Assessing beta-amyloid-induced NLRP3 inflammasome activation in primary 
microglia

Schnaars, M.; Beckert, H.; Halle, A.

doi:10.1007/978-1-62703-523-1_1

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Assessing beta-amyloid-induced NLRP3 inflammasome activation in primary microglia

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Schnaars, M.
Max Planck Research Group Neuroimmunology, Center of Advanced European Studies and Research (caesar), Max Planck Society;

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Beckert, H.
Max Planck Research Group Neuroimmunology, Center of Advanced European Studies and Research (caesar), Max Planck Society;

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Halle, A.
Max Planck Research Group Neuroimmunology, Center of Advanced European Studies and Research (caesar), Max Planck Society;

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http://www.ncbi.nlm.nih.gov/pubmed/23852592
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Citation

Schnaars, M., Beckert, H., & Halle, A. (2013). Assessing beta-amyloid-induced NLRP3 inflammasome activation in primary microglia. Methods in Molecular Biology, 1040, 1-8. doi:10.1007/978-1-62703-523-1_1.

Cite as: https://hdl.handle.net/11858/00-001M-0000-0028-6178-B

Abstract

Senile plaques are an important histological hallmark of Alzheimer's disease. They mainly consist of the fibrillar peptide beta-amyloid (Abeta) and are surrounded by activated microglia and astrocytes. Microglia in the vicinity of senile plaques express high levels of proinflammatory cytokines and neurotoxic substances, which are believed to influence disease progression. One important cytokine in Alzheimer's disease is IL-1beta. Stimulation of cultured primary microglia by synthetic fibrillar Abeta causes the release of IL-1beta via activation of the NLRP3 inflammasome.Here we provide protocols for the preparation of primary microglial cultures and synthetic oligomeric and fibrillar forms of Abeta.