Influence of cardiorespiratory fitness and MRI measures of neuroinflammation on hippocampal volume in multiple sclerosis

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This study investigated the impact of neuroinflammation and cardiorespiratory fitness (CRF) on hippocampal volume in patients with multiple sclerosis (MS), with a focus on differences between clinical phenotypes. A total of 81 MS patients were included, of whom 27 had relapsing–remitting MS (RRMS) and 54 had progressive MS (PMS). An additional 45 age- and sex-matched healthy controls were enrolled for structural brain imaging comparisons. All participants underwent high-resolution 3T MRI to assess normalized brain, gray matter, hippocampal, and thalamic volumes. In MS patients, aerobic capacity was assessed via maximum oxygen consumption (VO₂max) using cardiopulmonary exercise testing, while T2-hyperintense lesion volume (T2-LV) and choroid plexus volume (CPV) were quantified as MRI markers of neuroinflammation. Compared to healthy controls, both RRMS and PMS patients exhibited significantly lower brain and regional volumes, including the hippocampus, and higher T2-LV and CPV, reflecting increased neuroinflammation. Regression analyses revealed that T2-LV and CPV were the most influential predictors of global and regional brain atrophy in both MS phenotypes. Notably, VO₂max was identified as a significant predictor of hippocampal volume only in RRMS patients, explaining 16.9% of the variance and retained as a relevant predictor alongside T2-LV in multivariate models. In contrast, VO₂max had no significant explanatory value for hippocampal or other volumetric outcomes in PMS patients. These findings suggest a selective and clinically relevant association between aerobic fitness and hippocampal integrity in the early, relapsing phase of MS, possibly mediated by mechanisms such as neurogenesis or neuroprotection. In more advanced stages of the disease, such as PMS, widespread neurodegeneration may overshadow the potential benefits of aerobic capacity. The results underscore the importance of promoting CRF early in the disease course as a strategy to preserve hippocampal structure and potentially mitigate cognitive decline.

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