Linked Life Data

12485887

Source:http://linkedlifedata.com/resource/pubmed/id/12485887

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2002-12-17
pubmed:abstractText
Traumatic brain injury (TBI) is one of the few known risk factors for Alzheimers disease (AD) and for depression. The mechanisms by which trauma causes delayed cognitive deficits are largely unknown. In recent studies, it was demonstrated that the complement system (an important component of the immune system and a mediator of inflammation) is activated both in human AD and following experimental TBI in rats. Amyloid proteins are also present in AD and following TBI, and are known to activate complement in vitro. Based on these and other previous studies, it was hypothesized that regulation of the complement system will attenuate the long-term consequences of TBI. Vaccinia virus complement control protein (VCP) is a protein encoded by vaccinia virus. It blocks both the classic and alternative pathways of complement activation in vitro, and by doings so prevents the generation of proinflammatory chemotactic factors. Based on in vitro studies VCP can block the complement activation by the amyloid beta peptide. Using a fluid percussion rat model that causes traumatic brain injury (TBI), it was found that VCP significantly enhances functional recovery as determined by the Morris Water Maze test. Taken togther these studies indicate that potentially VCP could block molecular signals such as the formation of amyloid beta or the activation of complement to inhibit formation of AD following TBI.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0077-8923
pubmed:author
pubmed:issnType
Print
pubmed:volume
973
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
317-22
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Potential intervention by vaccinia virus complement control protein of the signals contributing to the progression of central nervous system injury to Alzheimer's disease.
pubmed:affiliation
Department of Microbiology and Immunology, University of Louisville School of Medicine, Louisville, Kentucky 40202, USA. gjk01@gwise.louisville.edu
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't