Apoptotic Mechanisms for Neuronal Cells in Early Brain Injury After Subarachnoid Hemorrhage

Yu Hasegawa; Hidenori Suzuki; Takumi Sozen; Orhan Altay; John H. Zhang

doi:10.1007/978-3-7091-0353-1_8

Apoptotic Mechanisms for Neuronal Cells in Early Brain Injury After Subarachnoid Hemorrhage

Yu Hasegawa, Hidenori Suzuki, Takumi Sozen, Orhan Altay, John H. Zhang

Research output: Chapter in Book/Report/Conference proceeding › Conference contribution

Abstract

Objects: The major causes of death and disability in subarachnoid hemorrhage (SAH) may be early brain injury (EBI) and cerebral vasospasm. Although cerebral vasospasm has been studied and treated by a lot of drugs, the outcome is not improved even if vasospasm is reversed. Based on these data, EBI is considered a primary target for future research, and apoptosis may be involved in EBI after experimental SAH. Methods: We reviewed the published literature about the relationship between SAH induced EBI and apoptosis in PubMed. Result: Most available information can be obtained from the endovascular filament perforation animal model. After onset of SAH, intracranial pressure is increased and then cerebral blood flow is reduced. Many factors are involved in the mechanism of apoptotic cell death in EBI after SAH. In the neuronal cells, both intrinsic and extrinsic pathways of apoptosis can occur. Some antiapoptotic drugs were studied and demonstrated a protective effect against EBI after SAH. However, apoptosis in EBI after SAH has been little studied and further studies will provide us more beneficial findings. Conclusions: The study of apoptosis in EBI after experimental SAH may give us new therapies for SAH. © 2011 Springer-Verlag/Wien.

Original language	American English
Title of host publication	Early Brain Injury or Cerebral Vasospasm
Subtitle of host publication	Volume 1: Pathophysiology
Publisher	Springer Vienna
Pages	43-48
Number of pages	6
ISBN (Electronic)	978-3-7091-0353-1
ISBN (Print)	9783709103524, 978-3-7091-1658-6
DOIs	https://doi.org/10.1007/978-3-7091-0353-1_8 https://doi.org/10.1007/978-3-7091-0353-1_8
State	Published - Jan 1 2011

Publication series

Name	Acta Neurochirurgica, Supplementum
Volume	110
ISSN (Print)	0065-1419
ISSN (Electronic)	0001-6268

ASJC Scopus Subject Areas

Surgery
Clinical Neurology

Keywords

Apoptosis
Cerebral blood flow
Early brain injury
Intracranial pressure
Subarachnoid hemorrhage
Oxidative Stress/physiology
Neurons/physiology
Humans
Brain Injuries/etiology
Signal Transduction/physiology
Subarachnoid Hemorrhage/complications
Animals
Apoptosis/physiology
Models, Biological
DNA Damage/physiology
Disease Models, Animal
PubMed/statistics & numerical data

Disciplines

Anesthesiology
Medicine and Health Sciences
Surgery
Neuroscience and Neurobiology

Access to Document

10.1007/978-3-7091-0353-1_8License: Unspecified
10.1007/978-3-7091-0353-1_8

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Full text

Cite this

Hasegawa, Y., Suzuki, H., Sozen, T., Altay, O., & Zhang, J. H. (2011). Apoptotic Mechanisms for Neuronal Cells in Early Brain Injury After Subarachnoid Hemorrhage. In Early Brain Injury or Cerebral Vasospasm: Volume 1: Pathophysiology (pp. 43-48). (Acta Neurochirurgica, Supplementum; Vol. 110). Springer Vienna. https://doi.org/10.1007/978-3-7091-0353-1_8, https://doi.org/10.1007/978-3-7091-0353-1_8

Apoptotic Mechanisms for Neuronal Cells in Early Brain Injury After Subarachnoid Hemorrhage. / Hasegawa, Yu; Suzuki, Hidenori; Sozen, Takumi et al.
Early Brain Injury or Cerebral Vasospasm: Volume 1: Pathophysiology. Springer Vienna, 2011. p. 43-48 (Acta Neurochirurgica, Supplementum; Vol. 110).

Research output: Chapter in Book/Report/Conference proceeding › Conference contribution

Hasegawa, Y, Suzuki, H, Sozen, T, Altay, O & Zhang, JH 2011, Apoptotic Mechanisms for Neuronal Cells in Early Brain Injury After Subarachnoid Hemorrhage. in Early Brain Injury or Cerebral Vasospasm: Volume 1: Pathophysiology. Acta Neurochirurgica, Supplementum, vol. 110, Springer Vienna, pp. 43-48. https://doi.org/10.1007/978-3-7091-0353-1_8, https://doi.org/10.1007/978-3-7091-0353-1_8

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abstract = "Objects: The major causes of death and disability in subarachnoid hemorrhage (SAH) may be early brain injury (EBI) and cerebral vasospasm. Although cerebral vasospasm has been studied and treated by a lot of drugs, the outcome is not improved even if vasospasm is reversed. Based on these data, EBI is considered a primary target for future research, and apoptosis may be involved in EBI after experimental SAH. Methods: We reviewed the published literature about the relationship between SAH induced EBI and apoptosis in PubMed. Result: Most available information can be obtained from the endovascular filament perforation animal model. After onset of SAH, intracranial pressure is increased and then cerebral blood flow is reduced. Many factors are involved in the mechanism of apoptotic cell death in EBI after SAH. In the neuronal cells, both intrinsic and extrinsic pathways of apoptosis can occur. Some antiapoptotic drugs were studied and demonstrated a protective effect against EBI after SAH. However, apoptosis in EBI after SAH has been little studied and further studies will provide us more beneficial findings. Conclusions: The study of apoptosis in EBI after experimental SAH may give us new therapies for SAH. {\textcopyright} 2011 Springer-Verlag/Wien.",

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N2 - Objects: The major causes of death and disability in subarachnoid hemorrhage (SAH) may be early brain injury (EBI) and cerebral vasospasm. Although cerebral vasospasm has been studied and treated by a lot of drugs, the outcome is not improved even if vasospasm is reversed. Based on these data, EBI is considered a primary target for future research, and apoptosis may be involved in EBI after experimental SAH. Methods: We reviewed the published literature about the relationship between SAH induced EBI and apoptosis in PubMed. Result: Most available information can be obtained from the endovascular filament perforation animal model. After onset of SAH, intracranial pressure is increased and then cerebral blood flow is reduced. Many factors are involved in the mechanism of apoptotic cell death in EBI after SAH. In the neuronal cells, both intrinsic and extrinsic pathways of apoptosis can occur. Some antiapoptotic drugs were studied and demonstrated a protective effect against EBI after SAH. However, apoptosis in EBI after SAH has been little studied and further studies will provide us more beneficial findings. Conclusions: The study of apoptosis in EBI after experimental SAH may give us new therapies for SAH. © 2011 Springer-Verlag/Wien.

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BT - Early Brain Injury or Cerebral Vasospasm

PB - Springer Vienna

ER -

Apoptotic Mechanisms for Neuronal Cells in Early Brain Injury After Subarachnoid Hemorrhage

Abstract

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ASJC Scopus Subject Areas

Keywords

Disciplines

Access to Document

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