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Systems Analysis of the Neuroinflammatory and Hemodynamic Response to Traumatic Brain Injury
Published on: May 27, 2022
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Acute Traumatic Brain Injury-Induced Neuroinflammatory Response and Neurovascular Disorders in the Brain
Duraisamy Kempuraj1,2,3, Mohammad Ejaz Ahmed4,5,6, Govindhasamy Pushpavathi Selvakumar4,5,6
1Department of Neurology, School of Medicine, University of Missouri, 1 Hospital Drive, Columbia, MO, USA. duraisamyk@health.missouri.edu.
Neurotoxicity Research
|September 21, 2020
Summary
Acute traumatic brain injury (TBI) disrupts the blood-brain barrier (BBB) by decreasing key proteins. Mast cell stabilizer cromolyn protected against this TBI-induced BBB damage in mice.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Acute traumatic brain injury (TBI) causes neuroinflammation and neurovascular damage.
- The precise mechanisms of TBI-induced neurovascular alterations remain unclear.
- Effective treatments to prevent TBI sequelae are lacking.
Purpose of the Study:
- To investigate TBI-induced neuroinflammatory and neurovascular alterations.
- To evaluate the protective effect of cromolyn on TBI-induced brain damage.
Main Methods:
- Mice underwent weight-drop-induced acute TBI.
- Neuroinflammation and neurovascular changes were assessed using immunofluorescence and ELISA.
- Cromolyn was administered to inhibit TBI's neuroinflammatory response.
Main Results:
- TBI significantly decreased pericyte marker PDGFR-β and BBB proteins JAM-A and ZO-1.
- Cromolyn administration prevented the TBI-associated decrease in PDGFR-β, JAM-A, and ZO-1.
- These findings indicate TBI-induced BBB/tight junction damage.
Conclusions:
- Acute TBI leads to damage of the blood-brain barrier and tight junctions.
- Cromolyn shows potential in protecting against acute TBI-induced brain damage and its long-term effects.
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