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Genetic vulnerability following traumatic brain injury: the role of apolipoprotein E
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  1. N Nathoo1,
  2. R Chetty2,
  3. J R van Dellen3,
  4. G H Barnett1
  1. 1Department of Neurosurgery, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, 44195 Ohio, USA
  2. 2Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto M5G 2M9, Ontario, Canada
  3. 3West London Neurosciences Centre and Imperial College School of Medicine, Charing Cross Hospital, London W6 8RF, UK
  1. Correspondence to:
 Dr N Nathoo, Department of Neurosurgery, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, 44195 Ohio, USA;
 nathoon{at}ccf.org

Abstract

Apolipoprotein E (APOE) is thought to be responsible for the transportation of lipids within the brain, maintaining structural integrity of the microtubule within the neurone, and assisting with neural transmission. Possession of the APOE ε4 allele has also been shown to influence neuropathological findings in patients who die from traumatic brain injury, including the accumulation of amyloid β protein. Previous clinical studies reporting varying outcome severities of traumatic brain injury, including cognitive and functional recovery, all support the notion that APOE ε4 allele possession is associated with an unfavourable outcome. Evidence from experimental and clinical brain injury studies confirms that APOE plays an important role in the response of the brain to injury.

  • apolipoprotein E
  • genetic vulnerability
  • outcome
  • traumatic brain injury
  • APOE, apolipoprotein E
  • APP, amyloid precursor protein
  • LDL, low density lipoprotein
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