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Association of early‐onset Alzheimer's disease with an interleukin‐1α gene polymorphism

Association of early‐onset Alzheimer's disease with an interleukin‐1α gene polymorphism Overexpression of the pluripotent cytokine interleukin‐1 (IL‐1) by microglial cells correlates with formation of neuritic β‐amyloid plaques in Alzheimer's disease (AD). We evaluated polymorphisms in the genes coding for the IL‐1α, IL‐1β, and IL‐1 receptor antagonist cytokines, and tested their association with the occurrence and age at onset of sporadic AD. We found a strong association between the IL‐1A T/T genotype and AD onset before 65 years of age (odds ratio, 4.86), with carriers of this genotype showing an onset of disease 9 years earlier than IL‐1A C/C carriers. A weaker association with the age at onset was also shown for the IL‐1B and IL‐1RN genes. These data suggest either a direct effect of the IL‐1 gene family, mainly IL‐1A, on the clinical onset of AD, or a linkage dysequilibrium with an unknown locus relevant to AD on chromosome 2. Ann Neurol 2000;47:361–365 http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Annals of Neurology Wiley

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References (238)

Publisher
Wiley
Copyright
Copyright © 2000 American Neurological Association
ISSN
0364-5134
eISSN
1531-8249
DOI
10.1002/1531-8249(200003)47:3<361::AID-ANA12>3.0.CO;2-N
Publisher site
See Article on Publisher Site

Abstract

Overexpression of the pluripotent cytokine interleukin‐1 (IL‐1) by microglial cells correlates with formation of neuritic β‐amyloid plaques in Alzheimer's disease (AD). We evaluated polymorphisms in the genes coding for the IL‐1α, IL‐1β, and IL‐1 receptor antagonist cytokines, and tested their association with the occurrence and age at onset of sporadic AD. We found a strong association between the IL‐1A T/T genotype and AD onset before 65 years of age (odds ratio, 4.86), with carriers of this genotype showing an onset of disease 9 years earlier than IL‐1A C/C carriers. A weaker association with the age at onset was also shown for the IL‐1B and IL‐1RN genes. These data suggest either a direct effect of the IL‐1 gene family, mainly IL‐1A, on the clinical onset of AD, or a linkage dysequilibrium with an unknown locus relevant to AD on chromosome 2. Ann Neurol 2000;47:361–365

Journal

Annals of NeurologyWiley

Published: Mar 1, 2000

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