Linked Life Data

19085270

Source:http://linkedlifedata.com/resource/pubmed/id/19085270

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2008-12-16
pubmed:abstractText
SPG3A/atlastin-1 gene mutations cause an autosomal dominant form of hereditary spastic paraplegia (SPG3A-HSP). We used positron emission tomography with [(11)C]DTBZ to assess nigrostriatal dopaminergic integrity in two unrelated adults with SPG3A-HSP due to the common SPG3A/atlastin-1 mutation, R239C. Nigrostriatal dopaminergic terminal density was normal. A difference from the human pattern of neurodegeneration is a critical limitation of this Drosophila model of SPG3A-HSP. This major difference between human SPG3A/atlastin-1 mutations and the Drosophila atl(l) phenotype has several possible explanations.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1563-5260
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
22
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
289-94
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Normal dopaminergic nigrostriatal innervation in SPG3A hereditary spastic paraplegia.
pubmed:affiliation
Geriatrics Research, Education, and Clinical Center, Ann Arbor VAHS, Ann Arbor, Michigan 48109-2200, USA. ralbin@umich.edu
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural