The brain has exceptionally high metabolic demands and depends on a continuous supply of oxygen and glucose to maintain neuronal activity and cognitive function. Despite accounting for only about 2 % of body weight, it consumes more than 20 % of the body's energy. This demand is met through tightly regulated cerebral blood flow mediated by neurovascular coupling (NVC), a process that links neuronal activity with local vascular responses. The cellular components responsible for this regulation including neurons, astrocytes, endothelial cells, pericytes, and vascular smooth muscle cells form the neurovascular unit (NVU), which maintains blood brain barrier (BBB) integrity, metabolic homeostasis, and efficient substrate delivery. Increasing evidence suggests that disruption of neurovascular and metabolic regulation is an early and critical contributor to Alzheimer's disease (AD). Impairment of NVU function leads to reduced cerebral blood flow, endothelial dysfunction, pericyte loss, and breakdown of the BBB. These vascular changes compromise the delivery of oxygen and glucose, resulting in cerebral hypometabolism that often precedes classical pathological hallmarks such as amyloid-β plaques and tau neurofibrillary tangles. Alterations in glucose transport across the BBB, particularly reduced expression of the GLUT1 transporter, further exacerbate neuronal energy deficits. Disturbances in lactate metabolism and mitochondrial dysfunction also contribute to oxidative stress and progressive neurodegeneration. Understanding the interaction between neurovascular dysfunction, impaired brain metabolism, and AD pathology provides important insight into disease progression. Therapeutic strategies aimed at restoring vascular function, improving metabolic substrate delivery, and enhancing neuronal energy metabolism may offer promising avenues for early intervention in AD.