From the Guidelines
Gliosis is a reactive process in the central nervous system where glial cells, primarily astrocytes, proliferate and undergo hypertrophy in response to brain or spinal cord injury. This process serves as the brain's attempt to repair damage and isolate injured areas, similar to how scar tissue forms elsewhere in the body. When injury occurs, astrocytes become activated, changing their morphology and increasing production of glial fibrillary acidic protein (GFAP). The resulting glial scar helps contain damage but can also impede neural regeneration by creating a physical and chemical barrier.
Key Characteristics of Gliosis
- Gliosis is not a disease itself but rather a response to various conditions including trauma, stroke, infection, autoimmune disorders, and neurodegenerative diseases.
- On imaging studies like MRI, gliosis appears as areas of increased signal intensity.
- While there's no specific treatment for gliosis itself, medical management focuses on addressing the underlying cause of neural injury and implementing neuroprotective strategies to minimize further damage. Understanding gliosis is important because it represents a fundamental process in neurological injury and repair, influencing recovery outcomes in many central nervous system disorders. Although the provided evidence 1 primarily discusses guidelines for the diagnosis and treatment of diffuse gliomas of adulthood, it does not directly address gliosis. However, the principles of neurological injury and repair are relevant across various conditions affecting the central nervous system.
From the Research
Definition of Gliosis
- Gliosis is defined as a nonneoplastic reaction (hypertrophy and/or proliferation) of astrocytes and/or microglial cells in the central nervous system (CNS) 2
- It is a frequent finding in the CNS in nonclinical safety studies, occurring at low incidence as a spontaneous finding and induced by various test articles 2
Characteristics of Gliosis
- Gliosis may accompany degeneration and/or necrosis of cells (mainly neurons) or neural parenchyma (neuron processes and myelin) 2
- Gliosis often follows inflammation (i.e., leukocyte accumulation causing parenchymal damage) or neoplasm formation 2
- Gliosis may appear as variably sized, randomly scattered foci of reactive glial cells in the absence of visible parenchymal damage or inflammation 2
Types of Gliosis
- Reactive gliosis, which occurs after traumatic brain injury (TBI) and is characterized by the transformation of quiescent type I radial glial cells (RGC) to proliferative type II RGCs 3
- Müller cell gliosis, which plays an important physiological role by maintaining retinal neuronal homeostasis and is associated with multiple pathological events in the retina, including optic nerve crush (ONC) injury 4
Factors Influencing Gliosis
- Aging, which can reduce microgliosis and astrogliosis after cortical stroke 5
- Recovery time, which can affect the extent of gliosis after cortical stroke 5
- Post-stroke treatment, such as memantine, which can reduce gliosis after cortical stroke 5
- MicroRNA-21 (miR-21), which can modulate Müller cell gliosis after ONC injury 4