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Neurology 2002;58:1566-1568
© 2002 American Academy of Neurology
Brief Communications

Are interleukin-1 gene polymorphisms risk factors or disease modifiers in AD?

E. K. Green, PhD, J. M. Harris, BSc, H. Lemmon, MA, J. C. Lambert, PhD, M. C. Chartier–Harlin, PhD, D. St. Clair, MD, D. M.A. Mann, PhD, T. Iwatsubo, MD and C. L. Lendon, PhD

From the Molecular Psychiatry Department (Drs. Green, Lambert, and Lendon, and J.M. Harris), Division of Neuroscience, Queen Elizabeth Psychiatry Hospital, University of Birmingham; Laboratory Medicine Academic Group (Dr. Mann), Department of Medicine, University of Manchester; Department of Mental Health (H. Lemmon and Dr. Clair), Foresterhill, University of Aberdeen, United Kingdom; INSERM 508 (Dr. Chartier–Harlin), Institut Pasteur de Lille, Lille Cédex, France; and Department of Neuropathology and Neuroscience (Dr. Iwatsubo), Graduate School of Pharmaceutical Sciences, University of Tokyo, Japan.

Address correspondence and reprint requests to Dr. Corinne Lendon, Molecular Psychiatry Department, Division of Neuroscience, Queen Elizabeth Psychiatry Hospital, University of Birmingham, Birmingham, B15 2QZ, UK; e-mail: c.l.lendon{at}bham.ac.uk

Polymorphisms in the interleukin-1 genes, IL-1A and IL-1B, have been associated with AD, but not in all studies. The authors genotyped the IL-1A(-889) and IL-1B(-511) polymorphisms in large independent cohorts of 503 control individuals and 395 patients with AD, and a further 100 with brain Aß load. No evidence was found of risk for AD with these variants, nor of an effect on age at onset. However, an impact of IL-1B(-511) on Aß40 load (p < 0.05) was detected.






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