title: No evidence for the presence of apolipoprotein epsilon4, interleukin-lalpha allele 2 and interleukin-1beta allele 2 cause an increase in programmed cell death following traumatic brain injury in humans.
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 pro-inflammatory cytokine IL-I.
  
  
  OBJECTIVE
  The principal aim of this study was to determine whether the presence of the ApoE epsilon4, IL- 1 alpha2 or IL- 1beta2 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 ApoEepsilon4, IL- 1 alpha allele 2 and IL- 1beta allele 2 and the amount of Tunel positivity.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Academic Unit of Neuropathology, University of Glasgow, Glasgow, Scotland, UK.
authors.forename: V E
authors.initials: VE
authors.lastname: Johnson
authors.forename: L
authors.initials: L
authors.lastname: Murray
authors.forename: R
authors.initials: R
authors.lastname: Raghupathi
authors.forename: J
authors.initials: J
authors.lastname: Stewart
authors.forename: J A R
authors.initials: JA
authors.lastname: Nicoll
authors.forename: M A
authors.initials: MA
authors.lastname: MacKinnon
authors.forename: T K
authors.initials: TK
authors.lastname: McIntosh
authors.forename: D I
authors.initials: DI
authors.lastname: Graham
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D053327:Apolipoprotein E4 / Q000235:genetics*; D017209:Apoptosis / Q000235:genetics*; D015415:Biomarkers / Q000378:metabolism; D001930:Brain Injuries / Q000235:genetics* / Q000276:immunology / Q000378:metabolism; D002452:Cell Count; D004252:DNA Mutational Analysis; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease / Q000235:genetics*; D005820:Genetic Testing; D005838:Genotype; D006624:Hippocampus / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D020287:In Situ Nick-End Labeling; D007375:Interleukin-1 / Q000235:genetics*; D053582:Interleukin-1alpha / Q000235:genetics; D053583:Interleukin-1beta / Q000235:genetics; D008297:Male; D008875:Middle Aged; D009410:Nerve Degeneration / Q000235:genetics* / Q000276:immunology / Q000378:metabolism; D011110:Polymorphism, Genetic / Q000235:genetics
chemical_list: D053327:Apolipoprotein E4; D015415:Biomarkers; D007375:Interleukin-1; D053582:Interleukin-1alpha; D053583:Interleukin-1beta