Central Nervous System Injury

The Scar Solution Natural Scar Removal

Scar Solution By Sean Lowry

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The lack of tissue regeneration in the CNS is due to a complex series of events that follow injury. Though these events are necessary for the restoration of the blood-brain barrier and minimization of secondary tissue damage, they also result in the formation of an environment which is not conducive to tissue regeneration. Damage to the CNS initiates an astrocytic response resulting in a glial scar. Damaged tissue releases molecular cues which promote astrocytic glial cell activity. Transforming growth factor b (TGFb) is among the molecular cues that increase immediately after injury and contribute to the initiation of reactive gliosis. Astrocytes migrate, proliferate, increase in size, and produce a glial scar rich in extracellular matrix (ECM) proteins, myelin, astrocytes, and oligodendro-cytes. While hypertrophic astrocytes comprise a significant portion of the glial scar, production of glycosaminoglycans is critical to glial scar formation. Reactive astrocytes produce a variety of proteoglycans including chondroitin

Fig. 1 Illustration of CNS glial scarring after injury. A series of events leads to the formation of an environment that is not conducive to tissue regeneration. Among these events, reactive astrocytes form an inhibitory glial scar. However, astrocytes have exhibited reduced activity on select nanomaterials. Figure adapted from (Silver and Miller 2004)

Fig. 1 Illustration of CNS glial scarring after injury. A series of events leads to the formation of an environment that is not conducive to tissue regeneration. Among these events, reactive astrocytes form an inhibitory glial scar. However, astrocytes have exhibited reduced activity on select nanomaterials. Figure adapted from (Silver and Miller 2004)

sulfate proteoglycans (CSPGs). CSPGs are known to aggressively inhibit axon outgrowth (Silver and Miller 2004). Glial scar tissue can prevent spontaneous neural tissue regeneration by serving as a physical and chemical barrier to tissue regeneration (Fig. 1). Axonal outgrowth from healthy tissue is impeded by this glial scar, preventing reinnervation of targets on the other side of the injury. Without a clear pathway for growing axons, neural tissue regeneration is impossible.

Beyond traumatic injury to the spine, damage as minimal as that which is caused by the insertion of a microelectrode into the brain can initiate an astrocytic response. Upon insertion of a microelectrode, neural cell tissue, as well as the blood-brain barrier, is damaged. To repair broken blood vessels, support damaged neural cells, and clean up cellular debris, microglia, astrocytes, and macrophages are recruited to the site of injury by molecular signaling. Though this cellular activity is necessary to repair the blood-brain barrier and minimize secondary damage, the result of overactive astrocytes is the formation of glial scar tissue similar to that which forms following traumatic injury. In this case, the formation of glial scar tissue compromises the effectiveness of the microelectrode. This chronic inflammatory response is a major complication for electrodes implanted for extended periods of time (Polikov et al. 2005). The utility of the microelectrode depends on a conductive interface to record or deliver electrical impulses. As the glial scar forms, the impedance at the electrode interface increases. Significantly reduced conductivity can render the electrode ineffective. Both spinal cord injury and microelectrode insertion result in compromised CNS tissue. Biomaterials, whether used for the fabrication of a microelectrode or formed into a scaffold for CNS tissue regeneration, aim to moderate astrocytic glial cell activity while promoting neural tissue growth. This is the promise for nanotechnology and nanomaterials.

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