Plasma GFAP and <i>p</i> ‐tau 181 were closely linked with longitudinal synaptic loss and cognition decline

CI patients have more longitudinal synapse loss and tau burden increases with one-year follow-up than HC participants. Baseline tau pathology(tau burden and plasma p-tau 181) and plasma GFAP were negatively associated with synaptic density and could predict longitudinal synapse loss. Tau pathology might trigger neuroinflammation leading to synaptic loss. Plasma p-tau 181 and GFAP could predict the longitudinal cognition decline. Tau pathology and neuroinflammation interaction resulted in synaptic loss and cognition decline.