Apolipoprotein E affects the central nervous system response to injury and the development of cerebral edema.
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.
Lynch
John R
JR
Multidisciplinary Neuroprotection Laboratory, Duke University Medical Center, Durham, NC 27710, USA.
Pineda
Jose A
JA
Morgan
Duncan
D
Zhang
Lin
L
Warner
David S
DS
Benveniste
Helen
H
Laskowitz
Daniel T
DT
D000208:Acute Disease; D000818:Animals; D001057:Apolipoproteins E / Q000235:genetics*; D001929:Brain Edema / Q000473:pathology / Q000503:physiopathology*; D004195:Disease Models, Animal; D015870:Gene Expression; D016489:Head Injuries, Closed / Q000473:pathology / Q000503:physiopathology*; D008279:Magnetic Resonance Imaging; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008817:Mice, Mutant Strains; D012333:RNA, Messenger / Q000032:analysis; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
D001057:Apolipoproteins E; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha