Essay On Astrogliosis

Astrogliosis
Normally, astrocytes can sense any changes in neuronal activity and extracellular space composition. Indeed, an abnormal increase in astrocytes number is observed in response to the destruction of nearby neurons from CNS trauma, infection, ischemia, stroke and other CNS injuries and diseases. This phenomenon is called astrogliosis. This reaction may entail any changes in neuronal signaling pathways or gene expression, such as an upregulation of GFAP, S100 or any other related protein expression (Sofroniew and Vinters 2010). The calcium binding protein, S100B, serve as a serum and/or cerebrospinal fluid biomarker of brain injury, such as epilepsy (Burda, Bernstein and Sodroniew 2015). Astrogliosis may harm or benefit neurons and other neural cells. Reactive astrocytes may undergo a series of changes that can be categorized
These changes may lead to gain or loss of astrocytes functions (M. V. Sofroniew 2009).
Mild astrogliosis is often associated with mild, noninvasive injury and lead to the activation of the innate immune system. Although there is an upregulation of GFAP has been documented, it does not lead to astrocyte proliferation. Proliferation of astrocytes does start in the second stage of astrogliosis, resulting in the extension of astrocyte processes, overlapping each other’s domain and disturbing astrocytes networks. Moreover, astrocyte proliferation is accompanied by cell hypertrophy. In the last category, which involves severe astrogliosis and glial scare formations along with upregulation of GFAP, a complete destruction of individual astrocytes domains accompanied with the formation of dense and narrow glial scar was observed. Glial scars act as protective