Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
26
pubmed:dateCreated
2004-7-1
pubmed:abstractText
Creatine mediates remarkable neuroprotection in experimental models of amyotrophic lateral sclerosis, Huntington's disease, Parkinson's disease, and traumatic brain injury. Because caspase-mediated pathways are shared functional mechanistic components in these diseases, as well as in ischemia, we evaluated the effect of creatine supplementation on an experimental stroke model. Oral creatine administration resulted in a remarkable reduction in ischemic brain infarction and neuroprotection after cerebral ischemia in mice. Postischemic caspase-3 activation and cytochrome c release were significantly reduced in creatine-treated mice. Creatine administration buffered ischemia-mediated cerebral ATP depletion. These data provide the first direct correlation between the preservation of bioenergetic cellular status and the inhibition of activation of caspase cell-death pathways in vivo. An alternative explanation to our findings is that creatine is neuroprotective through other mechanisms that are independent of mitochondrial cell-death pathways, and therefore postischemic ATP preservation is the result of tissue sparing. Given its safety record, creatine might be considered as a novel therapeutic agent for inhibition of ischemic brain injury in humans. Prophylactic creatine supplementation, similar to what is recommended for an agent such as aspirin, may be considered for patients in high stroke-risk categories.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1529-2401
pubmed:author
pubmed:issnType
Electronic
pubmed:day
30
pubmed:volume
24
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5909-12
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:15229238-Adenosine Triphosphate, pubmed-meshheading:15229238-Administration, Oral, pubmed-meshheading:15229238-Animals, pubmed-meshheading:15229238-Apoptosis, pubmed-meshheading:15229238-Brain Ischemia, pubmed-meshheading:15229238-Caspase 3, pubmed-meshheading:15229238-Caspases, pubmed-meshheading:15229238-Creatine, pubmed-meshheading:15229238-Drug Evaluation, Preclinical, pubmed-meshheading:15229238-Electron Transport Complex IV, pubmed-meshheading:15229238-Energy Metabolism, pubmed-meshheading:15229238-Enzyme Activation, pubmed-meshheading:15229238-Female, pubmed-meshheading:15229238-Infarction, Middle Cerebral Artery, pubmed-meshheading:15229238-Mice, pubmed-meshheading:15229238-Mice, Inbred C57BL, pubmed-meshheading:15229238-Neuroprotective Agents, pubmed-meshheading:15229238-Premedication
pubmed:year
2004
pubmed:articleTitle
Prophylactic creatine administration mediates neuroprotection in cerebral ischemia in mice.
pubmed:affiliation
Neuroapoptosis Laboratory, Department of Neurosurgery, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't