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Histopathology of traumatic brain injury to the developing brain

Vanya Goranova, Marco Sifringer, Chrissanthy Ikonomidou


Trauma to the developing brain leads to necrotic lesion at the site of injury and delayed apoptotic neurodegeneration at distant sites mainly in the thalamus, caudate nucleus and cortex. We studied the distribution and timely activation of monocytes/macrophages, microglia, astrocytes and two inflammatory cytokines, interleukin (IL)-1ß and IL-18, 2 h to 14 days following trauma using biochemistry and immunohistochemistry. A marked increase of mRNA and protein levels for IL-1ß and IL-18 was detected 2-12 h after injury. Apoptotic cell death affects mostly neuronal populations ipsilateral to the injury 6 h to 5 days later. Microglial activation was first evident at 12 h, peaked at 36-48 h and decreased substantially by 5 days. Astrocytic activation started at 18 h, peaked at 48 h and gradually declined by 14 days after trauma. The activation of immune and glial cells together with increased expression of both interleukins occurred at the site of primary and secondary damages. Our findings suggest that reactive microglia/astrocytes at the sites of secondary lesions might maintain apoptotic neurodegeneration over several days after traumatic injury to the immature brain but they might also promote tissue repair. Understanding the role of glial cells to progression of inflammation and apoptotic neurodegeneration together with tissue repair in the developing brain may provide valuable information to guide treatment after brain trauma.


developing brain; trauma; apoptosis; microglia; astroglia

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About The Authors

Vanya Goranova
Medical University of Varna

Department of Anatomy, Histology and Embryology

Marco Sifringer
Charité-Universitätsmedizin Berlin

Department of neonatology

Chrissanthy Ikonomidou
University of Wisconsin
United States

Department of neurology

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