Fig. 3

Schematic representation of the proposed relationship between Multiple Sclerosis, mitochondrial insufficiency and metabolic signatures. Underlying mitochondrial insuffciency possibly aggravated by an insult reduces mitochondrial capacity resulting in an increased flux through the peroxisomal β-oxidation system. This enhanced peroxisomal activity leads to elevated VLCFA and plasmalogens. Elevated VLCFA could result in CNS inflammation and demyelination. This metabolic derangement is hypothesized to start in early RRMS stage, culminating as a distinct metabolic phenotype in the SPMS stage. RRMS: Relapsing Remitting Multiple Sclerosis; SPMS: Secondary Progressive Multiple Sclerosis; VLCFA: Very Long Chain Fatty Acids; GTA: Gastrointestinal Tract Acids; DHA: Docosahexaenoic acid