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.

Highlights

  • 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]

  • Fatty acids are known to be involved in the inflammatory response, oxidative stress, and mitochondrial dysfunction

  • The authors go on to provide direct evidence that FABP5 and 7 inhibition limit oxidative stress-induced damage in EAE by targeting reactive microglia and protecting oligodendrocytes; these are considered as key strategies in limiting multiple sclerosis (MS) progression

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Summary

Introduction

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). The presence of proinflammation brought about by reactive T cells, microglia and astrocytes, oxidative stress, and mitochondrial dysfunction that perpetuate degeneration of neurons and glial cells, including oligodendrocytes, are common hallmarks of early MS.

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