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Polymorphisms in Inflammatory Genes and the Risk of Alzheimer Disease
Patrick L. McGeer, MD, PhD;
Edith G. McGeer, PhD
Arch Neurol. 2001;58:1790-1792.
The concept of inflammation as a
major factor in Alzheimer disease (AD) has heretofore been based on
postmortem findings of autodestructive changes associated with the
lesions coupled with epidemiological evidence of a protective effect of
anti-inflammatory agents.1 Now there is evidence that the
risk of AD is substantially influenced by a total of 10 polymorphisms
in the inflammatory agents interleukin 1 , interleukin 1ß,
interleukin 6, tumor necrosis factor ,
2-macroglobulin, and 1-antichymotrypsin.
The polymorphisms are all common ones in the general population, so
there is a strong likelihood that any given individual will inherit 1
or more of the high-risk alleles. The overall chances of an individual
developing AD might be profoundly affected by a "susceptibility
profile" reflecting the combined influence of inheriting multiple
high-risk alleles. Since some of the polymorphisms in question have
already been linked to peripheral inflammatory disorders, such as
juvenile rheumatoid arthritis, myasthenia gravis, and periodontitis,
associations between AD and several chronic degenerative diseases may
eventually be demonstrated. Such information could lead to strategies
for therapeutic intervention in the early stages of such disorders.
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From the Department of Psychiatry, Kinsmen Laboratory of
Neurological Research, University of British Columbia, Vancouver.
Corresponding author: Patrick L. McGeer, MD, PhD, Kinsmen Laboratory of
Neurological Research, University of British Columbia, 2255 Wesbrook
Mall, Vancouver, British Columbia, Canada V6T 1Z3 (e-mail: mcgeerpl{at}interchange.ubc.ca).
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