Abstract
To identify the differentially expressed peptides that influenced the generalized anxiety disorder (GAD) by adopting peptidomics and to further provide new targets for the diagnosis and treatment of clinical GAD. 20 patients with GAD as the experimental group and 20 healthy volunteers as the control group were included in the experiment. Differentially expressed peptides were compared and analyzed after collecting serum samples from the two groups and performing peptidomics testing. In addition, GO analysis, COG analysis, and enrichment pathway analysis were utilized to explore the biological processes and function distribution of the differentially expressed peptides. A total of 1149 significantly differentially expressed peptides were identified in the sera of patients with GAD compared to healthy controls (p< 0.05 or P-value-chitest< 0.05), the up-regulated polypeptides are predominant among them. Bioinformatics analysis revealed that the differentially expressed peptide precursor proteins are primarily involved in biological processes such as cellular cytoskeleton organization, intracellular signal transduction, and vesicular trafficking, and are primarily localized in subcellular structures such as the cytoplasm and vesicles, suggesting a possible role in the pathogenesis of GAD by influencing cellular cytoskeletal dynamics, synaptic plasticity, and intercellular signal transduction. Further analysis revealed that the corresponding proteins of these significantly differentially expressed peptides (such as SLAM family member 5, Talin-1, Clusterin, and IGHG1) are involved in immunoregulation, integrin activation, neuroprotection, and antibody-mediated immune responses, indicating that immune-inflammatory imbalance, abnormal synaptic structure, and function may be important molecular mechanisms in the pathogenesis of GAD. GAD is closely associated with immune-inflammatory imbalance and synaptic abnormalities, with significant differences in key proteins such as SLAM family member 5, Talin-1, Clusterin, and IGHG1. This study preliminarily explores differentially expressed peptides in GAD, providing new insights for clinical diagnosis and the screening of therapeutic targets.