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Key Players







Comment by Dr. Mladenoff


Astrocytes and microglial cells are key players in mTBI that are trigger into action after head trauma. If the patient is asymptomatic and is returned to play too soon, these cells continue to execute there search and destroy coded action. If any further inflammation presents to the brain via any pathway including: another hit to the head (even a subconcussive event), gut brain disturbances such as irritable bowel syndrome, asthma or allergies then the microglial cell activity is magnified and can lead to neurodegenerative changes.

The contribution of astrocytes and microglia to traumatic brain injury: Neuroinflammation and TBI
Article in British Journal of Pharmacology 173(4) · March 2015 with 63 ReadsDOI: 10.1111/bph.13125

Abstract
Traumatic brain injury (TBI) represents a major cause of death and disability in developed countries. Brain injuries are highly heterogeneous, and can also trigger other neurological complications, including epilepsy, depression and dementia. The initial injury often leads to the development of secondary sequelae; cellular hyper-excitability, vasogenic and cytotoxic oedema, hypoxia-ischemia, oxidative stress and inflammation, all of which influence expansion of the primary lesion.

It is widely known that inflammatory events in the brain following TBI contribute to the widespread cell death and chronic tissue degeneration. Neuro-inflammation is a multi-faceted response involving a number of cell types, both within the central nervous system (CNS) and in the peripheral circulation. Astrocytes and microglia, cells of the CNS, are considered key players in initiating an inflammatory response after injury. These cells are capable of secreting various cytokines, chemokines and growth factors, and following injury to the CNS, undergo changes in morphology. Ultimately, these changes can influence the local microenvironment and thus determine the extent of damage and subsequent repair. This review will focus on the roles of microglia and astrocytes following TBI, highlighting some of the key processes, pathways and mediators involved in this response. Additionally, both the beneficial and detrimental aspects of these cellular responses will be examined, using evidence from animal models and human post-mortem TBI studies. This article is protected by copyright. All rights reserved.
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