This Is MS Multiple Sclerosis Knowledge & Support Community

cheerleader wrote:
I've discussed the findings of The Lesion Project with a number of neurologists, and most of them are a bit skeptical of the findings. They say that even if a patient displays only one type of lesion postmortem, that does not mean that their lesions didn't evolve through different stages over time.

The different patterns could well just be due to the age of the lesion. And there's been no new research on the different "lesion patterns" since then. Lucchinetti has moved on to look at loss of gray matter in MS.

Well, now Luchinetti is back with a new article!!! And heterogeneity is again a real posibility. The age of the lesion is not associated with its type.

http://www.ncbi.nlm.nih.gov/pubmed/24771535

On the other hand, it seems that the Kir4.1 connection is not so clear as it seemed.

http://www.ncbi.nlm.nih.gov/pubmed/24756568

It is not explained in the abstract how the tests were performed but these are not positive news. We will have to wait for additional studies to see how this fixes in the global picture. Other groups still consider kir4.1 a possibility.

http://www.ncbi.nlm.nih.gov/pubmed/24817862 (no abstract but available in the next link)
http://journal.frontiersin.org/Journal/ ... 00062/full

Just to complement previous post, it seems that there is additional information about the negative finding of kir4.1 in the former french study (Lack of confirmation of anti-inward rectifying potassium channel 4.1 antibodies as reliable markers of multiple sclerosis. Nerrant E1, et al, Gui-de-Chauliac Hospital, France.).

The results are still surprising even for the group that found it. They commented their research here:

http://www.msdiscovery.org/news/new_fin ... wo-studies

It is hypothesed that the difference with previous results could be in the ELISA test:

"The ELISA used in the 2012 paper from Hemmer’s group and in the current Multiple Sclerosis Journal report immobilized the first extracellular loop and adjacent intramembrane regions on streptavidin-coated plates, to which anti-human Kir4.1 antibodies and patient samples were added. But apparently attachment of the antigen could not be precisely replicated."

“Many variables influence performance of ELISA,” Simon Rinaldi, Ph.D., of the Nuffield Department of Clinical Neurosciences at the University of Oxford told MSDF. “These include the nature of the peptide versus whole protein affixed to the plate, its concentration and binding density, the composition of the plate itself, the blocking steps, method of washing, temperatures used for primary and secondary steps, and perhaps most critically, the primary concentration and secondary antibody used.” Rinaldi was not involved in either of the Kir4.1 studies.