Apolipoprotein E affects the central nervous system response to injury and the development of cerebral edema. Ann Neurol 2002 Jan;51(1):113-7
Date
01/10/2002Pubmed ID
11782990DOI
10.1002/ana.10098Scopus ID
2-s2.0-0036135127 (requires institutional sign-in at Scopus site) 102 CitationsAbstract
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 alpha 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.
Author List
Lynch JR, Pineda JA, Morgan D, Zhang L, Warner DS, Benveniste H, Laskowitz DTMESH terms used to index this publication - Major topics in bold
Acute DiseaseAnimals
Apolipoproteins E
Brain Edema
Disease Models, Animal
Gene Expression
Head Injuries, Closed
Magnetic Resonance Imaging
Male
Mice
Mice, Inbred C57BL
Mice, Mutant Strains
RNA, Messenger
Tumor Necrosis Factor-alpha
