Research ArticleAlzheimer’s Disease

Complement C3 deficiency protects against neurodegeneration in aged plaque-rich APP/PS1 mice

See allHide authors and affiliations

Science Translational Medicine  31 May 2017:
Vol. 9, Issue 392, eaaf6295
DOI: 10.1126/scitranslmed.aaf6295

Avoiding complements

Complement C3 is an immune molecule that protects against pathogens and plays a role in refinement of the developing visual system by removing weak nerve connections (that is, synapses). C3 is up-regulated in Alzheimer’s disease and, therefore, may contribute to the synapse loss that underlies cognitive decline. Shi et al. now report that an aged transgenic mouse model of Alzheimer’s disease that lacks C3 was protected against synapse loss and cognitive decline even in the presence of Aβ plaques, possibly by altering the glial response to Aβ deposition. Thus, modulation of complement signaling may have potential as a new therapeutic strategy for Alzheimer’s disease.

View Full Text

Stay Connected to Science Translational Medicine