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Plasma glial fibrillary acidic protein (GFAP) mediated the relationship between CSF A\u03b2<jats:sub>42\/40<\/jats:sub> and A\u03b2\u2010PET, and CSF YKL\u201040 partly explained the association between A\u03b2\u2010PET, p\u2010tau<jats:sub>181<\/jats:sub>, and NfL.<\/jats:p><\/jats:sec><jats:sec><jats:title>DISCUSSION<\/jats:title><jats:p>Our results suggest that reactive astrogliosis, as indicated by different fluid biomarkers, influences the pathogenic cascade during the preclinical stage of AD. While plasma GFAP mediates the early association between soluble and insoluble A\u03b2, CSF YKL\u201040 mediates the latter association between A\u03b2 and downstream A\u03b2\u2010induced tau pathology and tau\u2010induced neuronal injury.<\/jats:p><\/jats:sec><jats:sec><jats:title>Highlights<\/jats:title><jats:p><jats:list list-type=\"bullet\">\n<jats:list-item><jats:p>Lower CSF A\u03b2<jats:sub>42\/40<\/jats:sub> was directly linked to higher plasma GFAP concentrations.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Plasma GFAP partially explained the relationship between soluble A\u03b2 and insoluble A\u03b2.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>CSF YKL\u201040 mediated A\u03b2\u2010induced tau phosphorylation and tau\u2010induced neuronal 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