Altered metabolism and endoplasmic reticulum-mitochondria contacts in multiple sclerosis neurons

Background

Genetic factors are estimated to account for approximately 30-50% of the risk for developing Multiple sclerosis (MS). Distinct mitochondrial variants, impairments in the respiratory chain, and mitochondrial dysfunction have been reported in individuals affected by MS. Mitochondria and the endoplasmic reticulum (ER) form membrane contact sites (ERMCs) that control important biological functions. Dysregulated ERMCs have been associated with a number of severe consequences for homeostasis, including altered mitochondrial calcium levels, impaired ATP production and abnormal lipid transfer. All of these mechanisms are thought to play an important role in the pathogenesis and disease progression of MS. Here, we investigated the hypothesis that the mitochondrial predisposition plays a crucial role in contributing to MS development.