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      Complement gene expression in human brain: comparison between normal and Alzheimer disease cases.

      Brain research. Molecular brain research
      Aged, Aged, 80 and over, Alzheimer Disease, genetics, metabolism, Amino Acid Isomerases, biosynthesis, Base Sequence, Brain, Carrier Proteins, Complement C1q, Complement C3, Complement C4, Complement Pathway, Classical, Female, Gene Expression, Humans, Male, Middle Aged, Molecular Sequence Data, Peptidylprolyl Isomerase, Polymerase Chain Reaction, RNA, Messenger, analysis

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          Abstract

          Many investigators have reported the presence of complement proteins in Alzheimer disease (AD) brains, but their origin is uncertain. We report the expression of complement genes C1q, C3 and C4 in RNA extracted from temporal cortex samples of post-mortem human brain. The transcripts for C3 and C4 were detected by Northern hybridization analysis, and the mRNAs for C1q, C3 and C4 were detected by polymerase chain reaction (PCR) amplification of brain derived complementary DNA (cDNA). The relative abundances of mRNAs for C3 and C4 were compared between samples of temporal cortex from neurologically normal and Alzheimer disease (AD) cases, using a semiquantitative PCR assay. There was a 3.01 fold mean increase in expression of C3 and a 3.27-fold mean increase in expression of C4 in AD samples compared to control cases. These results indicate that localized synthesis of some of the major complement components can occur in human brain. The factors causing activation of complement in AD still remain undetermined.

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