In this study, we applied an unsupervised learning framework to identify potential molecular subtypes exhibiting AD-related molecular patterns from large-scale blood protein expression data with limited clinical labels. A total of 2,933 blood-derived proteins obtained from 12,675 participants were initially analyzed, and after missingness-based quality control, 2,926 proteins and 11,953 samples were retained for downstream analyses. Dimensionality reduction was performed using principal component analysis (PCA) followed by uniform manifold approximation and projection (UMAP), and hierarchical density-based spatial clustering (HDBSCAN) was subsequently applied, resulting in the identification of three structurally distinct latent groups. Among these, Cluster -1 exhibited a distinct protein expression pattern and was observed in a separated region within the UMAP embedding space. Differential expression analysis and functional pathway enrichment analyses based on KEGG (Kyoto Encyclopedia of Genes and Genomes) and Reactome databases revealed that Cluster -1 was characterized by the enrichment of pathways showing biological relevance to previously reported AD-related molecular mechanisms, including DNA damage response, disruption of protein homeostasis, NF-κB signaling, and apoptosis. In contrast, Cluster 0 showed relatively mild dysregulation related to immune and metabolic processes and was therefore interpreted as an intermediate molecular state. Collectively, our findings demonstrate that an unsupervised learning-based approach can identify AD-related molecular subgroups solely from blood protein expression data, even in the absence of prior clinical label information. This framework provides a valuable foundation for the development of future biomarker-driven risk stratification and molecular subtype characterization for Alzheimer's disease.