|  Help  |  About  |  Contact Us

Publication : Complement C3 Is Activated in Human AD Brain and Is Required for Neurodegeneration in Mouse Models of Amyloidosis and Tauopathy.

First Author  Wu T Year  2019
Journal  Cell Rep Volume  28
Issue  8 Pages  2111-2123.e6
PubMed ID  31433986 Mgi Jnum  J:280229
Mgi Id  MGI:6369108 Doi  10.1016/j.celrep.2019.07.060
Citation  Wu T, et al. (2019) Complement C3 Is Activated in Human AD Brain and Is Required for Neurodegeneration in Mouse Models of Amyloidosis and Tauopathy. Cell Rep 28(8):2111-2123.e6
abstractText  Complement pathway overactivation can lead to neuronal damage in various neurological diseases. Although Alzheimer's disease (AD) is characterized by beta-amyloid plaques and tau tangles, previous work examining complement has largely focused on amyloidosis models. We find that glial cells show increased expression of classical complement components and the central component C3 in mouse models of amyloidosis (PS2APP) and more extensively tauopathy (TauP301S). Blocking complement function by deleting C3 rescues plaque-associated synapse loss in PS2APP mice and ameliorates neuron loss and brain atrophy in TauP301S mice, improving neurophysiological and behavioral measurements. In addition, C3 protein is elevated in AD patient brains, including at synapses, and levels and processing of C3 are increased in AD patient CSF and correlate with tau. These results demonstrate that complement activation contributes to neurodegeneration caused by tau pathology and suggest that blocking C3 function might be protective in AD and other tauopathies.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

17 Bio Entities

Trail: Publication

0 Expression