Neuronal expression of mRNAs for complement proteins of the classical pathway in Alzheimer brain.
To determine possible sources of complement proteins in the brain, we investigated by in situ hybridization expression of the mRNAs of C1q, C2, C3, C4, C5, C6, C7, C8 and C9 in postmortem Alzheimer disease (AD) and control brain tissue. We found detectable hybridization for all these components in the temporal cortex and hippocampus, with significantly higher levels being found in AD tissue. Hybridization signals were strongest over pyramidal neurons. Low or absent hybridization was seen in the visual cortex or cerebellum. These results suggest that the activated complement components found in association with AD lesions may be, in part, derived from neurons.
Shen
Y
Y
Department of Psychiatry and Behavioral Sciences, University of Louisville School of Medicine, KY 40292, USA.
Li
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R
McGeer
E G
EG
McGeer
P L
PL
D000368:Aged; D000369:Aged, 80 and over; D000544:Alzheimer Disease / Q000378:metabolism* / Q000473:pathology; D001921:Brain / Q000378:metabolism* / Q000473:pathology; D003171:Complement Pathway, Classical / Q000502:physiology*; D003165:Complement System Proteins / Q000235:genetics*; D006801:Humans; D009474:Neurons / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism*; D012016:Reference Values; D014018:Tissue Distribution
D012333:RNA, Messenger; D003165:Complement System Proteins