Citation

Cahill J, Cahill WJ, Calvert JW, Calvert JH, Zhang JH. J. Cereb. Blood Flow Metab. 2006; 26(11): 1341-1353.

Affiliation

Department of Physiology, Loma Linda University Medical School, Loma Linda, California 92354, USA.

Erratum On

J Cereb Blood Flow Metab 2006;26(11):1463.

Copyright

(Copyright © 2006, Nature Publishing Group)

DOI

10.1038/sj.jcbfm.9600283

PMID

16482081

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.

Language: en