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

Recent reports that complement proteins comprising the classical pathw ay are associated with senile plaques suggest that activation of the c lassical complement cascade in Alzheimer's disease tissue results in b ystander cell lysis and may contribute to AD neuropathology. Analysis of cerebrospinal fluid may prove to be a useful means of detecting cha nges in immunological activity in the brain. We use an enzyme-linked i mmunosorbent assay to measure levels of Clq, a subunit of the classica l complement cascade, in the CSF of patients clinically diagnosed with possible or probable AD. Significantly lower levels of Clq were detec ted in the CSF of the AIzheimer group as compared to control CSF[AD: m u = 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 sta tus such as the Mini-Mental State Exam (R = 0.45; p = 0.0072) and Bles sed's Information, Memory, and Concentration test (R = 0.42; p = 0.013 8) showed high correlations with decreased Clq levels. More specific m easures of cognitive function, such as word recall (R = 0.42; p = 0.01 2), word recognition (R = 0.52; p = 0.0017) and delayed recall(R = 0.4 5; p = 0.0062) memory tasks also correlated strongly with decreased Cl q levels.