Role of glial cells and neuroactive steroids in traumatic brain injury

Abstract

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Traumatic Brain Injury TBI is a major public health problem causing high rates of morbidity and mortality. Currently, there are no effective pharmaceutical strategies to prevent its secondary injury cascades, which includes oxidative stress and metabolic dysfunction that lead to increased tissue damage and cellular death. Although neuroprotective strategies using different approaches have been assessed to counteract TBI-induced neuroinflammation, none has shown promising results. In fact, most of these approaches have focused on neuronal population, rather than glial cells. The role of glial cells, mainly astrocytes, has been extensively studied in recent years due to their direct effect on the lesion and their ability to control pathological conditions associated with TBI. Experimental strategies targeting astrocytes are an important asset to reduce neuroinflammation and therefore improve the outcome in the damaged brain. More recently, estrogenic compounds have been used to control astroglial reactivity upon brain injury and also to modulate the expression of several genes involved in neural development, synaptic connectivity and survival of neurons. In this context, these neurosteroids are promising molecules thanks to their ability to modify brain response to injury by regulating astrogliosis. In this work, we highlight the role played by astrocytes during a pathological event, and discuss the potential effects of neuroactive steroids as a promising therapeutic approach to reduce brain damage.

Keywords

• Astrocytes
• Neuroprotection
• Traumatic Brain Injury
• Brain Injury
• Neuroactive steroids
• Neurosteroids
• estrogenic compounds