Differences in the choroid plexus volume and microstructure are associated with body adiposity.

Abstract

The choroid plexus (CP) is a cerebral structure located in the ventricles that functions in producing most of the brain’s cerebrospinal fluid (CSF) and transporting proteins and immune cells. Alterations in CP structure and function has been implicated in several pathologies including aging, multiple sclerosis, Alzheimer’s disease, and stroke. However, identification of changes in the CP remains poorly characterized in obesity, one of the main risk factors of neurodegeneration, including in the absence of frank central nervous system alterations. Our goal here was to characterize the association between obesity, measured by the body mass index (BMI) or waist circumference (WC) metrics, and CP microstructure and volume, assessed using advanced magnetic resonance imaging (MRI) methodology. This cross-sectional study was performed in the clinical unit of the National Institute on Aging and included a participant population of 123 cognitively unimpaired individuals spanning the age range of 22 – 94 years. Automated segmentation methods from FreeSurfer were used to identify the CP structure. Our analysis included volumetric measurements, quantitative relaxometry measures (T 1 and T 2), and the diffusion tensor imaging (DTI) measure of mean diffusivity (MD). Strong positive associations were observed between WC and all MRI metrics, as well as CP volume. When comparing groups based on the established cutoff point by the National Institutes of Health for WC, a modest difference in MD and a significant difference in T 1 values were observed between obese and lean individuals. We also found differences in T1 and MD between obese and overweight individuals as defined using the BMI cutoff. We conjecture that these observations in CP volume and microstructure are due to obesity-induced inflammation, diet, or, very likely, dysregulations in leptin binding and transport. These findings demonstrate that obesity is strongly associated with a decline in CP microstructural integrity. We expect that this work will lay the foundation for further investigations on obesity-induced alterations in CP structure and function.