Cece wrote:If KIR4.1 has to do with water transport, then its presence might be due to the abnormal cerebrospinal fluid hemodynamics, and it could also be a pre- and post-angioplasty biomarker for CCSVI patients.
The presence of KIR4.1 is interesting but there is more than one way to interpret it.
I really like the new blog, by the way. It is good to have all the information (and there is so much information!) in one easily linked place.
cheerleader wrote:Agree, Cece--this discvoery can be interpreted in many ways--but to jump to the conclusion that this is an autoimmune reaction to a water transport protein and discuss developing pharmaceutical treatments BEFORE understanding the mechanism behind this antibody response seems crazy-- this is what keeps getting us in to trouble with new MS medications.
It's taken from a press release from the upcoming American Academy of Neurology conference in Philadelphia in April. There were lots of different write ups about it. I just linked to the one that was open access.In the longitudinal analysis, pre-clinical MS patients had KIR4.1 antibodies several years prior to the first clinical attack.
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.
cheerleader wrote: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.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1416748/Treatment with plasmapheresis may fail in patients with multiple sclerosis because it does not remove antibrain antibodies from the intrathecal space.
Michal Schwartz’ studies revolutionized the current understanding of degenerative conditions of the central nervous system. Her theory not only broke long-held dogmas, but also shattered a conceptual wall between the brain and the immune system, which plays a fundamental role throughout life in supporting brain plasticity – with far-reaching clinical implications for behavior, cognition, stress, neurodegenerative and neurodevelopmental diseases. At Falling Walls, Schwartz explains the latest developments of her theory of “protective autoimmunity” that has inspired the search for new therapeutic strategies, harnessing or modulating immune cells to fight ageing, and acute and chronic neurodegenerative diseases.
As far as the Lucchinetti/Lesion Project research---Marc (Wheelchair Kamikazee) summed up what many on this board felt back in 2009 when I started a discussion on the Lesion Project--- general-discussion-f1/topic6851.htmlI'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.
cheerleader wrote:I'm hoping researchers look at the other situations where these KIR4.1 antibodies show up---in cerebral edema and hydrocephalus. There may be more clues in that line of research. http://ccsviinms.blogspot.com/2014/02/k ... cture.html
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