Inflammation as a mediator of the relationship between cortical thickness and metabolic syndrome.
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. 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 were chosen from the previous literature. Forty-three adults between the ages of 40 and 60 years underwent a health screen, neuropsychological testing and structural magnetic resonance imaging. Serum levels of pro-inflammatory markers (interleukin 1, interleukin 2, interleukin 6 and C-Reactive Protein) were measured using enzyme-linked immunosorbent assays. A higher number of MetS risk factors were associated with thinning in the inferior frontal ROI (β = -0.35, p = 0.019) as well as 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 gyrus (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 gyrus indicating successful statistical mediation. The results indicate a potentially important role for inflammation in linking MetS to cortical thinning and cognitive vulnerability.
Department of Psychology, The University of Texas at Austin, 108 E. Dean Keeton, Stop A8000, Austin, TX, 78712, USA.|Imaging Research Center, The University of Texas at Austin, Austin, TX, USA.
Sonya S
SS
Kaur
Department of Psychology, The University of Texas at Austin, 108 E. Dean Keeton, Stop A8000, Austin, TX, 78712, USA.|Imaging Research Center, The University of Texas at Austin, Austin, TX, USA.
Mitzi M
MM
Gonzales
Department of Psychology, The University of Texas at Austin, 108 E. Dean Keeton, Stop A8000, Austin, TX, 78712, USA.|Imaging Research Center, The University of Texas at Austin, Austin, TX, USA.
Danielle E
DE
Eagan
Department of Psychology, The University of Texas at Austin, 108 E. Dean Keeton, Stop A8000, Austin, TX, 78712, USA.
Katyoon
K
Goudarzi
Department of Kinesiology and Health Education, The University of Texas at Austin, Austin, TX, USA.|Imaging Research Center, The University of Texas at Austin, Austin, TX, USA.
Hirofumi
H
Tanaka
Department of Psychology, The University of Texas at Austin, 108 E. Dean Keeton, Stop A8000, Austin, TX, 78712, USA. haley@austin.utexas.edu.|Imaging Research Center, The University of Texas at Austin, Austin, TX, USA. haley@austin.utexas.edu.
Andreana P
AP
Haley
D000328:Adult; D001774:Blood Chemical Analysis; D002540:Cerebral Cortex / Q000473:pathology*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D024821:Metabolic Syndrome / Q000276:immunology* / Q000473:pathology*; D008875:Middle Aged; D015213:Neuroimmunomodulation; D009483:Neuropsychological Tests; D009929:Organ Size; D012307:Risk Factors
Cortical thickness; Inflammation; Metabolic syndrome