Hi Johnny--
good to hear from you. Your point on how it malfunctions in oxidative stress is a good one. It appears to malfunction in Alzheimer's, as well. I just wish the researchers would focus on mechanism of injury and preventative measures. Did you notice in the paper you linked how this process was reversed with antioxidants? That paper was a great find. Nice work!
Here were my thoughts on this from another thread -- and why I posted in on FB this morning.
What the researchers fail to mention is that this protein is found in neurodegenerative diseases and ischemic stroke. It's involved in axonal guidance, and comes in after injury.
Quote:
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)
http://www.ncbi.nlm.nih.gov/pubmed/21333637http://www.springerlink.com/content/l32u81587278q64t/http://www.landesbioscience.com/journal ... 1947614191
http://www.springerlink.com/content/t822327418652p81/Here's a study on modulating CRMP 2 in Alzheimers
Quote:
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.
http://mcb.asm.org/content/25/22/9973.fulland I don't think the full role of CRMP 2 is understood just yet. The Australian MS study used EAE in mice-
Quote:
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.
http://www.swimmunology.com/crmp-2-c.htmcheer
_________________
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
dual stents placed 5/09
CCSVI in MS