5 and it's ligands. Why aren't scientists and doctors realizing this.
Quote:
1. Long COVID leads to ongoing inflammation detectable in the blood, with patterns varying by symptom type, pointing towards personalized treatment needs.
2. Existing immune-modulating drugs, like IL-1 antagonists and JAK inhibitors, could offer potential treatment options for long COVID, suggesting a hopeful path for clinical trials.
They found that certain groups of symptoms appeared to be associated with specific proteins. For example, people with gastrointestinal symptoms had increased levels of a marker called SCG3, which has previously been linked to impaired communication between the gut and the brain.
https://neurosciencenews.com/inflammation-blo...vid-25880/
Leronlimab downregulates (antagonist) IL-1 and JAK1, 2 and 3. I took a look at the activation pathway for SCG3, It is upregulated by increased intracellular CA2+, by downregulating CA2+ leronlimab would downregulate SCG3. SGC3 is implicated in a host of diseases - Alzheimer's disease, Parkinson's disease, diabetic retinopathy, various cancers, macular degeneration, heart disease, stroke, and type 2 diabetes.
What SCG3 and so many other inflammatory and inflammation disease causing proteins link back to is CCR5 and it's ligands. Why aren't scientists and doctors realizing this.
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