Axotomy

Regeneration occurs because of microglial hyperplasia and astroglial hypertrophy, activities that are lacking in the central axotomy response.

[6] Central neurons, upon being severed, generally fail to up-regulate the expression of trophic factors, a type of regeneration-associated protein.

[citation needed] Multiple sclerosis is a disease that demyelinates the nerves of the central nervous system, leading to deteriorated bodily function.

Using what is known about the axotomy response, doctors and researchers are looking to implement neuro-protective rehabilitation to patients in the early stages of multiple sclerosis in order to prevent the disease from running its course and causing irreversible disability.

These rehabilitations would include the utilization of trophic factors to aid in neuron survival and maintenance of synapsing function.

Researchers are currently working towards utilizing this potential for recovery to develop therapies for patients with traumatic brain injuries.

Two mechanisms that aid in the reinnervation process are acute inflammation and the activation of molecules in the extracellular matrix surrounding the synapse.

This cytokine, called osteopontin, may be able to aid in axon regeneration by exposing its integrin receptor binding sites.

A study done by Julie L. Chan proves the functionality of osteopontin in initiating the immune response necessary for synaptic repair and reorganization after injury (axotomy).

Altering the inflammatory response may unintentional halt the beneficial aspects of inflammation and have devastating effects on the brain's ability to heal itself.