Is it easy to cure EAE in mice? Maybe...
Given Nader's blurb that three mice were rescued from the mouse model of Multiple Sclerosis, which was offered in the Thomas Barnard interview at this link:
https://www.investorvillage.com/smbd.asp?mb=1...d=21091991
I wondered how easy is it to cure Multiple Sclerosis in mice?
The MS mouse model is called Experimental Autoimmune Encephalomyelitis (EAE). EAE is induced in ordinary mice by injecting the mice with Myelin Oligodenctrocye Glycoprotein (MOG). Its pretty easy to make the EAE mouse model. Just inject some mice with the MOG protein.
The EAE mouse model is very widely used as a preclinical indicator by MS drug developers.
Unfortunately, curing EAE in mice is not so predictive of succes in humans as one might hope, as reported in this article:
https://www.nature.com/articles/nature11102
Apparently there are many cures for EAE in mice but none of them have worked in humans.
So I have to wonder, why did Nader make a big deal about leronlimab curing EAE in three mice, and why did that bring some near to "tears"? Is there something different about Cytodyn's EAE mouse experiments? Surely the scientists running those tests must be familiar with the many cures of EAE in mice that did not translate into humans?
Perhaps the Cytodyn scientists are focused on the really massive amount of literature that identifies M1 macrophages, both infiltrating the CNS from the blood stream and also resident in the CNS tissue (CNS resident macrophages are called microglia). Patterson's results on repolarizing M1 macrophages to M2 are certainly persuasive that leronlimab can help MS given the massive number of experiments identifying M1 macrophages as a key component of the MS disease pathway.
So a lot of evidence that leronlimab will be effective in MS, but it doesn't seem the slam dunk that Pourhassan seemed to be describing in the Thomas Barnard interview.
I found three things that can cure EAE in mice, but there must be many others.
Infection with some random parasite:
https://www.sciencedirect.com/science/article...110400054X
Some sort of partial bone marrow transplant:
https://www.pnas.org/content/pnas/112/52/15994.full.pdf
And CAR Tregs where the CAR is myelin oigodendrocyte glycoprotein (MOG):
https://link.springer.com/article/10.1186/1742-2094-9-112
Note that the Treg CAR targets MOG, the same protein that induces EAE in the mice. At least a few Treg cell therapy startups have active MS programs using the MOG protein as their engineered CAR target.
I wonder what, if anything, was different about the Cytodyn MS mice that were cured of EAE and how the Cytodyn experiments may have been different from other EAE cures.
Given Nader's blurb that three mice were rescued from the mouse model of Multiple Sclerosis, which was offered in the Thomas Barnard interview at this link:
https://www.investorvillage.com/smbd.asp?mb=1...d=21091991
I wondered how easy is it to cure Multiple Sclerosis in mice?
The MS mouse model is called Experimental Autoimmune Encephalomyelitis (EAE). EAE is induced in ordinary mice by injecting the mice with Myelin Oligodenctrocye Glycoprotein (MOG). Its pretty easy to make the EAE mouse model. Just inject some mice with the MOG protein.
The EAE mouse model is very widely used as a preclinical indicator by MS drug developers.
Unfortunately, curing EAE in mice is not so predictive of succes in humans as one might hope, as reported in this article:
https://www.nature.com/articles/nature11102
Apparently there are many cures for EAE in mice but none of them have worked in humans.
So I have to wonder, why did Nader make a big deal about leronlimab curing EAE in three mice, and why did that bring some near to "tears"? Is there something different about Cytodyn's EAE mouse experiments? Surely the scientists running those tests must be familiar with the many cures of EAE in mice that did not translate into humans?
Perhaps the Cytodyn scientists are focused on the really massive amount of literature that identifies M1 macrophages, both infiltrating the CNS from the blood stream and also resident in the CNS tissue (CNS resident macrophages are called microglia). Patterson's results on repolarizing M1 macrophages to M2 are certainly persuasive that leronlimab can help MS given the massive number of experiments identifying M1 macrophages as a key component of the MS disease pathway.
So a lot of evidence that leronlimab will be effective in MS, but it doesn't seem the slam dunk that Pourhassan seemed to be describing in the Thomas Barnard interview.
I found three things that can cure EAE in mice, but there must be many others.
Infection with some random parasite:
https://www.sciencedirect.com/science/article...110400054X
Some sort of partial bone marrow transplant:
https://www.pnas.org/content/pnas/112/52/15994.full.pdf
And CAR Tregs where the CAR is myelin oigodendrocyte glycoprotein (MOG):
https://link.springer.com/article/10.1186/1742-2094-9-112
Note that the Treg CAR targets MOG, the same protein that induces EAE in the mice. At least a few Treg cell therapy startups have active MS programs using the MOG protein as their engineered CAR target.
I wonder what, if anything, was different about the Cytodyn MS mice that were cured of EAE and how the Cytodyn experiments may have been different from other EAE cures.
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