Long-term intracerebral inflammatory response after experimental focal brain injury in rat.
Head injury is a risk factor for development of the sporadic form of Alzheimer's disease (AD) and chronic anti-inflammatory treatment reduces the prevalence of AD. This study was undertaken to test the hypothesis that inflammatory reactions persist in the long term. Rats were subjected to moderate focal brain injury. The brains were analyzed after 3 months by immunohistochemistry. Persistent major histocompatibility complex (MHC)-II up-regulation, mononuclear phagocytes, interleukin (IL)-1-beta and tumor necrosis factor (TNF)-alpha synthesis (p < 0.01) were detected in large areas of the ipsilateral hemisphere. The fact that a long-term inflammation is detectable following experimental brain injury corroborates the hypothesis that persistent post-traumatic inflammation is a possible factor in the causative chain of traumatically induced dementia.
Holmin
S
S
Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden.
Mathiesen
T
T
D000818:Animals; D001930:Brain Injuries / Q000276:immunology*; D002540:Cerebral Cortex / Q000166:cytology / Q000276:immunology / Q000293:injuries; D004660:Encephalitis / Q000276:immunology*; D000949:Histocompatibility Antigens Class II / Q000032:analysis; D007124:Immunoenzyme Techniques; D007375:Interleukin-1 / Q000032:analysis; D007963:Leukocytes, Mononuclear / Q000737:chemistry / Q000276:immunology; D015213:Neuroimmunomodulation / Q000502:physiology*; D010587:Phagocytosis / Q000276:immunology; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
D000949:Histocompatibility Antigens Class II; D007375:Interleukin-1; D014409:Tumor Necrosis Factor-alpha