Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2010-9-9
pubmed:abstractText
Multiple systems atrophy (MSA) is a neurodegenerative disorder characterized by oligodendrocytic accumulations of alpha-synuclein (alphasyn). Oxidative stress is a key mechanism proposed to underlie MSA pathology. To address the role of alphasyn modifications, over and above general oxidative modifications, this study examined the effects of 3-nitropropionic acid (3NP) administration, a technique used to model MSA, in knock-out mice lacking alphasyn (alphasynKO). Although susceptible to 3NP-induced oxidative stress, alphasynKO mice display reduced neuronal loss and dendritic pathology. The alphasynKO mice are resistant to 3NP-induced motor deficits and display attenuated loss of tyrosine hydroxylase and dopamine transporter striatal immunoreactivity. The results suggest that deficits in MSA are not due to general oxidative protein modification but in addition may be related to specific alphasyn modifications.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/20224454-11062131, http://linkedlifedata.com/resource/pubmed/commentcorrection/20224454-11073803, http://linkedlifedata.com/resource/pubmed/commentcorrection/20224454-11895375, http://linkedlifedata.com/resource/pubmed/commentcorrection/20224454-12376616, http://linkedlifedata.com/resource/pubmed/commentcorrection/20224454-12846977, http://linkedlifedata.com/resource/pubmed/commentcorrection/20224454-12857790, http://linkedlifedata.com/resource/pubmed/commentcorrection/20224454-15147505, http://linkedlifedata.com/resource/pubmed/commentcorrection/20224454-15288507, http://linkedlifedata.com/resource/pubmed/commentcorrection/20224454-15382209, http://linkedlifedata.com/resource/pubmed/commentcorrection/20224454-15496679, http://linkedlifedata.com/resource/pubmed/commentcorrection/20224454-15743798, http://linkedlifedata.com/resource/pubmed/commentcorrection/20224454-16291942, http://linkedlifedata.com/resource/pubmed/commentcorrection/20224454-16298531, http://linkedlifedata.com/resource/pubmed/commentcorrection/20224454-18053987, http://linkedlifedata.com/resource/pubmed/commentcorrection/20224454-1821673, http://linkedlifedata.com/resource/pubmed/commentcorrection/20224454-18695506, http://linkedlifedata.com/resource/pubmed/commentcorrection/20224454-19032594, http://linkedlifedata.com/resource/pubmed/commentcorrection/20224454-19405128, http://linkedlifedata.com/resource/pubmed/commentcorrection/20224454-7499323, http://linkedlifedata.com/resource/pubmed/commentcorrection/20224454-8734302, http://linkedlifedata.com/resource/pubmed/commentcorrection/20224454-9130677, http://linkedlifedata.com/resource/pubmed/commentcorrection/20224454-9923766
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1473-558X
pubmed:author
pubmed:issnType
Electronic
pubmed:day
21
pubmed:volume
21
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
457-62
pubmed:dateRevised
2011-9-26
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Alpha-synuclein deficient mice are resistant to toxin-induced multiple system atrophy.
pubmed:affiliation
Department of Neurosciences, University of California San Diego, School of Medicine, La Jolla, California 92093-0624, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural