Chewing the fat on an emerging target in multiple sclerosis.

Abstract

In this article of EBioMedicine, An Cheng and colleagues show that blocking the function of fatty acid-binding proteins (FABPs) pharmacologically, alleviates the severity of the inflammatory demyelinating neurological condition in the experimental autoimmune encephalomyelitis (EAE) mouse model [1]. Suggesting that targeting lipid metabolism may be a viable therapeutic strategy against several pathological hallmarks of multiple sclerosis (MS). To appreciate this finding, we need to examine the role of FABP and its relationship with MS.