Traumatic injury to the brain elicits physical damage to the vascular networks and neural circuit architecture alike. Gliosis is a reactive cellular process that occurs after injury. As with scarring in other organs and tissues, the glial scar is the body's mechanism to protect and begin the healing process in the nervous system. Unfortunately, the glial scar also serves as a major barrier to regenerating axons, and therefore, its emergence in evolution amongst higher vertebrates appears counterproductive (Rolls 2009).

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As part of scar formation in the brain, astrocytes form a dense network of gap junctions that generate a physical barrier to axon extensions. (Cregg 2014). Coupled with many neuro-development inhibitor molecules that are secreted by the cells within the glial scar, physical and functional recovery from chronic injury is inhibited. Consequently, we believe that the recovery can be attributed to one or more of the following hypothesized mechanisms of action:

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• Reductions in neuroinflammation being achieved through down-regulation of pro-inflammatory genes and up-regulation of anti-inflammatory genes (Teng-Chao 2021, Mamber 2011)

• Reversal of gliosis associated with post-concussive syndrome.

• Reduced scarring in damaged areas of the cerebrovascular system potentially leading to improved brain hemodynamics.

• Lowered fibrin levels lessening the physical interference of scar tissue with normal transmission of brain signals and restoring the extracellular matrix (Mamber 2004).

• Inhibition of microglial infiltration of the wound area decreasing inflammation and gliosis (Beech Tree Labs / Harvard Medical School).

• Induction of neuron remyelination; observations of remyelination in peripheral nerves (B.E.T.) may be broadened to encompass all neurons.

• Stimulation of dendritic cells signaling macrophages to shift from their active state (which can be destructive if uncontrolled) to a resting phase which facilitates healing (Sanders, Mitchell – personal communication).