Last reviewed: June 1, 2026
2019Cell Reports
Complement C3 Is Activated in Human AD Brain and Is Required for Neurodegeneration in Mouse Models of Amyloidosis and Tauopathy
Wu T, Dejanovic B, Gandin VD, et al.
Abstract summary
Showed elevated complement activity in blood and brain of Alzheimer's disease patients. C1q deposits co-localize with amyloid plaques and synapses. C3 knockout mice show reduced synaptic elimination and attenuated cognitive deficits in AD models. Provides therapeutic rationale for complement inhibition in AD.
Evidence labels
human tissueanimal model
Diseases
- Alzheimer's disease
Species
human, mouse
Methods
ELISA, immunohistochemistry, mouse genetics
Therapeutic relevance
Complement inhibition validated as an approach to limit microglial-mediated synapse loss in Alzheimer's disease.
Last reviewed: June 1, 2026