Neuroinflammation and immune dysregulation are increasingly recognized as central contributors to the progression of neurodegenerative disorders such as Alzheimer's disease. While central nervous system mechanisms have been extensively studied, the contribution of peripheral processes and their interaction with disease-associated pathways remain incompletely understood. Recent advances in high-throughput technologies, including large-scale proteomics and single-cell approaches (scRNA-seq), enable detailed characterization of unique cell populations and their functional states across biological compartments, along with global pathway dysregulation. These datasets are high-dimensional and require computationally intensive approaches to extract biologically meaningful patterns. This project aims to investigate molecular alterations associated with inflammatory and immune-related pathways in the context of neuroinflammation. Using publicly available proteomics and scRNA-seq datasets from neurodegeneration-focused consortia, we will perform integrative analyses across multiple datasets derived from various tissues. The study will involve processing and analysis of large protein expression matrices and single-cell transcriptomic data, including quality control, normalization, and statistical modeling of differential expression. For scRNA-seq data, analyses will include cell-type identification, clustering, and characterization of immune cell subpopulations. Computational approaches will be applied to perform pathway enrichment analysis, network-based modeling, and cross-dataset comparisons to identify consistent signatures of immune activation, dysfunction, and exhaustion. Integration of proteomics and single-cell datasets will require scalable workflows and efficient handling of high-dimensional data. Given the scale and complexity of these datasets, the project will rely on computational resources for data processing, statistical analysis, and systems-level modeling. Data-driven approaches may also be used to identify patterns associated with disease states and tissue-specific phenotypes. This exploratory study aims to generate insights into peripheral immune contributions to neurodegenerative disease and to identify pathway-level alterations associated with dysregulated inflammatory processes. By combining large-scale proteomic and single-cell data with computational analysis, the project seeks to improve understanding of neuroimmune interactions and provide a foundation for future mechanistic and translational research.