Commentary 10.1172/JCI135906

Intrinsic antiviral immunity drives neurodegeneration in Alzheimer disease

Stefano Pluchino and Cory Willis

Department of Clinical Neurosciences and NIHR Biomedical Research Centre, University of Cambridge, Cambridge, United Kingdom.

Address correspondence to: Stefano Pluchino, Clifford Allbutt Building, Cambridge Biosciences Campus, Hills Road, CB2 0HA Cambridge, United Kingdom. Phone: 44.1223.331163; Email: spp24@cam.ac.uk.

Find articles by Pluchino, S. in: JCI | PubMed | Google Scholar |

Department of Clinical Neurosciences and NIHR Biomedical Research Centre, University of Cambridge, Cambridge, United Kingdom.

Address correspondence to: Stefano Pluchino, Clifford Allbutt Building, Cambridge Biosciences Campus, Hills Road, CB2 0HA Cambridge, United Kingdom. Phone: 44.1223.331163; Email: spp24@cam.ac.uk.

Find articles by Willis, C. in: JCI | PubMed | Google Scholar

First published March 9, 2020 - More info

Published in Volume 130, Issue 4 on April 1, 2020
J Clin Invest. 2020;130(4):1622–1624. https://doi.org/10.1172/JCI135906.
© 2020 American Society for Clinical Investigation
First published March 9, 2020 - Version history

β-Amyloid aggregates found in brain plaques are viewed as triggers of cytotoxicity and neuroinflammation in Alzheimer disease (AD). However, the main β-amyloid (Aβ) species and what imbues the aggregates with such toxic potential are still not yet understood. In this issue of the JCI, Roy et al. show that Aβ complexed with nucleic acids triggers an antiviral type I interferon response in neuroglia, resulting in complement-mediated synapse elimination in AD models. These findings identify a putative endogenous immune signaling axis that drives neurodegeneration in AD and has strong implications for the development of precise therapeutic strategies.

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