Linked Life Data

12657883

Source:http://linkedlifedata.com/resource/pubmed/id/12657883

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2003-3-26
pubmed:abstractText
Sandhoff disease (SD) is a heritable lysosomal storage disease resulting from impaired degradation of GM2 ganglioside. The hallmark pathology of the SD model mouse brain is GM2 ganglioside accumulation in neurons. In the present study, we immunohistochemically investigated the neuronal pathology in SD mouse brains, and demonstrated neuronal accumulation of alpha- and beta-synucleins in addition to GM2 ganglioside. Synuclein-positive neurons were extensively observed throughout SD mouse brains, although the distribution of beta-synuclein was less extensive than that of alpha-synuclein. Synuclein-positive neurons were negative to ubiquitin and PHF-tau. These findings suggest that neuronal synucleins may accumulate secondarily to GM2 ganglioside in SD mouse brains, and that neuronal accumulation of synucleins may be more critical than that of GM2 ganglioside for SD mice.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0959-4965
pubmed:author
pubmed:issnType
Print
pubmed:day
24
pubmed:volume
14
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
551-4
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Neuronal accumulation of alpha- and beta-synucleins in the brain of a GM2 gangliosidosis mouse model.
pubmed:affiliation
Department of Psychiatry, Yokohama City University School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama 236-0004, Japan. kyon@mail.cc.tohoku.ac.jp
pubmed:publicationType
Journal Article, Comparative Study