Glial fibrillary acidic protein was described. Patients with GFAP astrocytopathy developed meningoencephalomyelitis with inflammation of the meninges, the brain parenchyma, and the spinal cord. About one third of cases were associated with various cancers and many also expressed other CNS autoantibodies. There are multiple disorders associated with improper GFAP regulation, and injury can cause glial cells to react in detrimental ways. Glial scarring is a consequence of several neurodegenerative conditions, as well as injury that severs neural material. The scar is formed by astrocytes interacting with fibrous tissue to re-establish the glial margins around the central injury core and is partially caused by up-regulation
Satellite glial cell found in different cells. Although SGCs express glial fibrillary acidic protein (GFAP) and different S-100 proteins, the most useful marker available today for SGC identification is glutamine synthetase (GS). The levels of GS are relatively low at rest, but they greatly increase if the neuron undergoes axonal damage. Furthermore, SGCs also possess mechanisms to release cytokines, adenosine triphosphate (ATP), and other chemical messengers. Research is currently ongoing in determining the physiological role of satellite glial cells. Current theories suggest that SGCs have a significant role in controlling the microenvironment of the sympathetic ganglia. This is based on the observation that