The mechanisms underpinning accelerated cognitive decline in metabolic syndrome (MetS) are poorly understood. Neurovascular coupling (NVC) is the coordinated matching of blood flow to neuronal activation and is dependent on endothelial function. NVC may drive blood flow dysregulation that contributes to neuronal damage and cognitive decline. The purpose was to assess NVC, peripheral endothelial function, and cognitive performance in older adults with MetS and healthy controls (CON), and the association of these factors. Older adults with and without MetS were recruited to complete a neurocognitive battery, assessment of NVC, and endothelial function. NVC was measured in the frontoparietal regions using functional near infrared spectroscopy (fNIRS) while participants completed the n-back task (0-,1-,2-back). Changes in oxyhemoglobin (HbO) and deoxyhemoglobin (HbR) signal reflected NVC during the n-back task. Endothelial function was measured using brachial ultrasound measurements of flow mediated dilation (%FMD). MetS (n=22; age: 66±6) demonstrated poorer NVC during higher cognitive loads, reflected by an attenuated increase in HbO in the premotor cortex during the 2-back task compared to CON (n=26; age: 64±5) (p =0.036). MetS also demonstrated poorer FMD (5.55 ±1.35% vs. 4.42 ±1.71%, p =0.01) and 2-back accuracy compared to CON (MetS: 81.7 ± 6.4%; CON: 86.0 ±6.1%, p =0.027), with a significant positive association between these two factors (r=0.37, p =0.012). Impairments in NVC of the frontal cortex may be an early cerebrovascular mechanism underpinning cognitive decline in MetS and is discernible during higher cognitive loads. Peripheral endothelial dysfunction may be implicated in this mechanism.