| Literature DB >> 28106546 |
Patrick C G Haddick1, Jessica L Larson2, Nisha Rathore3, Tushar R Bhangale3, Qui T Phung4, Karpagam Srinivasan5, David V Hansen5, Jennie R Lill4, Margaret A Pericak-Vance6,7, Jonathan Haines8, Lindsay A Farrer9,10,11,12,13, John S Kauwe14, Gerard D Schellenberg15, Carlos Cruchaga16,17, Alison M Goate18,19, Timothy W Behrens3, Ryan J Watts5, Robert R Graham3, Joshua S Kaminker2, Marcel van der Brug1.
Abstract
The common p.D358A variant (rs2228145) in IL-6R is associated with risk for multiple diseases and with increased levels of soluble IL-6R in the periphery and central nervous system (CNS). Here, we show that the p.D358A allele leads to increased proteolysis of membrane bound IL-6R and demonstrate that IL-6R peptides with A358 are more susceptible to cleavage by ADAM10 and ADAM17. IL-6 responsive genes were identified in primary astrocytes and microglia and an IL-6 gene signature was increased in the CNS of late onset Alzheimer's disease subjects in an IL6R allele dependent manner. We conducted a screen to identify variants associated with the age of onset of Alzheimer's disease in APOE ɛ4 carriers. Across five datasets, p.D358A had a meta P = 3 ×10-4 and an odds ratio = 1.3, 95% confidence interval 1.12 -1.48. Our study suggests that a common coding region variant of the IL-6 receptor results in neuroinflammatory changes that may influence the age of onset of Alzheimer's disease in APOE ɛ4 carriers.Entities:
Keywords: Alzheimer’s disease; IL-6; astrocytes; metalloproteases; microglia
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Year: 2017 PMID: 28106546 PMCID: PMC5667357 DOI: 10.3233/JAD-160524
Source DB: PubMed Journal: J Alzheimers Dis ISSN: 1387-2877 Impact factor: 4.472