title: Early brain injury following aneurysmal subarachnoid hemorrhage: emphasis on cellular apoptosis.
abstract: Subarachnoid hemorrhage (SAH) due to intracranial aneurysm rupture is a complex     clinical disease with high mortality and morbidity. Recent studies suggest that     early brain injury (EBI) rather than vasospasm might be responsible for     morbidity and mortality within 24-72 hours after SAH. The rise in intracranial     pressure following SAH causes a significant drop in cerebral perfusion pressure     that leads to global cerebral ischemia and initiates the acute injury cascade.     Various molecular mechanisms have been shown to involve in the pathophysiology     of EBI including cellular apoptosis. In this review, we summarize apoptotic     molecular mechanisms involved in the etiology of EBI and its potential as a     target for future therapeutic intervention.
authors.affiliation: Koç University, Faculty of Medicine, Neuroscience Research Lab., Sariyer, Istanbul, Turkey.
authors.forename: Simge
authors.initials: S
authors.lastname: Yuksel
authors.forename: Yusuf Berk
authors.initials: YB
authors.lastname: Tosun
authors.forename: Julian
authors.initials: J
authors.lastname: Cahill
authors.forename: Ihsan
authors.initials: I
authors.lastname: Solaroglu
mesh_terms: D017209:Apoptosis / Q000502:physiology*; D001930:Brain Injuries / Q000209:etiology* / Q000473:pathology*; D002545:Brain Ischemia / Q000209:etiology; D006801:Humans; D009422:Nervous System Diseases / Q000209:etiology; D013345:Subarachnoid Hemorrhage / Q000150:complications* / Q000473:pathology* / Q000503:physiopathology; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000502:physiology
chemical_list: D016159:Tumor Suppressor Protein p53