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(Stroke. 2003;34:e193.)
© 2003 American Heart Association, Inc.

Research Reports

Association Between Interleukin-1A Polymorphism and Cerebral Amyloid Angiopathy–Related Hemorrhage

M.O. McCarron, MRCP, MD; J. Stewart; P. McCarron, PhD, MFPHM; S. Love, PhD, FRCP, FRCPath; H.V. Vinters, MD; J.W. Ironside, FRCPath; D.M.A. Mann, PhD, FRCPath; D.I. Graham, PhD, FRCPath J.A.R. Nicoll, MD, FRCPath

From the Departments of Neurology (M.O.M.) and Epidemiology and Public Health (P.M.), Royal Victoria Hospital, Belfast, UK; Department of Neuropathology, Institute of Neurological Sciences, Southern General Hospital, Glasgow, UK (J.S., D.I.G.); Department of Neuropathology, Frenchay Hospital, Bristol, UK (S.L.); Department of Pathology and Laboratory Medicine, UCLA Medical Center, Los Angeles, Calif (H.V.V.); Neuropathology Laboratory, Department of Pathology, University of Edinburgh, UK (J.W.I.); Greater Manchester Neurosciences Centre, University of Manchester, Hope Hospital, Salford, UK (D.M.A.M.); and Department of Neuropathology, Southampton General Hospital, Southampton, UK (J.A.R.N.).

Correspondence to Dr Mark McCarron, Department of Neurology, Royal Victoria Hospital, Belfast, BT12 6BA, UK. E-mail markmccarron{at}doctors.org.uk

Background and Purpose— 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 2 or 4 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.

Key Words: cerebral amyloid angiopathy • interleukins • intracerebral hemorrhage