Mouse model EAE is not a useful multiple sclerosis model...

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MSUK
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Mouse model EAE is not a useful multiple sclerosis model...

Post by MSUK »

Mouse model EAE is not a useful multiple sclerosis model - study

EAE is not a useful model for demyelinating disease

Peter O. Behanemail, Abhijit Chaudhuri

Abstract

Experimental allergic encephalomyelitis (EAE) is the commonest, readily induced, organspecific, autoimmune disorder of laboratory animals of its kind.

It is an artificial disorder brought about by the immunisation of susceptible animals with brain antigens in complete Freund׳s adjuvant (CFA).

Variations can be induced by altering the nature of the antigen and the conditions involving immunisation.

Whilst it is often described as a demyelinating disease, in strict terms it is not, since the primary pathologic process is not demyelination but rather an encephalomyelitis that is immunologically induced. Rather, the prototype demyelinating disease is multiple sclerosis and its variants.

In this paper, the central question we ask is whether the data gleaned from the EAE model contributes to our understanding of the pathological events in MS.

Towards answering this, we describe the historical development of EAE and its hyperacute form, and discuss the findings studied extensively in the non-human primate which show that ordinary EAE is an exact model for ADEM in the human, and that the hyperacute form of EAE is represented by AHLE in the human. Additionally, we shall comment on the latest research on new variants of EAE, and explain our opinion regarding the use of EAE models in research aiming to understand the pathogenesis of multiple sclerosis.

Full article - http://www.msard-journal.com/article/S2 ... 7/fulltext

Source: Multiple Sclerosis and related disorders Copyright © 2014 Elsevier Inc (19/08/14)
MS-UK - http://www.ms-uk.org/
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NHE
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Re: Mouse model EAE is not a useful multiple sclerosis model

Post by NHE »

Also see their earlier paper...

The sad plight of multiple sclerosis research (low on fact, high on fiction): critical data to support it being a neurocristopathy.
Inflammopharmacology. 2010 Dec;18(6):265-90.
  • The literature for evidence of autoimmunity in multiple sclerosis (MS) is analysed critically. In contrast to the accepted theory, the human counterpart of the animal model experimental autoimmune demyelinating disease, experimental allergic encephalomyelitis (EAE), is not MS but a different demyelinating disorder, i.e. acute disseminated encephalomyelitis and acute haemorrhagic leucoencephalitis. Extrapolation of EAE research to MS has been guided largely by faith and a blind acceptance rather than sound, scientific rationale. No specific or sensitive immunological test exists that is diagnostic of MS despite the extensive application of modern technology. Immunosuppression has failed to have any consistent effect on prognosis or disease progression. The available data on MS immunotherapy are conflicting, at times contradictory and are based on findings in animals with EAE. They show predominantly a 30% effect in relapsing/remitting MS which suggests powerful placebo effect. Critical analysis of the epidemiological data shows no association with any specific autoimmune diseases, but does suggest that geographic factors and age at development posit an early onset possibly dependent on environmental influences. Certain neurological diseases are, however, found in association with MS, namely hypertrophic peripheral neuropathy, neurofibromatosis-1, cerebral glioma, glioblastoma multiforme and certain familial forms of narcolepsy. These share a common genetic influence possibly from genes on chromosome 17 affecting cell proliferation. A significant number of these disorders are of neural crest origin, the classical example being abnormalities of the Schwann cell. These and other data allow us to propose that MS is a developmental neural crest disorder, i.e. a cristopathy, implicating glial cell dysfunction with diffuse blood-brain barrier breakdown. The data on transcription factor SOX10 mutations in animals may explain these bizarre clinical associations with MS and the phenotypic variability of such alterations (Cossais et al. 2010). Research directed to the area of neural crest associations is likely to be rewarding.
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Re: Mouse model EAE is not a useful multiple sclerosis model

Post by CureOrBust »

The sad plight of multiple sclerosis research (low on fact, high on fiction): critical data to support it being a neurocristopathy wrote:...The available data on MS immunotherapy are conflicting, at times contradictory and are based on findings in animals with EAE. They show predominantly a 30% effect in relapsing/remitting MS which suggests powerful placebo effect....
I am not a fan of EAE, but still not sure how that statement made it through the peer review process (or was ever written). My understanding of the trial process is that they were getting 30% OVER the placebo effect.
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