I decided to dig a little deeper into why Monteluk
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Quote:
We know from published research that montelukast crosses the blood-brain barrier and accumulates in the brain over time and at levels substantially higher than other body tissues after 24 hours. Montelukast inhibits GPR172, a G-protein coupled receptor that is expressed on neurons and glial cells in the human brain. This may contribute to neuropsychiatric events. But the FDA has admitted the exact mechanisms of the medication are not well understood.
https://www.fda.gov/media/158486/download#:~:...c%20events.
The FDA may want to take note. GPR172 is also known as human riboflavin transporter 3 ((hRFT3). Riboflavin also known as Vitamin B2 can downregulate some of the same inflammatory chemokines that leronlimab also downregulates, ROS (reactive oxygen species) that leronlimab downregulates and reduce mitochondrial dysfunction like leronlimab. It does not seem to do so as effectively as leronlimab because it does not effect the binding ligands and the broader production of chemokines.
But GPR172 does offer some neuroprotection and blocking it could definitely be the cause of the psychiatric events. In addition low levels of riboflavin have been shown to have some effect in Alzheimer's, Parkinson's disease, multiple sclerosis and other neurodegenerative diseases.