A Neural Signature of Metabolic Syndrome—Preliminary Results

As of 2012, metabolic syndrome (MetS) has been estimated to impact 34.7% of the U.S. population (Aguilar, 2015). Meeting the criteria for MetS increases one’s risk for developing cardiovascular disease and type 2 diabetes mellitus (T2DM). However, only recently have researchers begun to probe its effects on brain structure and function. Recent studies have shown that in humans, increased levels of obesity and hyperglycemia are correlated with decreased executive function, processing speed, memory, as well as higher incidences of depression, among others (Yates, 2012). Evidence also suggests that effects of MetS and neurocognitive dysfunction are bidirectional and complex, with genetic, environmental, and behavioral causes playing an important role (Biessels, 2014). In our study, we use voxel-based morphometry (VBM), a well-established structural MRI imaging analysis, to investigate regional gray matter atrophy differences between age- and sex-matched healthy controls (n = 108) and individuals meeting the International Diabetes Federation criteria for MetS (n = 108) from a homogenous Mexican-American cohort. We find that, indeed, there is a significant difference in gray matter density between individuals meeting the criteria for MetS and their age- and sex-matched healthy controls with statistically significant involvement in the following brain regions: bilateral caudate nuclei, orbitofrontal cortex, right parahippocampus/amygdala, right posterior insula, and posterior cerebellum. Additionally, when regressing out key components of MetS such as waist circumference and obesity, we find diverging gray matter atrophy patterns suggesting differential involvement of MetS components on gray matter structure.