growth cone in the damaged regions. Among inhibitory factors, oligodendrocyte and myelin-derived inhibitory ligands are membrane-bound, meaning that, in the case of injury, those factors are not upregulated or overexpressed, rather it is from direct contact between intact or degraded myelin (or oligodendrocytes) and newly forming neurons. Nevertheless, with scar formation, many cell types in the brain release growth-inhibitory ligands such as basal lamina components, inhibitory axon guidance molecules and chondroitin sulfate proteoglycans. Inhibitory action of such factors may be a protection of the brain from inflammation. Okano and Sawamoto used an astrocyte-selective conditional Stat3-deficient mice model to examine the role of reactive astrocytes. The result was increased widespread CD11b-positive inflammatory cell invasion and demyelination. Application Brain damage itself can induce endogenous regeneration. Many studies have proven endogenous regeneration as a possible treatment of brain damage. However, the inhibitory reaction of the surrounding tissue of damaged region must be overcome before the treatment produces significant improvement. Traumatic brain injury In the study of the endogenous regeneration of the brain done by Scharff and co-researchers, damaged neurons in a songbird brain are regenerated with the same neuronal types where regeneration occurs (in the case of the study, the hippocampus). However, in places where normal regeneration of the neuron does not occur, there was no replacement of damaged neurons. Thus, recovering brain function after a brain injury was supposed to have limitations. However, a current study revealed that neurons are repaired to some degree after damage, from the SVZ. The migrating ability of progenitor cells in the SVZ form chain-like structures and laterally move progenitor cells towards the injured region. Along with progenitor cells, thin astrocytic processes and blood vessels also play an important role in the migration of neuroblasts, suggesting that the blood vessels may act as a scaffold. Other factors that contribute of the migration are slit proteins (produced at the choroid plexus) and their gradient (generated by the flow of cerebrospinal fluid). However, only 0.2% of new neurons survived and functioned in this study. Enhancing neurogenesis can be done by injecting growth factors such as fibroblast growth factor-2 (FGF-2) and epidermal growth factor (EGF). However, enhanced neurogenesis also have the possibility of epilepsy resulting in prolonged seizures. Parkinson's Disease Although endogenous regeneration methods are showing some promising evidence in treating brain ischemia, the current body of knowledge regarding promoting and inhibiting endogenous regeneration is not sufficient to treat Parkinson's