title: Association between interleukin-1A polymorphism and cerebral amyloid angiopathy-related hemorrhage.
abstract: OBJECTIVE
  It has been suggested that the interleukin-1A (IL-1A) allele 2 is a risk factor for Alzheimer's disease (AD). Because cerebral amyloid angiopathy-related hemorrhage (CAAH) often coexists with AD, we examined the IL-1A polymorphism in CAAH.
  
  
  METHODS
  In a case-control study, patients with pathologically verified CAAH, AD patients without intracerebral hemorrhage, and neuropathologically normal control subjects were studied. DNA was extracted from brain tissue, and IL-1A was genotyped. Logistic regression was used to examine the IL-1A polymorphism in CAAH patients with and without AD compared with AD and non-AD control subjects.
  
  
  RESULTS
  There were 42 patients with CAAH, 232 AD patients, and 167 non-AD control subjects. In age-adjusted analyses, there was no association between possession of IL-1A allele 2 and risk of CAAH compared with AD control subjects (odds ratio [OR], 0.94; 95% confidence interval [CI], 0.45 to 1.97; P=0.87) or non-AD control subjects (OR, 0.94; 95% CI, 0.47 to 1.87; P=0.86). Stratifying for the presence of apolipoprotein E epsilon2 or epsilon4 demonstrated the known increased risk of CAAH from these lipoprotein E alleles. Subgroup analyses demonstrated a nonsignificant excess of the IL-1A 2,2 genotype in patients with CAAH and AD compared with those CAAH patients who did not have histological evidence indicating AD (OR, 2.17; 95% CI, 0.15 to 122.3; P=0.64). Comparisons between CAAH patients with AD and AD control subjects and between CAAH patients without AD and non-AD control subjects did not demonstrate an association between CAAH and possession of either the IL-1A allele 2 or the 2,2 genotype.
  
  
  CONCLUSIONS
  The IL-1A allele 2 or 2,2 genotype does not appear to be a major risk factor for CAAH.
authors.affiliation: Department of Neurology, Royal Victoria Hospital, Belfast, BT12 6BA, UK. markmccarron@doctors.org.uk
authors.forename: M O
authors.initials: MO
authors.lastname: McCarron
authors.forename: J
authors.initials: J
authors.lastname: Stewart
authors.forename: P
authors.initials: P
authors.lastname: McCarron
authors.forename: S
authors.initials: S
authors.lastname: Love
authors.forename: H V
authors.initials: HV
authors.lastname: Vinters
authors.forename: J W
authors.initials: JW
authors.lastname: Ironside
authors.forename: D M A
authors.initials: DM
authors.lastname: Mann
authors.forename: D I
authors.initials: DI
authors.lastname: Graham
authors.forename: J A R
authors.initials: JA
authors.lastname: Nicoll
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000544:Alzheimer Disease / Q000453:epidemiology / Q000473:pathology; D053329:Apolipoprotein E2; D053318:Apolipoprotein E3; D001057:Apolipoproteins E / Q000235:genetics; D016022:Case-Control Studies; D016657:Cerebral Amyloid Angiopathy / Q000453:epidemiology / Q000235:genetics*; D002543:Cerebral Hemorrhage / Q000453:epidemiology / Q000235:genetics*; D015897:Comorbidity; D005787:Gene Frequency; D006801:Humans; D007375:Interleukin-1 / Q000235:genetics*; D008875:Middle Aged; D016017:Odds Ratio; D011110:Polymorphism, Genetic; D012016:Reference Values; D018570:Risk Assessment; D012307:Risk Factors
chemical_list: D053329:Apolipoprotein E2; D053318:Apolipoprotein E3; D001057:Apolipoproteins E; D007375:Interleukin-1