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Posted On: 09/12/2020 6:57:32 PM
Post# of 148908
Thanks for your reply, ohm.
Yres, so much reporting on CCR5 in Multiple sclerosis.
The literature on this is so vast, I wondered just what kind of a reason Dr. Maddon and Dr. Burger might have for doubting the possible effectiveness of leronlimab in MS. Pourhassan made a big deal out of Burger's and Maddon's reluctance to pursue other leronlimab indications in his interview with Thomas Barnard.
Especially when the mouse model experiment is dirt cheap to conduct. Just get a few mice, inject them with MOG, watch EAE develop, then inject with leronlimab and watch them recover. It seems so easy anyone could do it. The mice are so small the whole experiment takes only one vial!
So why were Maddon and Burger resistant to this MS path?
I sure couldn't find any reason.
But is it CCR5 generally or is it the macrophages?
I believe its the macrophages specifically that destroy the myelin sheath.
So stop the macrophages and prevent myelin destruction and MS progression stops.
One more piece of data is that homosyzous CCR5delta32 mutants can still suffer MS. I saw several articles on whether heterozygous CCR5delta32 is protective for MS. Each is a few hundred patients from some limited world geography. Some studies say protective, some say not protective. So not really conclusive.
Another data point I found is that CCR5 knockout mice are not fully protected from MS.
Nader's blurb in the Barnard interview says the three mice were fully rescued.
So why is leronlimab better than CCR5 gene knockout in mice?
Well, if its the M1 macrophages that infiltrated from the bloodstream that are destroying the myelin sheath, perhaps that is the answer.
In any event, the simple MS mouse experiment should have been done years ago and I can't understand why anyone would be opposed to it. It seems like such a small and inexpensive exercise that its a no brainer to do it. But for some reason Pourhassan had to think it up himself and overcome some internal resistance, however mild, to get it done. Very interesting.
Another pice of data is
Yres, so much reporting on CCR5 in Multiple sclerosis.
The literature on this is so vast, I wondered just what kind of a reason Dr. Maddon and Dr. Burger might have for doubting the possible effectiveness of leronlimab in MS. Pourhassan made a big deal out of Burger's and Maddon's reluctance to pursue other leronlimab indications in his interview with Thomas Barnard.
Especially when the mouse model experiment is dirt cheap to conduct. Just get a few mice, inject them with MOG, watch EAE develop, then inject with leronlimab and watch them recover. It seems so easy anyone could do it. The mice are so small the whole experiment takes only one vial!
So why were Maddon and Burger resistant to this MS path?
I sure couldn't find any reason.
But is it CCR5 generally or is it the macrophages?
I believe its the macrophages specifically that destroy the myelin sheath.
So stop the macrophages and prevent myelin destruction and MS progression stops.
One more piece of data is that homosyzous CCR5delta32 mutants can still suffer MS. I saw several articles on whether heterozygous CCR5delta32 is protective for MS. Each is a few hundred patients from some limited world geography. Some studies say protective, some say not protective. So not really conclusive.
Another data point I found is that CCR5 knockout mice are not fully protected from MS.
Nader's blurb in the Barnard interview says the three mice were fully rescued.
So why is leronlimab better than CCR5 gene knockout in mice?
Well, if its the M1 macrophages that infiltrated from the bloodstream that are destroying the myelin sheath, perhaps that is the answer.
In any event, the simple MS mouse experiment should have been done years ago and I can't understand why anyone would be opposed to it. It seems like such a small and inexpensive exercise that its a no brainer to do it. But for some reason Pourhassan had to think it up himself and overcome some internal resistance, however mild, to get it done. Very interesting.
Another pice of data is
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