Linked Life Data

12384220

Source:http://linkedlifedata.com/resource/pubmed/id/12384220

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2002-10-17
pubmed:abstractText
In the superoxide dismutase 1 (SOD1)(G93A G1H) transgenic mouse, the primary pathology and disease signs are associated with the degeneration of motor neurons in the lumbar spinal cord. It is unclear if the descending motor pathways from the cortex and brainstem are also compromised. The retrograde tracer Fluorogold was inserted into the T(12) segment of the spinal cord and the number of labelled neurons counted in the sensorimotor cortex and brainstem of 60, 90 and 110 day-old mice. A small loss of corticospinal and bulbospinal projections was detected at 60 days. By 110 days, 53% of corticospinal, 41% of bulbospinal and 43% of rubrospinal neurons were lost. The progressive loss of corticospinal axons was confirmed using the stereological fractionator method. These findings suggest that the expression of the SOD1(G93A G1H) mutant protein results in a disease that resembles the late stages of human motor neuron disease. This involves not only the destruction of lower motor neurons in the spinal cord, but also additional loss of descending cortical and bulbar neurons.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0304-3940
pubmed:author
pubmed:copyrightInfo
Copyright 2002 Elsevier Science Ireland Ltd.
pubmed:issnType
Print
pubmed:day
31
pubmed:volume
332
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
99-102
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Degeneration of corticospinal and bulbospinal systems in the superoxide dismutase 1(G93A G1H) transgenic mouse model of familial amyotrophic lateral sclerosis.
pubmed:affiliation
Department of Anatomy and Cell Biology, PO Box 13C, Monash University, Victoria 3800, Australia.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't