TREM2 expression in a model of traumatic brain injury: implications for the development of post-traumatic epilepsy
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Abstract
RATIONALE: Traumatic brain injury (TBI) often leads to long-term neurological complications, including the development of post-traumatic epilepsy (PTE), which significantly impacts patients' quality of life. Understanding the pathogenesis of TBI and PTE development can help identify potential therapeutic targets to mitigate brain injury, prevent seizures, and potentially improve patient outcomes.
OBJECTIVE: The objective of the study is to investigate the role of TREM2 (Triggering Receptors Expressed on Myeloid Cells 2) in the post-traumatic changes in the brain of rats with moderate to severe TBI. TREM2 is a protein that plays a crucial role in regulating microglial activation, and its significance has gained greater attention in the context of neuroinflammatory diseases, such as PTE. This study aims to provide insights into the putative relevance of TREM2 to PTE development.
METHODS: Signal analysis of coronal brain sections from adult male Sprague Dawley rats subjected to lateral fluid percussion injury (LFPI) and stained with an anti-TREM2 specific antibody using immunohistochemistry. TREM2 immuno-stained rat brains were made available by Dr. Galanopoulou (Albert Einstein College of Medicine) from previous projects that were approved by the Albert Einstein College of Medicine Institutional Animal Care and Use Committee. No animals were handled or sacrificed by the student. Signal densitometry of TREM2 expression was done using Fiji:ImageJ software, while blinded to group allocation, to ensure unbiased results.
RESULTS: Following LFPI, TREM2-immunoreactivity (TREM2-ir) was significantly elevated compared to sham rats in cerebral cortical, hippocampal and thalamic regions ipsilateral only to the side of the injury.
CONCLUSION: There is elevated TREM2-ir in ipsilateral to the injury cortico-thalamic and hippocampal brain regions in LFPI compared to sham rats. The increase in TREM2-ir suggests a lateralized, region-specific inflammatory response likely linked to microglial activation and tissue repair following brain injury.The combined effort of all these elements may be crucial in understanding PTE development.
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2025