Gliosis is a reaction of brain tissue to injury of any kind, consisting of the proliferation of astrocytes and which ultimately results in the formation of glial scarring. Gliosis is often a consequence of traumatic, ischemic, demyelinating, tumor and neurodegenerative brain damage. Gliosis is the analogue of the systemic defense reaction - fibrosis.

Gliosis is initiated by damage to brain tissue. Since any injury in most cases means the loss of functional brain tissue (neurons), the first intention of the gliosis process is to fill the gap formed in the brain tissue. This is done mainly in two ways:

  • astrocyte hypertrophy and migration (astrogliosis) - astrocyte hypertrophy is largely due to the secretion of glial fibrillar acidic protein (GFAP), a protein with important functions in the synthesis of the neuronal cytoskeleton and cell expansion through the formation of pseudopods. Namely the formation of pseudopods determines the formation of a dense glial network consisting of the outgrowths of hypertrophied astrocytes. It has recently been demonstrated in experimental conditions that astrocytes that do not divide under normal conditions, in the case of tissue injury, gain the ability to proliferate, thus giving rise to a specific subpopulation for the process of gliosis - reactive astrocytes. Both hypertrophy and astrocytic proliferation result in filling of the space formed by the lesion neuronal loss.
  • synthesis and secretion of extracellular matrix components. Among the secreted molecules are laminin, fibronectin, tenescin C and proteoglycans.

Another component of the gliosis is the activation of microglia. Microglia represent the analogue of systemic macrophages, being involved in nonspecific local defense. The microglia cells activate rapidly around the focus of the lesion secreting significant amounts of cytokines, active biolipids, coagulation factors and neurotrophic factors. As a result of the secretion of these compounds, fibroblasts and endothelial cells are activated and recruited. Activation of these cell groups directly leads to the process of sclerosis and angiogenesis, respectively. It has been estimated that the number of blood vessels in the gliosis region is 2 times higher than in normal brain tissue.

The positive effects of gliosis

  • Restoring the physical and chemical integrity of brain tissue
  • Formation of a barrier between damaged and intact tissue in order to prevent the spread of infection or cell damage
  • Glial scarring through its components (secreted active substances) causes an improvement in vascularity, trophics and metabolic support of brain tissue in the lesion focus.

Negative effects of gliosis

  • Prevention of neuronal expansion: after a brain injury as a rule neurons tend to expand their axons to form new connections and regain lost functions with the loss of brain tissue. The glial scar in this case has a negative influence on this process, by preventing axonal expansion both physically, the gliotic tissue being more difficult to penetrate, and chemically by secreting factors to inhibit neuronal growth.
  • Replacing brain tissue with dysfunctional connective tissue. This can be the explanation for motor or any other sequelae after a brain or spinal cord injury. This may be a potential therapeutic target in spinal cord injuries, in which modulation of the gliosis process could leave patients with a chance for a fuller recovery of lost function.