ApoE mimetic ameliorates motor deficit and tissue damage in rat spinal cord injury.

Published

Journal Article

Apolipoprotein E (apoE), a plasma protein responsible for transporting lipid and cholesterol, modulates responses of the central nervous system to injury. Small peptides derived from the receptor-binding region of apoE can simulate some important bioactivities of apoE holoprotein and offer neuroprotection against brain injury. We tested whether COG1410, an apoE-mimetic peptide, provides protection in a rat model of spinal cord injury (SCI). Traumatic injury was created at T8 by a cortical impact device. Injured rats were randomized to four treatment groups: vehicle, 0.15, 0.3, or 0.6 mg/kg COG1410; sham surgery rats received vehicle. Basso, Beattie, Bresnahan neurological score was evaluated prior to injury and at 1, 3, 7, and 14 days after injury. Histological changes were evaluated at 14 days. All injured rats lost body weight during the first week following injury. Body weight recovery was significantly improved in rats treated with COG1410. Mechanical impact resulted in severe motor deficit, and most animals had a BBB score of 0-1 at 24 hours postinjury. COG1410-treated rats showed significantly improved functional recovery and ameliorated motor deficit at 14 days postinjury. Histological analysis showed that COG1410 groups had a significantly reduced lesion size at the site of injury, a larger preserved luxol fast blue-stained area, and more visible neurons in the surrounding area of injury. Microglial activation was also significantly suppressed. These findings indicate that this apoE mimetic effectively improved neurological and histological outcome following SCI in rats, and the effect was associated with inhibition of microglial activation.

Full Text

Duke Authors

Cited Authors

  • Wang, R; Hong, J; Lu, M; Neil, JE; Vitek, MP; Liu, X; Warner, DS; Li, F; Sheng, H

Published Date

  • July 2014

Published In

Volume / Issue

  • 92 / 7

Start / End Page

  • 884 - 892

PubMed ID

  • 24633884

Pubmed Central ID

  • 24633884

Electronic International Standard Serial Number (EISSN)

  • 1097-4547

Digital Object Identifier (DOI)

  • 10.1002/jnr.23371

Language

  • eng

Conference Location

  • United States