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Astrocytes are a subtype of glial cells that make up the majority of cells in the human central nervous system (CNS). They perform metabolic, structural, homeostatic, and neuroprotective tasks such as clearing excess neurotransmitters, stabilizing and regulating the blood-brain barrier, and promoting synapse formation.[1][2][3][4] Unlike neurons and other cells in the nervous system, they do not conduct electrical signals. Instead, they ensure the continued function of their signal-relaying counterparts.[1] Due to their diverse array of responsibilities, science has viewed them as both targets for treatment and causes of disease. Thus, it is crucial for clinicians to understand the histology and purpose of astrocytes and to identify their roles in both healthy and pathological states.

Astrocyte pathologies tend to manifest in two main forms: astrocytopathy and astrogliosis.[5]  Astrocytopathy includes any genetic, traumatic, toxic, or other insult that can alter the existing functions or capabilities of astrocytes.[5] Such pathologies affect the astrocyte network's ability to carry out one or more of its many essential functions, which can lead to a variety of neurological diseases. The category of astrogliosis is understood to be a neuroimmunological malfunction. Reactive astrogliosis is a complex process in which signals from microglia, synapses, neurons, and sites of injury cause astrocytes to undergo rapid remodeling.[5][6] Astrocytes can react in this way to a variety of ions, transcription factors, metabolic molecules, and even pro-inflammatory signals such as interleukin-6 (IL-6), transforming growth factor-alpha (TGF-alpha), leukemia inhibitory factor (LIF), and ciliary neurotrophic factor (CNTF).[5] These signals promote increased expression of GFAP and vimentin, hypertrophy of foot processes, and expression of pro-inflammatory gene products that allow astrocytes to perform neuroprotective duties.[5] Studies have shown that astrogliosis tends to isolate damaged CNS tissues while protecting healthy tissue, creating glial scars, and repairing damage to the blood-brain barrier while guiding post-traumatic neuroplasticity.[5] The exact response depends on the specific brain region in which astrogliosis gets triggered, but as with many immune responses, there is a risk for pathological damage if the process becomes dysregulated.[5]