We have standardized and validated the adult zebrafish EAE model. This model can help get a quick idea of in vivo activity of drugs in a week using very low quantities of candidate compounds. Further work will be required to define this model particularly as it is found that zebrafish may not express a MOG homologue.
- Zebrafish develop EAE
- Zebrafish EAE is treated with MS DMT
- You don't need to use mice, or larger animals, to look for Immunosuppressive treatments
- Another nail in the rodent EAE coffin?
- If this work is true, and it needs to be repeated, the authors lucked out
As anyone who works on animals in the EU, you are committed to consider the 3Rs (refinement, reduction replacement) of animals in research.
People take the argument for using mice because there is no other less sentient animal to do the study.
This rug is being pulled from under the carpet and if this work proves to be true, it could set the cat amongst the pigeons.
Zebrafish are one of the model organisms that people use because the offspring are transparent and you can make transgenic ,gene-altered fish. There are quite a few myelination projects going on in these fish.
However, this study says you can get EAE in fish, by immunizing them with myelin peptides just like you would do in a mouse.
Is this the end of mouse EAE,. Maybe if the ethics committee eat this study up.
However, is it true?
It will be repeated and I guess this will be starting today or tomorrow being monday
The authors started by injecting myelin oligodendrocyte glycoprotein (MOG) in adjuvant to induce a paralytic disease. So far so good but as the fish do not produce MOG, how can this occur? There is no target to be attacked by the immune system.
Next they used fingolimod, which traps T (& B) cells in lymph glands so they can't get in the blood so thet can't get in the brain. However, fish don't have lmyph glands, but fingolimod blocks the EAE. How can that be?
The study "smells fishy"
This could mean it is all tosh, but maybe it is a lucky study.
The simple solution is for someone else to repeat it, but this takes fishy studies into a new level of ethics
Studies in the mouse report that immune responses to the MOG peptide can cross react with a immune responses to a nerve protein to induce the disease? Does this operate here? We don't know because there were no T cell responses measured.
This will mean repeating the work, but this may be another signal for killing off those EAE, that are justified in the name of MS research, that have so little real relevance.
I get that bad Home office (Animal Inspectors) feeling coming .