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
Radial glial cell to replace lost or damaged tissue in a process known as gliosis. Radial glial cells originate from the transformation of neuroepithelial cells that form the neural plate during the early phases of pre-natal neurogenesis. This process is mediated through the down-regulation of epithelium-related protein expression (such as tight junctions) and an up-regulation of glial-specific features such as glycogen granules, the astrocyte glutamate transporter (GLAST), the intermediate filament vimentin, and, in some instances, including humans, glial fibrillary acidic protein (GFAP). After this transition, radial glia retain many of the original characteristics of neuroepithelial cells including: their apical-basal polarity, their position along