Persistent neuroinflammation and neurodegeneration after brain injury

Authors

  • Shafiq Ur Rehman
  • Tahir Ali
  • Danish Ali Khan
  • Syed Alamdar Hussain
  • Usman Farooq

Abstract

ABSTRACT
INTRODUCTION: Traumatic brain injury (TBI) is a major global health issue in both civilians and war-affected military personnel and has no proper cure or treatment. Survivors of TBI exhibit long-term cognitive dysfunction and even permanent disabilities. As TBI patients exhibit multiple pathological conditions and the exact mechanism of neuroinflammation and neurodegeneration is still remain elusive. Therefore, we assess the prolonged effects of penetrating brain injury in animal model to further explore the neuroinflammation-associated neuropathological conditions in clinical studies.
OBJECTIVE: To determine the long term neuroinflammatory and neurodegenerative effects after penetrating brain injury in preclinical model.
METHODOLOGY: In the present study, we developed a penetrating brain injury and examined compare the neuroinflammatory effects after seven days and two months following brain injury in animal model. We used confocal laser microscopy to assess the expression of neuroinflammatory mediators in the mice group.
RESULTS: These findings provide evidence that penetrating brain injury have prolonged effects after two months. Using confocal laser microscopy, we found that the expression of GFAP (reactive astrocytes marker) and IL-1β (inflammatory marker) in the mice brain were significantly sustained after two months following brain injury, suggesting the prolonged neuroinflammatory effects after penetrating brain injury. Here, we found fascinating results that severity of neuroinflammation was higher at day 7 as compare to two months in animal brains.
CONCLUSION: These findings provide evidence that penetrating brain injury is critically involved in prolonged neuroinflammation which effect the cognitive ability and neurological impairments in the brain. Furthermore, these findings would be supportive in the preclinical and clinical settings.
KEY WORDS: inflammation, Traumatic brain injury, Astrocytes, interleukin beta.

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Published

2020-11-19