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001     151661
005     20240223115101.0
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024 7 _ |a 10.1016/j.celrep.2020.02.025
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024 7 _ |a 2211-1247
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024 7 _ |a 2639-1856
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037 _ _ |a DZNE-2020-01240
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Friker, Lea L.
|b 0
245 _ _ |a β-Amyloid Clustering around ASC Fibrils Boosts Its Toxicity in Microglia
260 _ _ |a [New York, NY]
|c 2020
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520 _ _ |a Alzheimer’s disease is the world’s most common neurodegenerative disorder. It is associated with neuroinflammation involving activation of microglia by β-amyloid (Aβ) deposits. Based on previous studies showing apoptosis-associated speck-like protein containing a CARD (ASC) binding and cross-seeding extracellular Aβ, we investigate the propagation of ASC between primary microglia and the effects of ASC-Aβ composites on microglial inflammasomes and function. Indeed, ASC released by a pyroptotic cell can be functionally built into the neighboring microglia NOD-like receptor protein (NLRP3) inflammasome. Compared with protein-only application, exposure to ASC-Aβ composites amplifies the proinflammatory response, resulting in pyroptotic cell death, setting free functional ASC and inducing a feedforward stimulating vicious cycle. Clustering around ASC fibrils also compromises clearance of Aβ by microglia. Together, these data enable a closer look at the turning point from acute to chronic Aβ-related neuroinflammation through formation of ASC-Aβ composites.
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588 _ _ |a Dataset connected to CrossRef
650 _ 2 |a Amyloid beta-Peptides: metabolism
|2 MeSH
650 _ 2 |a Amyloid beta-Peptides: toxicity
|2 MeSH
650 _ 2 |a Amyloid beta-Peptides: ultrastructure
|2 MeSH
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a CARD Signaling Adaptor Proteins: metabolism
|2 MeSH
650 _ 2 |a Caspase 1: metabolism
|2 MeSH
650 _ 2 |a Cells, Cultured
|2 MeSH
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Inflammasomes: metabolism
|2 MeSH
650 _ 2 |a Interleukin-1beta: metabolism
|2 MeSH
650 _ 2 |a Mice, Inbred C57BL
|2 MeSH
650 _ 2 |a Microglia: drug effects
|2 MeSH
650 _ 2 |a Microglia: metabolism
|2 MeSH
650 _ 2 |a Microglia: pathology
|2 MeSH
650 _ 2 |a Models, Biological
|2 MeSH
650 _ 2 |a NLR Family, Pyrin Domain-Containing 3 Protein: metabolism
|2 MeSH
650 _ 2 |a Proteolysis: drug effects
|2 MeSH
650 _ 2 |a Pyroptosis: drug effects
|2 MeSH
650 _ 2 |a Signal Transduction: drug effects
|2 MeSH
650 _ 2 |a Toll-Like Receptor 2: metabolism
|2 MeSH
650 _ 2 |a Toll-Like Receptor 4: metabolism
|2 MeSH
700 1 _ |a Scheiblich, Hannah
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700 1 _ |a Hochheiser, Inga V.
|b 2
700 1 _ |a Brinkschulte, Rebecca
|b 3
700 1 _ |a Riedel, Dietmar
|b 4
700 1 _ |a Latz, Eicke
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700 1 _ |a Geyer, Matthias
|b 6
700 1 _ |a Heneka, Michael T.
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773 _ _ |a 10.1016/j.celrep.2020.02.025
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856 4 _ |u https://www.sciencedirect.com/science/article/pii/S2211124720301868
856 4 _ |u https://pub.dzne.de/record/151661/files/DZNE-2020-01240.pdf
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
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