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Are interleukin-1 gene polymorphisms risk factors or disease modifiers in AD?
E K Green1, J M Harris, H Lemmon
1Molecular Psychiatry Department, Division of Neuroscience, Queen Elizabeth Psychiatry Hospital, University of Birmingham, United Kingdom.
Neurology
|May 30, 2002
Summary
Interleukin-1 gene variants (IL-1A and IL-1B) do not appear to increase Alzheimer's disease (AD) risk or affect onset age. However, IL-1B(-511) may influence amyloid-beta 40 (Abeta40) levels in the brain.
Area of Science:
- Genetics
- Neuroscience
- Immunology
Background:
- Interleukin-1 (IL-1) gene polymorphisms have been inconsistently linked to Alzheimer's disease (AD) risk.
- Previous studies show conflicting results regarding the association between IL-1 gene variants and AD.
Purpose of the Study:
- To investigate the association between IL-1A(-889) and IL-1B(-511) polymorphisms and Alzheimer's disease risk.
- To examine the effect of these polymorphisms on age at AD onset and brain amyloid-beta (Abeta) load.
Main Methods:
- Genotyping of IL-1A(-889) and IL-1B(-511) polymorphisms in large cohorts of AD patients and control individuals.
- Analysis of AD risk, age at onset, and brain Abeta load in relation to identified genotypes.
Main Results:
- No significant evidence found for an increased risk of AD associated with the studied IL-1A and IL-1B polymorphisms.
- These genetic variants did not demonstrate an effect on the age of AD onset.
- A statistically significant impact of the IL-1B(-511) polymorphism on brain Abeta(40) load was observed (p < 0.05).
Conclusions:
- The investigated IL-1A and IL-1B polymorphisms are unlikely to be major risk factors for Alzheimer's disease.
- The IL-1B(-511) polymorphism may play a role in modulating amyloid-beta pathology, specifically Abeta(40) levels, in the brain.