DECREASED LEVELS OF C1Q IN CEREBROSPINAL-FLUID OF LIVING ALZHEIMER PATIENTS CORRELATE WITH DISEASE STATE

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 Clq, a subunit of the classical complement cascade, in the CSF of patients clinically diagnosed with possible or probable AD. Significantly lower levels of Clq were detected in the CSF of the AIzheimer group as compared to control CSF[AD: mu = 268 ng/ml, SD = 84; non-AD: mu = 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 Clq 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 Clq levels.