Ischemic tolerance and endogenous neuroprotection.
Practically any stimulus capable of causing injury to a tissue or organ can, when applied close to (but below) the threshold of damage, activate endogenous protective mechanisms--thus potentially lessening the impact of subsequent, more severe stimuli. A sub-threshold ischemic insult applied to the brain, for example, activates certain cellular pathways that can help to reduce damage caused by subsequent ischemic episodes--a phenomenon known as 'ischemic preconditioning' (IP) or 'ischemic tolerance' (IT). Although investigated for some time in model organisms, IP/IT has recently been shown in human brain. This opens a window into endogenous neuroprotection and, potentially, a window of opportunity to utilize these mechanisms in the clinic to treat patients with stroke and other CNS disorders.
Experimental Neurology, Charite Hospital, Humboldt University, 10098 Berlin, Germany. ulrich.dirnagl@charite.de
Ulrich
U
Dirnagl
Roger P
RP
Simon
John M
JM
Hallenbeck
D000222:Adaptation, Physiological; D000818:Animals; D001921:Brain / Q000098:blood supply / Q000378:metabolism* / Q000503:physiopathology; D002545:Brain Ischemia / Q000503:physiopathology* / Q000517:prevention & control; D004195:Disease Models, Animal; D004921:Erythropoietin / Q000378:metabolism; D006801:Humans; D019194:Ischemic Preconditioning; D018696:Neuroprotective Agents / Q000627:therapeutic use
D018696:Neuroprotective Agents; D004921:Erythropoietin