Immunometabolic dysregulation is associated with reduced cortical thickness of the anterior cingulate cortex

免疫代谢失调与前扣带皮层厚度减少有关

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作者:Laura S van Velzen, Lianne Schmaal, Yuri Milaneschi, Marie-José van Tol, Nic J A van der Wee, Dick J Veltman, Brenda W J H Penninx

Background

Immunometabolic dysregulation (low-grade inflammation and metabolic dysregulation) has been associated with the onset and more severe course of multiple psychiatric disorders, partly due to neuroanatomical changes and impaired neuroplasticity. We examined the effect of multiple markers of immunometabolic dysregulation on hippocampal and amygdala volume and anterior cingulate cortex thickness in a large sample of patients with depression and/or anxiety and healthy subjects (N=283).

Conclusions

Multiple serum, but not genetic immunometabolic dysregulation markers were found to relate to rostral ACC structure, suggesting that inflammation and metabolic dysregulation may impact the ACC through similar mechanisms.

Methods

Interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-a), c-reactive protein (CRP), triglyceride levels and HDL-cholesterol and genomic profile risk scores (GPRS) for immunometabolic dysregulation were determined in peripheral blood and T1 MRI scans were acquired at 3T. Regional brain volume and cortical thickness was assessed using FreeSurfer. Covariate-adjusted linear regression analyses were performed to examine the relationship between immunometabolic dysregulation and brain volume/thickness across all subjects.

Results

Multiple immunometabolic dysregulation markers (i.e. triglyceride levels and inflammation) were associated with lower rostral ACC thickness across all subjects. IL-6 was inversely associated with hippocampal and amygdala volume in healthy subjects only. GPRS for immunometabolic dysregulation were not associated with brain volume or cortical thickness. Conclusions: Multiple serum, but not genetic immunometabolic dysregulation markers were found to relate to rostral ACC structure, suggesting that inflammation and metabolic dysregulation may impact the ACC through similar mechanisms.

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