Abstract

especially in early disease stages. In late stages of AD Abeta and tauprotein levels have become static and are therefore unsuitable to reflect ongoing dynamic processes of AD-related neurodegeneration, such as glia cell-related pathobiology. But, it is well established that amyloid plaques are associated with activated astrocytes. Thus, astrocyte-derived proteins like glial fibrillary acidic protein (GFAP) and S100B that are detectable in CSF might serve as markers of pathophysiological events especially in advanced AD. Methods: For a sample of 68 human CSF aliquots commercially available ELISA were used for the quantitative analysis of GFAP (IBL-International, Hamburg, Germany) and S100B (IBL). We included AD patients, healthy and disease controls. First we correlated standard biomarkers (abeta and tau-protein) and glia-derived proteins, furthermore we compared biomarker levels of controls and AD patients at different disease stages. Results: When calculating the correlation coefficient (Spearman) we found a significant correlation of t-tau and GFAP (r 1⁄4 0.261, P <0.05). In contrast, no correlation of S100B and t-Tau levels was detected. Comparing groups of patients at different disease stages, we found that for both markers, S100B and GFAP the average concentrations are highest in AD-patients with moderate dementia at presumably advanced disease stages. Conclusions: Astrocyte-derived proteins like GFAP and S100B can be reliably detected in CSF and might serve as markers for late pathophysiological events in the course of the disease. Additional measurement of astroglial biomarkers might allow an improved pathobiological staging of AD.

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