Beyond transcriptomics, several other cellular pathways and molecular mechanisms could contribute to the regional heterogeneity and the observed differential vulnerability in Alzheimer's disease. One such pathway is the immune response, particularly the activation of microglia and the release of pro-inflammatory cytokines, which play a critical role in neuroinflammation and neuronal damage in Alzheimer's disease. Dysregulation of synaptic plasticity and neurotransmitter systems, such as glutamatergic and GABAergic signaling, could also contribute to regional vulnerability by affecting synaptic function and neuronal communication. Additionally, alterations in mitochondrial function, oxidative stress, and protein misfolding pathways, including the ubiquitin-proteasome system and autophagy, may impact cellular health and contribute to neurodegeneration in specific brain regions. Epigenetic modifications, such as DNA methylation and histone acetylation, could further influence gene expression patterns and cellular responses to Alzheimer's pathology, adding another layer of complexity to regional heterogeneity. Understanding the interplay of these diverse cellular pathways and molecular mechanisms is essential for unraveling the full spectrum of factors contributing to the differential vulnerability observed in Alzheimer's disease and for developing comprehensive therapeutic strategies targeting multiple aspects of the disease process.