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

Ann Neurol. 2002 Jan;51(1):113-7. 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 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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Acute Disease
  • Animals
  • Apolipoproteins E / genetics*
  • Brain Edema / pathology
  • Brain Edema / physiopathology*
  • Disease Models, Animal
  • Gene Expression
  • Head Injuries, Closed / pathology
  • Head Injuries, Closed / physiopathology*
  • Magnetic Resonance Imaging
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Mutant Strains
  • RNA, Messenger / analysis
  • Tumor Necrosis Factor-alpha / genetics


  • Apolipoproteins E
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha