Review Article

Contribution of Neurons and Glial Cells to Complement-Mediated Synapse Removal during Development, Aging and in Alzheimer’s Disease

Table 3

Cellular localization of complement components in Alzheimer’s disease.

Cell typeLocalizationExperimental modelMethodRef.

C1q
 NeuronCellularHuman tissueIHC, in situ hybridization[88]
Synaptic punctaIn vivo: J20 miceIF[8]
 MicrogliaIn vivo: J20 miceIF[8]
 AstrocyteCellularIn vitro: human primary culture
In vivo: 5xFAD mice
ELISA, IF[84, 89]
ExosomesHuman plasma samplesImmunoassay[34]
C3
 NeuronSynaptic punctaIn vivo: J20 miceIF[8]
 MicrogliaIn vitro: mice primary culture
In vivo: APPswe/PS1dE9 mice
qPCR, IP, in situ hybridization[35, 37]
 AstrocyteIn vitro: mice primary culture
In vivo: APP/TTA, APPswe/PS1dE9 mice
qPCR, in situ hybridization, IC[30, 37]
CellularIn vivo: APP miceIF[124]
Human tissueqPCR, in situ hybridization[14]
ExosomesHuman plasmaImmunoassay[34]
CR3
 MicrogliaCellularIn vitro: mice primary culture, BV2 cell line
In vivo: J20 mice
IF, WB[8, 91]
C3aR
 NeuronIn vitro: mice primary culture
In vivo: APP/TTA mice
IF[118]
 MicrogliaIn vitro: mice primary culture
In vivo: APPswe/PS1dE9 mice
qPCR, in situ hybridization[37]

qRT-PCR: semiquantitative PCR; ICC: immunocytochemistry; IHC: immunohistochemistry; WB: Western blot; IF: immunofluorescence; FACS: fluorescence-activated cell sorting; IP: immunoprecipitation.