EAE Defense
In a previous post we pointed to a review article that concluded that EAE is a poor model for MS.
Now we have a couple of MS research heavy-weights defending EAE. They claim that EAE led directly to the development of: glatiramer acetate, mitoxantrone, and natalizumab.
I guess I'm confused. GA (Copaxone) was developed to *replace* EAE and create a better animal model, it was tried in EAE after is was invented - EAE did not *lead* to its creation - just its use in MS. Similarly for mitoxantrone (Novantrone), which was originally developed for cancer. Natalizumab (Tysabri) will need to be discounted in this argument because one of the rebuttal's authors (and Accelerated Cure Project advisor), Larry Steinman, has publicly stated that he fought to keep natalizumab from being used in humans due to the potential for immuno-compromise.
Even if we allow for those 3 "successes", we have to ask ourselves what we mean by a "good" or "working" model if this is all we get out of 73 years of use. What about all the drugs that worked on EAE and not in MS? What about all the drugs that may have worked in MS, but because they didn't work in EAE were never tried? Let's take the money we spend on EAE and spend it on developing a better model.
Funny and sad
eae
"We have produced evidence which now clearly demonstrates that an incorrect scientific assumption has previously been made, with regard to the process by which the disease progresses, and which also explains why so little progress has been made in multiple sclerosis research during the last three decades. Our research has further clarified the incorrect scientific assumption that findings can be extrapolated to this area of research from the closest animal model, experimental allergic encephalomyelitis (EAE). Whilst the human counterpart of EAE was previously thought to be MS we can now confirm that this is not the case and that the human counterpart to EAE is, in fact, acute disseminated encephalomyelitis (ADEM) and acute haemorrhagic leukoencephalitis (AHLE). This important clarification should enable more effective and targeted research to be carried out and, together with our conclusion that MS is a neurodegenerative and metabollic disorder with the predominant genes being on chromosome 17, takes us one step closer in the hunt for the cause of MS".
2002 article published by Royal College of Physicians of Edinburgh