MLN1202

A board to discuss future MS therapies in early stage (Phase I or II) trials.

MLN1202

Postby bromley » Mon Jul 25, 2005 6:40 am

Another drug / another trial

Is there anyone out there with MS who isn't on a drug or a drug trial?

http://investor.millennium.com/phoenix. ... highlight=

Bromley
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Postby OddDuck » Mon Jul 25, 2005 8:13 am

Unfortunately, I have a feeling these folks may be barking up the wrong tree (but who knows, right?) At least there are attempts at just about everything! That is something anyway.

Personally speaking, I wouldn't hold my breath about that particular study (i.e. blocking CCR2) yielding any real promising results.


(American Journal of Pathology. 2003;162:139-150.)
© 2003 American Society for Investigative Pathology

Experimental Autoimmune Encephalomyelitis (EAE) in CCR2-/- Mice
Susceptibility in Multiple Strains


Stefanie Gaupp*, David Pitt*, William A. Kuziel, Barbara Cannella* and Cedric S. Raine*
From the Departments of Pathology (Neuropathology),*Neurology,and Neuroscience,Albert Einstein College of Medicine, Bronx, New York; and the Section of Molecular Genetics and Microbiology,University of Texas at Austin, Austin, Texas

Chemokines are low molecular weight cytokines which act as chemoattractants for infiltrating cells bearing appropriate receptors (CCR) to sites of inflammation. It has been proposed that CCR2 on monocytes is responsible for their recruitment into the central nervous system (CNS) in experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis, and two previous reports have described resistance of CCR2-/- mice to EAE. The present study examined three different mouse strains with CCR2 deletions for susceptibility to EAE. Animals were studied up to 4 months post-sensitization and were examined by neuropathology, RNase protection assay, in situ hybridization, and in vitro assays. All three strains were found to be susceptible to EAE: C57BL/6 x J129 and Balb c strains, 100%; and C57BL/6, 67%. Unusual in CNS lesions of CCR2-/- mice was an overabundance of neutrophils versus monocytes in wild-type animals. An attempt of the immune system to develop compensatory mechanisms for the lack of CCR2 was evidenced by a corresponding increase in mRNA for other chemokines and CCR. Inasmuch as neutrophils replaced monocytes and led to demyelination, our findings support the concept that promiscuity of chemokines and CCR was able to surmount the deletion of CCR2, still resulting in full expression of this autoimmune disease.
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Postby OddDuck » Mon Jul 25, 2005 8:37 am

I did some further research.

If anyone wants to really get into the chemokine connection with relationship to MS, go here:

http://www.jneuroinflammation.com/content/2/1/7

That is an EXCELLENT overall study to read.

The bottom line is that it could be promising, but is pretty complex, and depends upon the specific model of MS, at what point in the MS cascade of events this treatment is initiated, the length of time of treatment, etc. etc.

Basically, though, it boils down to the treatment of inflammation (which some MS doesn't involve inflammation). But, still, could be promising.

(I do also have to note, though, that this treatment and study indicates how important stopping the migration of macrophages across the BBB is in MS.)

Interesting anyway..........

Best,

Deb
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Postby Sharon » Mon Jul 25, 2005 2:56 pm

What a pleasant surprise, Deb! Nice to have you posting once again.
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