The protein they're blocking is CRMP 2
http://www.dailypioneer.com/home/online ... rosis.html
What the researchers fail to mention is that this protein is found in neurodegenerative diseases and ischemic stroke.
http://www.landesbioscience.com/journal ... 1947614191
Collapsin response mediator protein2 (CRMP2) is a brain-specific protein involved in neuronal polarity and axonal guidance, and phosphorylation of CRMP2 regulates the function and the activity. CRMP2 has shown to be implicated in several neurodegenerative diseases (Alzheimer's disease, epilepsy and ischemia)
I'm kind of sick of these research press releases that mention MS, and not the other associated diseases where these "NEW discoveries" are also found....where is the collaborative effort to understand WHY there is ischemic injury in the MS brain?
Here's a study on modulating CRMP 2 in Alzheimers
In another study, we have recently found that CRMP-2 interacts with Specifically Rac1-Associated protein (Sra-1/CYFIP1) (43a), which directly interacts with actin filaments (45). Thus, CRMP-2 may associate with actin filaments through Sra-1 in growth cones. In this study, Rho kinase-induced phosphorylation of CRMP-2 had no effect on the actin binding ability of CRMP-2. CRMP-2 is a highly conserved phosphoprotein, and its phosphorylation states alter upon NGF-induced neuronal differentiation or in the formation of degenerating neurites in the brains of patients with Alzheimer's disease (12, 33). These findings raise the possibility that other kinases up- or down-regulate CRMP-2 activity and mediate actin reorganization in the Rho family GTPase-mediated signal cascade. Further studies characterizing the protein kinases may shed some light on other functions of CRMP-2.
and I don't think the full role of CRMP 2 is understood just yet. The Australian MS study used EAE in mice (sou was right) and the human brain is different....it has a purpose.
Since CRMP-2 is present in adult and aged brains, there is reason to speculate that it may have a role in neuritic and axonal growth and regeneration and thus contribute to a high level of plasticity in adult brains. In some disease states, CRMP-2 has been shown to be reduced, such as in Down syndrome fetal brain, epilepsy brain hippocampus and areas of traumatic brain injury. In Alzheimer’s disease, CRMP-2 has been shown to be associated with the paired helical filaments (PHF) in degenerating neurons. This PHF-associated CMPR-2 has been shown to be highly phosphorylated. This hyperphosphorylated form of CMPR-2 may lead to its inactivation and may accelerate the neuritic degeneration in Alzheimer’s disease.
but the headline sure looked good, huh?