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  Microglia-derived ASC specks cross-seed amyloid-beta in Alzheimer's disease.

Venegas, C., Kumar, S., Franklin, B. S., Dierkes, T., Brinkschulte, R., Tejera, D., et al. (2017). Microglia-derived ASC specks cross-seed amyloid-beta in Alzheimer's disease. Nature, 552(7685), 355-361. doi:10.1038/nature25158.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-002E-A451-A Version Permalink: http://hdl.handle.net/11858/00-001M-0000-002E-A456-F
Genre: Journal Article

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 Creators:
Venegas, C., Author
Kumar, S., Author
Franklin, B. S., Author
Dierkes, T., Author
Brinkschulte, R., Author
Tejera, D., Author
Vieira-Saecker, A., Author
Schwartz, S., Author
Santarelli, F., Author
Kummer, M. P., Author
Griep, A., Author
Gelpi, E., Author
Beilharz, M., Author
Riedel, D.1, Author              
Golenbock, D. T., Author
Geyer, M., Author
Walter, J., Author
Latz, E., Author
Heneka, M. T., Author
Affiliations:
1Facility for Electron Microscopy, MPI for biophysical chemistry, Max Planck Society, ou_578615              

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 Abstract: The spreading of pathology within and between brain areas is a hallmark of neurodegenerative disorders. In patients with Alzheimer's disease, deposition of amyloid-beta is accompanied by activation of the innate immune system and involves inflammasome-dependent formation of ASC specks in microglia. ASC specks released by microglia bind rapidly to amyloid-beta and increase the formation of amyloid-beta oligomers and aggregates, acting as an inflammation-driven cross-seed for amyloid-beta pathology. Here we show that intrahippocampal injection of ASC specks resulted in spreading of amyloid-beta pathology in transgenic double-mutant APP(Swe)PSEN1(dE9) mice. By contrast, homogenates from brains of APP(Swe)PSEN1(dE9) mice failed to induce seeding and spreading of amyloid-beta pathology in ASC-deficient APP(Swe)PSEN1(dE9) mice. Moreover, co-application of an anti-ASC antibody blocked the increase in amyloid-beta pathology in APP(Swe)PSEN1(dE9) mice. These findings support the concept that inflammasome activation is connected to seeding and spreading of amyloid-beta pathology in patients with Alzheimer's disease.

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Language(s): eng - English
 Dates: 2017-12-202017-12-21
 Publication Status: Published in print
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 Rev. Method: Peer
 Identifiers: DOI: 10.1038/nature25158
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Title: Nature
Source Genre: Journal
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Pages: - Volume / Issue: 552 (7685) Sequence Number: - Start / End Page: 355 - 361 Identifier: -