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No evidence for the presence of apolipoprotein epsilon-4, interleukin-1 alpha allele 2 and interleukin-1 beta allele 2 cause an increase in programmed cell death following traumatic brain injury in humans

No evidence for the presence of apolipoprotein epsilon-4, interleukin-1 alpha allele 2 and interleukin-1 beta allele 2 cause an increase in programmed cell death following traumatic brain injury in humans
No evidence for the presence of apolipoprotein epsilon-4, interleukin-1 alpha allele 2 and interleukin-1 beta allele 2 cause an increase in programmed cell death following traumatic brain injury in humans
Background: Brain injury after trauma is an important cause of mortality and morbidity in society. There is evidence in both man and laboratory animals that in addition to necrosis, cell loss may occur as a result of programmed cell death (PCD). The cellular and molecular responses after head injury are partly influenced by genetic polymorphisms of apolipoprotein E and the proinflammatory cytokine IL-1.
Aim: The principal aim of this study was to determine whether the presence of the ApoE epsilon(4), IL-1(alpha 2) or IL-I beta(2) allele types influenced the amounts of PCD after head injury compared with controls. Methods: Paraffin sections from the hippocampus of 38 patients (32 M : 6 F, aged 15-75, mean 38 years, survival 7-576 hours; mean 36 hours) who died after a head injury were stained by Tunel histochemistry and quantified, and genotyping was undertaken by PCR "blind" to clinical detail.
Results: There were more Tunel+ cells (neurons and glia) after head injury than in controls with statistically increased numbers in all sectors of the hippocampus including the dentate fascia. However, there was no correlation between ApoE epsilon(4), IL-1 alpha allele 2 and IL-1 beta allele 2 and the amount of Tunel positivity.
Conclusion: Given that both the ApoE and IL-1 influence outcome after various forms of acute brain injury, further work will be required to determine the mechanism underlying this relationship
risk-factors, brain, apoptosis, rats, acute brain injury, apolipoprotein e, injuries, spinal-cord-injury, fatal head-injury, survival, programmed cell death, traumatic brain injury, in-situ, head injury
0722-5091
255-264
Johnson, V.E.
b52e7298-560d-4c08-87e2-2316a15c65b0
Murray, L.
bfd60879-aefc-4bb8-abc2-9c10f1646a57
Raghupathi, R.
fc57cd49-4426-4bb1-8f0d-a5b8ca1970a0
Stewart, J.
856808fb-3362-46ea-b9ed-aa64db4fc983
Nicoll, J.A.R.
88c0685f-000e-4eb7-8f72-f36b4985e8ed
MacKinnon, M.A.
fb44a0bc-2ee2-4499-a759-034d38a2766f
McIntosh, T.K.
d0ef37a5-b713-403d-9b85-62fab5c474ca
Graham, D.I.
0b1c9c9e-94b2-44fa-b189-8e04501b3a67
Johnson, V.E.
b52e7298-560d-4c08-87e2-2316a15c65b0
Murray, L.
bfd60879-aefc-4bb8-abc2-9c10f1646a57
Raghupathi, R.
fc57cd49-4426-4bb1-8f0d-a5b8ca1970a0
Stewart, J.
856808fb-3362-46ea-b9ed-aa64db4fc983
Nicoll, J.A.R.
88c0685f-000e-4eb7-8f72-f36b4985e8ed
MacKinnon, M.A.
fb44a0bc-2ee2-4499-a759-034d38a2766f
McIntosh, T.K.
d0ef37a5-b713-403d-9b85-62fab5c474ca
Graham, D.I.
0b1c9c9e-94b2-44fa-b189-8e04501b3a67

Johnson, V.E., Murray, L., Raghupathi, R., Stewart, J., Nicoll, J.A.R., MacKinnon, M.A., McIntosh, T.K. and Graham, D.I. (2006) No evidence for the presence of apolipoprotein epsilon-4, interleukin-1 alpha allele 2 and interleukin-1 beta allele 2 cause an increase in programmed cell death following traumatic brain injury in humans. Clinical Neuropathology, 25 (6), 255-264.

Record type: Article

Abstract

Background: Brain injury after trauma is an important cause of mortality and morbidity in society. There is evidence in both man and laboratory animals that in addition to necrosis, cell loss may occur as a result of programmed cell death (PCD). The cellular and molecular responses after head injury are partly influenced by genetic polymorphisms of apolipoprotein E and the proinflammatory cytokine IL-1.
Aim: The principal aim of this study was to determine whether the presence of the ApoE epsilon(4), IL-1(alpha 2) or IL-I beta(2) allele types influenced the amounts of PCD after head injury compared with controls. Methods: Paraffin sections from the hippocampus of 38 patients (32 M : 6 F, aged 15-75, mean 38 years, survival 7-576 hours; mean 36 hours) who died after a head injury were stained by Tunel histochemistry and quantified, and genotyping was undertaken by PCR "blind" to clinical detail.
Results: There were more Tunel+ cells (neurons and glia) after head injury than in controls with statistically increased numbers in all sectors of the hippocampus including the dentate fascia. However, there was no correlation between ApoE epsilon(4), IL-1 alpha allele 2 and IL-1 beta allele 2 and the amount of Tunel positivity.
Conclusion: Given that both the ApoE and IL-1 influence outcome after various forms of acute brain injury, further work will be required to determine the mechanism underlying this relationship

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More information

Published date: June 2006
Keywords: risk-factors, brain, apoptosis, rats, acute brain injury, apolipoprotein e, injuries, spinal-cord-injury, fatal head-injury, survival, programmed cell death, traumatic brain injury, in-situ, head injury

Identifiers

Local EPrints ID: 62429
URI: http://eprints.soton.ac.uk/id/eprint/62429
ISSN: 0722-5091
PURE UUID: 0861514b-cf84-44c1-a7fd-e14d4036e14c
ORCID for J.A.R. Nicoll: ORCID iD orcid.org/0000-0002-9444-7246

Catalogue record

Date deposited: 12 Sep 2008
Last modified: 08 Jan 2022 02:55

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Contributors

Author: V.E. Johnson
Author: L. Murray
Author: R. Raghupathi
Author: J. Stewart
Author: J.A.R. Nicoll ORCID iD
Author: M.A. MacKinnon
Author: T.K. McIntosh
Author: D.I. Graham

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