To conclude, the pathway enrichment analysis reveals a complex interplay of shared and disease-specific molecular mechanisms across AD, PD and FTD, with converging pathways suggesting common immune (CLU and TGFB1), glycolytic (ENO1 and ENO2) and matrisome (ADAM10 and MMP7) disruptions, whereas distinct proteomic signatures underscore disease-specific pathophysiological processes such as apoptosis (CASP3 and CASP7) in AD, ER-Phagosome (PSME1 and PSMD5) impairment in PD and platelet dysregulation (SOD1 and CD36) in FTD. Here, ENO2 is linked to frontotemporal dementia.