Decreased levels of C1q in cerebrospinal fluid of living Alzheimer patients correlate with disease state

Matthew D. Smyth, David H. Cribbs, Andrea J. Tenner, W. Rodman Shankle, Malcolm Dick, J. Patrick Kesslak, Carl W. Cotman

Research output: Contribution to journalArticlepeer-review

41 Scopus citations

Abstract

Recent reports that complement proteins comprising the classical pathway are associated with senile plaques suggest that activation of the classical complement cascade in Alzheimer's disease tissue results in bystander cell lysis and may contribute to AD neuropathology. Analysis of cerebrospinal fluid may prove to be a useful means of detecting changes in immunological activity in the brain. We use an enzyme-linked immunosorbent assay to measure levels of C1q, a subunit of the classical complement cascade, in the CSF of patients clinically diagnosed with possible or probable AD. Significantly lower levels of C1q were detected in the CSF of the Alzheimer group as compared to control CSF [AD: μ = 268 ng/ml, SD = 84; non-AD: μ = 340 ng/ml, SD = 76; F(1, 44) = 5.84, p = 0.02]. Diminished performance on global measures of mental status such as the Mini-Mental State Exam (R = 0.45; p = 0.0072) and Blessed's Information, Memory, and Concentration test (R = 0.42; p = 0.0138) showed high correlations with decreased C1q levels. More specific measures of cognitive function, such as word recall (R = 0.42; p = 0.012), word recognition (R = 0.52; p = 0.0017) and delayed recall (R = 0.45; p = 0.0062) memory tasks also correlated strongly with decreased C1q levels.

Original languageEnglish
Pages (from-to)609-614
Number of pages6
JournalNeurobiology of Aging
Volume15
Issue number5
DOIs
StatePublished - 1994

Keywords

  • Alzheimer's disease
  • C1q
  • Cerebrospinal fluid
  • Complement
  • ELISA
  • Inflammation

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