Linked Life Data

15350647

Source:http://linkedlifedata.com/resource/pubmed/id/15350647

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2004-9-7
pubmed:abstractText
The superoxide dismutase 1 (SOD1)G93A mouse was recently established as transgenic model of amyotrophic lateral sclerosis. We were interested to know whether the SOD1 G93A mutation promotes neuronal injury after intraluminal middle cerebral artery thread occlusion and/or retinal ganglion cell (RGC) axotomy in mice, which are highly reproducible and clinically relevant in vivo models of acute and subacute neuronal degeneration, respectively. In our experiments, G93A mutant SOD1 neither influenced ischemic injury after 90 or 30 min of focal ischemia, nor had an impact on the severity of RGC degeneration after optic nerve transection, when human SOD1 G93A mutant mice were compared to human wild-type SOD1 mice. Our data indicate that the clinically relevant SOD1 G93A mutation, which leads to amyotrophic lateral sclerosis in humans and mice, does not necessarily worsen neuronal degeneration in other pathologies. Thus, the G93A mutation may be counterbalanced in non-motor neurons of young animals, and region-specific and age-related factors may be necessary so that neurodegeneration is re-enforced.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0306-4522
pubmed:author
pubmed:issnType
Print
pubmed:volume
128
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
359-64
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
The superoxide dismutase1 (SOD1) G93A mutation does not promote neuronal injury after focal brain ischemia and optic nerve transection in mice.
pubmed:affiliation
Department of Neurology, University Hospital Zürich, Frauenklinikstrasse 26, CH-8091, Switzerland. ertugrul.kilic@usz.ch
pubmed:publicationType
Journal Article