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Increasing evidence indicates that neuronal loss is not driven by a single terminal event, but emerges from interacting regulated cell death (RCD) programs. These programs are closely coupled to mitochondrial injury, proteostatic collapse, lysosomal stress, metabolic imbalance, glial state transitions, and chronic neuroinflammation. Yet, how distinct death pathways are organized across cell types, disease stages, and disease\u2010specific microenvironments remains unresolved. This review examines RCD as an integrated pathogenic network in major NDs. Caspase and B\u2010cell lymphoma 2 (BCL2) family signaling, receptor\u2010interacting protein kinase 1 (RIPK1), RIPK3, and mixed lineage kinase domain\u2010like protein activation, NOD\u2010like receptor family pyrin domain containing 3 and gasdermin signaling, GPX4\u2010linked lipid peroxidation control, and autophagy lysosomal failure are discussed as convergent stress response modules rather than isolated pathways. Across Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and Huntington's disease, these modules shape neuronal fate through disease\u2010specific interactions with mitochondrial dysfunction, iron dyshomeostasis, inflammasome activation, and microglial metabolic remodeling. 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