Linked Life Data

17495518

Source:http://linkedlifedata.com/resource/pubmed/id/17495518

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2007-8-8
pubmed:abstractText
Animal models of cathepsin D (CD) deficiency are characterized by a progressive and relentless neurodegenerative phenotype similar to that observed in Neuronal Ceroid Lipofuscinoses (NCL), a group of pediatric neurodegenerative diseases known collectively as Batten Disease. We have shown recently that the targeted deletion of the pro-apoptotic molecule Bax prevents apoptotic markers but not neuron death and neurodegeneration induced by CD deficiency, which suggests that alterations in the macroautophagy-lysosomal degradation pathway can mediate neuron death in NCL/Batten Disease in the absence of apoptosis. Herein, we review CD deficiency in the broader context of NCL and offer potential mechanisms for neuron death and neurodegeneration induced by CD deficiency.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1554-8627
pubmed:author
pubmed:issnType
Print
pubmed:volume
3
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
474-6
pubmed:dateRevised
2007-12-3
pubmed:meshHeading
pubmed:articleTitle
Cathepsin D deficiency and NCL/Batten disease: there's more to death than apoptosis.
pubmed:affiliation
Department of Pathology, Neuropathology Division, University of Alabama at Birmingham, Birmingham, Alabama 35294-0017, USA. shacka@uab.edu
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural