Cortical thickness and inflammation in Metabolic Syndrome
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Metabolic Syndrome (MetS), the clustering of obesity, high blood pressure, and disordered glucose and lipid/lipoprotein metabolism within a single individual, is associated with poorer cognitive function and dementia in later life. It has been hypothesized that cognitive impairment in MetS occurs primarily within the context of inflammation. MetS risk factors are also associated with thinning of the cerebral cortex. However, the mechanisms by which MetS and inflammation affect the brain are poorly understood. The present study used statistical mediation to examine the relationship between MetS risk factors, cortical thickness in a priori regions of interest (ROIs) and inflammation. ROIs in the inferior frontal, superior temporal, middle frontal, supra marginal, anterior cingulate and middle occipital regions were chosen from the previous literature. Serum levels of pro-inflammatory markers (interleukin 1, interleukin 2, interleukin 6 and C-Reactive Protein) were measured using enzyme-linked immunosorbent assays. Forty-three adults between the ages of 40 and 60 years underwent a health screen, neuropsychological testing and structural magnetic resonance imaging. A higher number of MetS risk factors was associated with thinning in the inferior frontal ROI (β=-0.35, p = 0.019). A higher number of MetS risk factors was also associated with higher levels of serum interleukin 2 (β=0.31, p=0.04). A higher level of serum interleukin 2 was also associated with reduced thickness in the inferior frontal ROI (β=-0.41, p=0.013). After accounting for the effects of interleukin 2, the number of MetS risk factors was no longer associated with cortical thickness in the inferior frontal ROI indicating successful statistical mediation and pointing towards a potentially important role for imflammation in linking MetS to cortical thinning and cognitive vunlerability.