Apolipoprotein E affects the central nervous system response to injury and the development of cerebral edema

• Published in: Annals of neurology 2002-01, Vol.51 (1), p.113-117
• Main Authors: Lynch, John R., Pineda, Jose A., Morgan, Duncan, Zhang, Lin, Warner, David S., Benveniste, Helen, Laskowitz, Daniel T.
• Format: Article
• Language: English
• Subjects: Acute Disease; Animals; Apolipoproteins E - genetics; Biological and medical sciences; Brain Edema - pathology; Brain Edema - physiopathology; Disease Models, Animal; Gene Expression; Head Injuries, Closed - pathology; Head Injuries, Closed - physiopathology; Injuries of the nervous system and the skull. Diseases due to physical agents; Magnetic Resonance Imaging; Male; Medical sciences; Mice; Mice, Inbred C57BL; Mice, Mutant Strains; RNA, Messenger - analysis; Traumas. Diseases due to physical agents; Tumor Necrosis Factor-alpha - genetics
• ISSN: 0364-5134; 1531-8249
• DOI: 10.1002/ana.10098

Apolipoprotein E has been implicated in modifying neurological outcome after traumatic brain injury, although the mechanisms by which this occurs remain poorly defined. To investigate the role of endogenous apolipoprotein E following acute brain injury, noninvasive magnetic resonance imaging was performed on anesthetized mice following closed head injury. Effacement of the lateral ventricle was used as a radiographic surrogate for cerebral edema. At 24 hours following injury, apolipoprotein E‐deficient animals had a greater degree of cerebral edema as compared to matched controls. In addition, the brains of apolipoprotein E‐deficient animals had a significantly greater upregulation of tissue necrosis factor α messenger ribonucleic acid as compared to controls as early as 1‐hr post injury. Thus, modulation of the endogenous central nervous system inflammatory response may be one mechanism by which apolipoprotein E affects outcome following acute brain injury.