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
Glial scar molecules that chemically prevent axonal extensions. Moreover, the basal membrane component is expected to generate an additional physical and chemical barrier to axonal extensions. The formation of the glial scar is a complex process. Several main classes of molecular mediators of gliosis have been identified and are briefly discussed below. Two neuronally-important subclasses of transforming growth factor family of molecules are TGFβ-1 and TGFβ-2 that directly stimulate astrocytes, endothelial cells, and macrophages. TGFβ-1 has been observed to increase immediately after injury to the central nervous system, whereas TGFβ-2 expression occurs more slowly near the injury site. Further, TGFβ-2 has been