Mechanisms of Early Brain Injury after Subarachnoid Hemorrhage
Top Cited Papers
- 1 November 2006
- journal article
- review article
- Published by SAGE Publications in Journal of Cerebral Blood Flow & Metabolism
- Vol. 26 (11) , 1341-1353
- https://doi.org/10.1038/sj.jcbfm.9600283
Abstract
Apoptosis is the term given to programmed cell death, which has been widely connected to a number of intracranial pathologies including stroke, Alzheimer's disease, and more recently subarachnoid hemorrhage (SAH). Subarachnoid hemorrhage is a disease, without any form of effective treatment, that affects mainly the young and middle aged and as a result is responsible for severe disability in otherwise healthy and productive individuals. Despite intense research efforts in the field, we currently possess a very limited understanding of the underlying mechanisms that result in injury after SAH. However, a number of studies have recently indicated that apoptosis may be a major player in the pathogenesis of secondary brain injury after SAH. As a result, the apoptotic cascades present a number of potential therapeutic opportunities that may ameliorate secondary brain injury after SAH. Experimental data suggest that these cascades occur very early after the initial insult and may be related directly to physiologic sequela commonly associated with SAH. It is imperative, therefore, to obtain a thorough understanding of the early events that occur after SAH, which will enable future therapies to be developed.Keywords
This publication has 148 references indexed in Scilit:
- Endothelin-1 levels in plasma and cerebrospinal fluid of patients with cerebral vasospasm after aneurysmal subarachnoid hemorrhageSurgical Neurology, 2005
- The role of p53 in hypoxia-induced apoptosisBiochemical and Biophysical Research Communications, 2005
- The role of p53-induced apoptosis in cerebral ischemia: effects of the p53 inhibitor pifithrin ?Experimental Neurology, 2004
- Role of brain natriuretic peptide in cerebral vasospasmActa Neurochirurgica, 2003
- Hypoxia Links ATR and p53 through Replication ArrestMolecular and Cellular Biology, 2002
- Hypoxia death stimulus induces translocation of p53 protein to mitochondriaFEBS Letters, 2001
- Evidence for Apoptosis After Intracerebral Hemorrhage in Rat StriatumJournal of Cerebral Blood Flow & Metabolism, 2000
- Intracranial AneurysmsNew England Journal of Medicine, 1997
- Fas(CD95)/FasL interactions required for programmed cell death after T-cell activationNature, 1995
- Cerebral arterial flow dynamics during aneurysm haemorrhageActa Neurochirurgica, 1978