Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2000-9-18
pubmed:abstractText
Thanks largely to cloning the genes for several neurodegenerative diseases over the past decade and the existence of mouse mutants, the molecular basis of neurodegeneration is finally beginning to yield some of its secrets. We discuss what has been learned about the pathogenesis of "triplet repeat" diseases through mouse models for spinocerebellar ataxia types 1 and 3 and Huntington disease, including the roles of nuclear aggregates and protein cleavage. We also discuss the neurologic phenotypes that arise from mutations in neurotransmitter receptors (lurcher mice) and ion channels (weaver, leaner, and tottering mice), drawing parallels between ischemic cell death and the neurodegeneration that occurs in the lurcher mouse. Finally, we discuss common mechanisms of cell death and lessons learned from these mouse models that might have broader relevance to other neurologic disorders.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0066-4278
pubmed:author
pubmed:issnType
Print
pubmed:volume
62
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
779-802
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Insights from mouse models into the molecular basis of neurodegeneration.
pubmed:affiliation
Howard Hughes Medical Institute, Rockefeller University, New York, New York 10021, USA. heintz@rockvax.rockefeller.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review, Research Support, Non-U.S. Gov't