The traditional view of Alzheimer's as purely a brain disorder is giving way to recognition that immune cells throughout the body actively shape disease progression. This paradigm shift opens entirely new therapeutic avenues for the 55 million people worldwide living with dementia. Comprehensive analysis of genetic risk factors reveals that numerous Alzheimer's susceptibility genes operate specifically within immune cells, not neurons. T cells, B cells, monocytes, macrophages, and neutrophils orchestrate a complex inflammatory cascade that directly influences amyloid plaque formation, tau protein tangles, and chronic brain inflammation. The mechanisms involve peripheral inflammatory signals that breach the blood-brain barrier, immune cell exhaustion that impairs the brain's natural cleanup processes, and metabolic dysfunction that amplifies toxic inflammation while reducing protein clearance capacity. This immune-centric perspective represents a fundamental reconceptualization of Alzheimer's pathophysiology. Rather than viewing inflammation as merely a consequence of neurodegeneration, evidence now positions immune dysfunction as a primary driver. The implications extend beyond basic science to immediate therapeutic possibilities, including repurposing existing immune checkpoint inhibitors and cytokine-blocking drugs already proven safe in cancer and autoimmune conditions. However, significant knowledge gaps remain, particularly the urgent need for human-derived immune profiling data to replace reliance on animal models. The field appears poised for personalized immunotherapy approaches that integrate individual genetic risk profiles with immune system aging patterns, potentially offering more precise interventions than current one-size-fits-all strategies targeting amyloid alone.