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A genetic variation of the inflammatory cytokine interleukin‐6 delays the initial onset and reduces the risk for sporadic Alzheimer's disease
Author(s) -
Papassotiropoulos Andreas,
Bagli Metin,
Jessen Frank,
Bayer Thomas A.,
Maier Wolfgang,
Rao Marie Luise,
Heun Reinhard
Publication year - 1999
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/1531-8249(199905)45:5<666::aid-ana18>3.0.co;2-3
Subject(s) - disease , neurodegeneration , cytokine , immune system , allele , immunology , alzheimer's disease , medicine , inflammation , genotype , interleukin , biology , genetics , gene , pathology
Local inflammatory processes surrounding the amyloid plaques contribute to the progression and acceleration of the Alzheimer's disease (AD)–related neurodegeneration. Interleukin‐6 (IL‐6) is an inflammatory cytokine with possible involvement in the local immune response occurring in the central nervous system of AD patients. We tested the hypothesis as to whether a genetic polymorphism of the IL‐6 gene ( IL‐6 ) modifies the age at onset and risk for sporadic AD. Our results support an association of the C allele of the IL‐6 genotype with a delayed initial onset and reduced disease risk and indicate that genetically determined alterations of the immune response may modify the course of AD. Ann Neurol 1999;45:666–668