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This process involves both molecular and morphological changes in the astrocytes, including increased expression of GFAP, vimentin and nestin, uptake of excitotoxic glutamate, protection from oxidative stress by the production of GSH, neuroprotection by release of adenosine, degradation of amyloid-beta peptides, facilitation of blood-brain barrier, increased formation of gap junctions between astrocytes, formation of scars and, in some cases release of inflammatory cytokines, including tumor necrosis factor- (TNF-), and production of ROS [3,35,38-40]

TB-500 reduces production of pro-inflammatory cytokines at injury sites, creating a more permissive environment for nerve regeneration

This effect is mediated through the PTEN/AKT/FOXO1 signaling pathway, which is crucial for muscle growth and maintenance 7