In summary, this study demonstrated that patients with early poststroke aphasia exhibit distinct alterations in serum levels of synaptic-associated proteins—including elevated α-SYN, BDNF, and TrkB alongside reductions in CREB and GAP-43—accompanied by widespread gray matter structural decline across language-related regions, as reflected by reduced GMV, CT, and SULC. Here, GAP43 is linked to Aphasia.