Traumatic brain injury exacerbates neurodegenerative pathology: improvement with an apolipoprotein E-based therapeutic.

Journal Article (Journal Article)

Cognitive impairment is common following traumatic brain injury (TBI), and neuroinflammatory mechanisms may predispose to the development of neurodegenerative disease. Apolipoprotein E (apoE) polymorphisms modify neuroinflammatory responses, and influence both outcome from acute brain injury and the risk of developing neurodegenerative disease. We demonstrate that TBI accelerates neurodegenerative pathology in double-transgenic animals expressing the common human apoE alleles and mutated amyloid precursor protein, and that pathology is exacerbated in the presence of the apoE4 allele. The administration of an apoE-mimetic peptide markedly reduced the development of neurodegenerative pathology in mice homozygous for apoE3 as well as apoE3/E4 heterozygotes. These results demonstrate that TBI accelerates the cardinal neuropathological features of neurodegenerative disease, and establishes the potential for apoE mimetic therapies in reducing pathology associated with neurodegeneration.

Full Text

Duke Authors

Cited Authors

  • Laskowitz, DT; Song, P; Wang, H; Mace, B; Sullivan, PM; Vitek, MP; Dawson, HN

Published Date

  • November 2010

Published In

Volume / Issue

  • 27 / 11

Start / End Page

  • 1983 - 1995

PubMed ID

  • 20812776

Electronic International Standard Serial Number (EISSN)

  • 1557-9042

Digital Object Identifier (DOI)

  • 10.1089/neu.2010.1396


  • eng

Conference Location

  • United States