Abstract
There is no specific test for diagnosing neuromyelitis optica spectrum disorder (NMOSD), a disabling autoimmune disease of the central nervous system. Instead, diagnosis relies on ruling out other related disorders with overlapping clinical symptoms. An urgency for NMOSD biomarker discovery is underscored by adverse responses to treatment following misdiagnosis and poor prognosis following the delayed onset of treatment. Pathogenic autoantibiotics that target the water channel aquaporin-4 (AQP4) and myelin oligodendrocyte glycoprotein (MOG) contribute to NMOSD pathology. The importance of early diagnosis between AQP4-Ab+ NMOSD, MOG-Ab+ NMOSD, AQP4-Ab− MOG-Ab− NMOSD, and related disorders cannot be overemphasized. Here, we provide a comprehensive data collection and analysis of the currently known metabolomic perturbations and related proteomic outcomes of NMOSD. We highlight short chain fatty acids, lipoproteins, amino acids, and lactate as candidate diagnostic biomarkers. Although the application of metabolomic profiling to individual NMOSD patient care shows promise, more research is needed.
Highlights
The term ‘neuromyelitis optica spectrum disorder’ (NMOSD) was established as a way to unify and classify neuromyelitis optica (NMO), formerly known as Devic’s disease, and a variety of related neurodegenerative syndromes and autoimmune disorders in order to improve individual patient care [1]
Has begun and initial studies show great promise, as they associate a battery of metabolites that link cells, proteins, metabolic pathways, and soluble mediators that may facilitate the pathophysiology of NMOSD
A select group of short-chain fatty acid (SCFA), lipids, lipoproteins, and amino acids that are associated with energy metabolism and glycolysis appears to be promising as candidate biomarkers for disease diagnosis, progression, and response to treatment
Summary
The term ‘neuromyelitis optica spectrum disorder’ (NMOSD) was established as a way to unify and classify neuromyelitis optica (NMO), formerly known as Devic’s disease, and a variety of related neurodegenerative syndromes and autoimmune disorders in order to improve individual patient care [1]. The probability that the continued use of single-candidate approach studies, that may not capture the dynamic complexity of the underlying cause(s) of NMOSD or mechanism(s) of disease progression is limited. The objective of this review is to provide a comprehensive data collection and analysis of the currently known metabolomic perturbations and related proteomics outcomes of NMOSD and relate these immune cell function. Our hope is that this extensive data resource will facilitate additional metabolomic profiling to expedite biomarker discovery. An individual’s metabolomic profile is reportedly as unique as one’s fingerprint given that no two individuals have exactly the same enzyme activity at any given time—and holds great promise to facilite precision medicine approaches for NMOSD patient care.
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