The metabolic syndrome (MetS) is a cluster of risk factors that together increase the risk of developing cardiovascular disease and diabetes relative to the risk associated with each individual component alone. It is estimated that 34% of Americans over the age of 20 meet criteria for MetS, and the prevalence of MetS is estimated to climb to 45% in adults who are 60 years of age or older. Previous research has shown MetS and its individual components are associated with lower cognitive function and increased risk for future cognitive decline and dementia in both middle-aged and older adults. The present study used archival structural MRI data to investigate differences in cortical thickness and subcortical volumes between adults with and without MetS. A total of twenty-six middle age and older age adults with and without MetS (n = 14, n = 12, respectively) were included in the present study. Clinical data were acquired prior to the imaging session and included measurements of body mass index, waist circumference, and blood pressure. T-1 weighted structural MRI scans were processed using the Freesurfer image analysis suite, which allows for the study of cortical and subcortical anatomy via cortical reconstruction and volumetric segmentation. It was hypothesized that (1) Adults with MetS would have smaller values for cortical thickness and subcortical volume in brain areas related to executive functioning, memory, taste and reward processing, regulation of food intake and appetite, and behavioral inhibition, (2) Cortical and subcortical measurements would be negatively associated with measures of adiposity, and (3) Cortical and subcortical measurements would be negatively associated with metabolic risk factor burden. Analyses of covariance revealed group differences in cortical thickness in structures of the medial temporal lobe, controlling for age and gender. The MetS group had smaller values for cortical thickness in the left entorhinal cortex, left parahippocampal gyrus, left temporal pole, and right temporal pole. Correlation analyses revealed a number of significant relationships between clinical data and cortical thickness in these medial temporal structures. Both measures of adiposity and metabolic risk factor burden were negatively associated with cortical thickness in these areas. Further, exploratory analyses showed cortical thickness in medial temporal structures was negatively associated with the presence of hypertension and diabetes. The principal finding of the present study was that adults with MetS had smaller values for cortical thickness in medial temporal lobe structures relative to metabolically healthy adults. The medial temporal lobe is implicated in early Alzheimer's disease pathology and its structures are important to memory function. In group comparisons, the largest effect size was seen in the left entorhinal cortex, an area suggested to be the first site of neuropathological changes seen in Alzheimer's disease. Given the established connections between medial temporal lobe atrophy and cognitive decline and dementia, our findings suggest that middle-age and older adults with MetS may be at increased risk for cognitive decline and future dementia.