Linked Life Data

16464659

Source:http://linkedlifedata.com/resource/pubmed/id/16464659

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2006-2-8
pubmed:abstractText
Signaling through the insulin/IGF-1 pro-survival pathway is widely recognized to be neuroprotective as well as important for neuronal growth and physiology. In mammals, age-associated decline in circulating IGF-1 levels has been associated with neuronal aging and symptoms of neurodegeneration. Defects in IGF-1 receptor associated signaling has, however, been shown to significantly extend lifespan in models ranging from invertebrates to mouse. At least in C. elegans, restoring such defects in neurons alone reduces lifespan to wild-type levels. As we seek to delay brain aging and age-associated neuronal degeneration via nutritional and endocrinal supplements, an understanding of the mechanistic basis of this apparent paradox is important. Recent elucidation of the role of the protein deacetylase SIRT1 in cell survival and data associating IGF-1 with the regulation of SIRT1 expression may provide a direction towards resolving this issue.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0197-4580
pubmed:author
pubmed:issnType
Print
pubmed:volume
27
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
501-5
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
SIRT1, neuronal cell survival and the insulin/IGF-1 aging paradox.
pubmed:affiliation
Department of Biochemistry and Programme in Neurobiology and Aging, National University of Singapore, 8 Medical Drive, Singapore 117597, Singapore. bchtbl@nus.edu.sg
pubmed:publicationType
Journal Article, Review