Astrocytopathy

Astrogliosis
Formation of reactive astrocytes after CNS injury.
Anatomical terminology []

Astrogliosis (also known as astrocytosis or referred to as reactive astrocytosis) is an abnormal increase in the number of astrocytes due to the destruction of nearby neurons from CNS trauma, infection, ischemia, stroke, autoimmune responses, and neurodegenerative disease. In healthy neural tissue, astrocytes play critical roles in energy provision, regulation of blood flow, homeostasis of extracellular fluid, homeostasis of ions and transmitters, regulation of synapse function, and synaptic remodeling. Astrogliosis changes the molecular expression and morphology of astrocytes, causing scar formation and, in severe cases, inhibition of axon regeneration.

Reactive astrogliosis is a spectrum of changes in astrocytes that occur in response to all forms of central nervous system (CNS) injury and disease. Changes due to reactive astrogliosis vary with the severity of the CNS insult along a graduated continuum of progressive alterations in molecular expression, progressive cellular hypertrophy, proliferation and scar formation.

Insults to neurons in the central nervous system caused by infection, trauma, ischemia, stroke, autoimmune responses, or other neurodegenerative diseases may cause reactive astrocytes.

When the astrogliosis is pathological itself, instead of a normal response to a pathological problem, it is referred to as astrocytopathy.

Reactive astrocytes may benefit or harm surrounding neural and non-neural cells. They undergo a series of changes that may alter astrocyte activities through gain or loss of functions lending to neural protection and repair, glial scarring, and regulation of CNS inflammation.

Proliferating reactive astrocytes are critical to scar formation and function to reduce the spread and persistence of inflammatory cells, to maintain the repair of the blood-brain barrier (BBB), to decrease tissue damage and lesion size, and to decrease neuronal loss and demyelination.