Journal
NEUROSCIENCE LETTERS
Volume 617, Issue -, Pages 188-194Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2016.02.025
Keywords
Traumatic brain injury; Neuroinflammation; Site-targeted complement inhibition; CR2-conjugated pharmacological compounds; Secondary brain injury
Categories
Funding
- Colorado Traumatic Brain Injury Trust Fund
Ask authors/readers for more resources
Intracerebral complement activation after severe traumatic brain injury (TBI) leads to a cascade of neuroinflammatory pathological sequelae that propagate host-mediated secondary brain injury and adverse outcomes. There are currently no specific pharmacological agents on the market to prevent or mitigate the development of secondary cerebral insults after TBI. A novel chimeric CR2-fH compound (mTT30) provides targeted inhibition of the alternative complement pathway at the site of tissue injury. This experimental study was designed to test the neuroprotective effects of mTT30 in a mouse model of closed head injury. The administration of 500 mu g mTT30 i.v. at 1 h, 4 h and 24 h after head injury attenuated complement C3 deposition in injured brains, reduced the extent of neuronal cell death, and decreased post-injury microglial activation, compared to vehicle-injected placebo controls. These data imply that site-targeted alternative pathway complement inhibition may represent a new promising therapeutic avenue for the future management of severe TBI. (C) 2016 Published by Elsevier Ireland Ltd.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available