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Apolipoprotein E affects the central nervous system response to injury and the development of cerebral edema
Author(s) -
Lynch John R.,
Pineda Jose A.,
Morgan Duncan,
Zhang Lin,
Warner David S.,
Benveniste Helen,
Laskowitz Daniel T.
Publication year - 2002
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.10098
Subject(s) - medicine , cerebral edema , central nervous system , edema , apolipoprotein e , endogeny , endocrinology , apolipoprotein b , magnetic resonance imaging , closed head injury , pathology , traumatic brain injury , anesthesia , radiology , cholesterol , disease , psychiatry
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.