Alzheimer's disease (AD) and delirium, though distinct in clinical tempo, converge mechanistically at the intersection of neurovascular dysfunction, glial activation, and metabolic collapse. This chapter explores the integrative framework of neurovascular-glia crosstalk, emphasizing how endothelial injury, astrocytic reactivity, and microglial hyperactivation collectively undermine brain energy metabolism. We highlight evidence that blood-brain barrierc (BBB) breakdown, mitochondrial insufficiency, and oxidative stress establish a "metabolic vulnerability state" predisposing the AD brain to delirium. Single-cell and transcriptomic analyses delineate shared molecular circuits involving MAPK, TP53, APOE, and δ-secretase (LGMN)-the latter regulated by disease-relevant miRNAs such as miR-124 and miR-146a. These networks couple neuroinflammation with impaired energy dynamics, bridging chronic neurodegeneration and acute encephalopathic stress. We further discuss how tyrosine-kinase signaling, serotonergic dysregulation, and glial-vascular miscommunication coalesce into a unified pathophysiological axis. Therapeutic repurposing strategies-ranging from tyrosine kinase inhibitors (nilotinib, imatinib) to metabolic modulators (metformin, pioglitazone)-offer promising cross-disease interventions. Finally, we underscore the transformative role of artificial intelligence (AI) and large language models (LLMs) in accelerating drug repurposing through integrative omics and pathway-based reasoning. Together, these advances redefine the AD-delirium nexus as a systems-level disorder of energy and communication, opening translational avenues for precision therapeutics that restore neurovascular balance and cognitive resilience.