The standard model with its inconsistencies

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

The standard model with its inconsistencies

Postby frodo » Mon Mar 30, 2015 11:55 am

Given that most people around here is contrary to the accepted standard model of MS, I think is good to know its details and discuss its inconsistencies.

I have found a video that explains the model quite good (good explanation, even if it explains a bad model)

The link

https://www.youtube.com/watch?v=mYCwkor7dsU

First problem I notice is that they assume three different pathways for breaking the BBB. One for activated lymphocytes, other for b-cells and other for Th17 cells. Each of these cell cross the BBB with different pathways. I find more easy to accept that the BBB is previously weakened and they cross it without any problem.

Other thing that is not explained is the NAWM presence before the BBB breakdown.

Maybe we could make here a list of the problems that this standard model presents?
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Re: The standard model with its inconsistencies

Postby Rogan » Mon Mar 30, 2015 3:53 pm

Two problems with the standard model.

1. Hasn't found a root cause in 50 years.
2. The model's entire evidence base is off of inflicting healthy mice with EAE.

Mice are not humans and humans with "MS" don't get EAE.
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Re: The standard model with its inconsistencies

Postby Cece » Mon Mar 30, 2015 6:34 pm

No auto-antigen has been identified in MS.
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Re: The standard model with its inconsistencies

Postby NHE » Tue Mar 31, 2015 2:47 am

Rogan wrote:Two problems with the standard model.

1. Hasn't found a root cause in 50 years.
2. The model's entire evidence base is off of inflicting healthy mice with EAE.

Mice are not humans and humans with "MS" don't get EAE.


...and EAE mice, aka the SJL/J strain, are pretty messed up to begin with.

http://jaxmice.jax.org/strain/000686.html
SJL mice display a very high incidence of reticulum cell sarcomas resembling Hodgkin's disease by approximately one year of age. This strain is also characterized by extreme aggression in males and its susceptibility to experimental autoimmune encephalomyelitis (EAE) for multiple sclerosis research. SJL/J mice develop a spontaneous myopathy resulting from a splice-site mutation in the Dysferlin gene resulting in decreased levels of dysferlin protein in SJL/J mice and making this strain a good model for limb girdle muscular dystrophy 2B. SJL mice, fed an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat), fail to develop atherosclerotic aortic lesions in contrast to several highly susceptible strains of mice. SJL are immunocompetent but have elevated levels of circulating T cells.
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