Solve SCI
Goal: Allow Glial Scar to be Growth-Permissive
Stop Production of Molecules that (potentially) cause gliosis
TNF-alpha
endothelin-1
thrombin
IL-1
IL-6
CNTF
Cytokines
Mitigate effects of glial scar molecules that inhibit neurological regeneration
Phosphacan
Slit proteins
Ephrin B-2
Brevican
Tenascin
Versican
Semaphorin 3
Chondroitin Sulfate Proteoglycans
Removing or preventing the production of sugar epitopes on proteoglycan molecules allows for axonal regeneration. (Bradbury, et al., 2002; Grimpe and Silver, 2004; McKeon, et al., 1995; McKeon, et al., 1991; Steinmetz, et al., 2005)
Enzyme which degrades Chondroitin Sulfate Proteoglycan shows local efficacy in enhancing axonal growth. (Cafferty et al., 2007)
Injured corticospinal fibers and uninjured serotonergic fibers increase sprouting after enzymatic treatment to remove sugar epitopes (Barritt et al., 2006)
In vivo studies have revealed remarkable long-distance regeneration of adult axons though CNS white matter tracts after enzymatic treatment to digest these proteoglycan side chains (Steinmetz, et al., 2005)
Neurocan
Introduce Growth-Promoting Factors
cAMP & NT-3 combination has been shown to allow regeneration past lesion site
Intrathecally delivered NT-3, NGF, and GDNF can promote axonal regeneration across the dorsal root entry zone (Ramer et al., 2002; Ramer et al., 2000)
L-1
Polysialic Acid Neural Cell Adhesion Molecule
Oncomodulin
Extracellular Matrix
A-Cell Product
Remyelenize Axons
RXR agonist 9 cis retinoic acid. (Jeffrey K Huang, Andrew A Jarjour)
Subtopic