Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2006-9-1
pubmed:abstractText
Autophagy, a lysosomal pathway for degrading organelles and long-lived proteins, is becoming recognized as a key adaptive response that can preclude death in stressed or diseased cells. However, during development strong induction of autophagy in specific cell populations mediates a type of programmed cell death that has distinctive 'autophagic' morphology and a requirement for autophagy activity. The recent identification of autophagosomes in neurons in a growing number of neurodegenerative disorders has, therefore, sparked controversy about whether these structures are contributing to neuronal cell death or protecting against it. Emerging evidence supports the view that induction of autophagy is a neuroprotective response and that inadequate or defective autophagy, rather than excessive autophagy, promotes neuronal cell death in most of these disorders. In this review, we consider possible mechanisms underlying autophagy-associated cell death and their relationship to pathways mediating apoptosis and necrosis.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0166-2236
pubmed:author
pubmed:issnType
Print
pubmed:volume
29
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
528-35
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Autophagy in neurodegenerative disease: friend, foe or turncoat?
pubmed:affiliation
Center for Dementia Research, Nathan S. Kline Institute, Orangeburg, NY 10962, USA. nixon@nki.rfmh.org
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural