Linked Life Data

21519046

Source:http://linkedlifedata.com/resource/pubmed/id/21519046

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2011-6-24
pubmed:abstractText
?-Amyloid protein (A?) accumulation, caspase activation, apoptosis, and hypoxia-induced neurotoxicity have been suggested to be involved in Alzheimer disease neuropathogenesis. A? is produced from amyloid precursor protein through proteolytic processing by the aspartyl protease ?-site amyloid precursor protein-cleaving enzyme (BACE) and ?-secretase. Inhaled anesthetics have long been considered to protect against neurotoxicity. However, recent studies have suggested that the inhaled anesthetic isoflurane may promote neurotoxicity by inducing caspase activation and apoptosis, and by increasing levels of BACE and A?. We therefore sought to determine whether isoflurane can induce concentration-dependent dual effects on hypoxia-induced caspase-3 activation and increases in BACE levels: protection versus promotion.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1526-7598
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
113
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
145-52
pubmed:dateRevised
2011-11-9
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
The potential dual effects of anesthetic isoflurane on hypoxia-induced caspase-3 activation and increases in ?-site amyloid precursor protein-cleaving enzyme levels.
pubmed:affiliation
Geriatric Anesthesia Research Unit, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, 149 13th St., Room 4310, Charlestown, MA 02129-2060, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural