ArticleBiomolecules2023
LC-MS/MS-Based Proteomics Approach for the Identification of Candidate Serum Biomarkers in Patients with Narcolepsy Type 1.
Article in Biomolecules, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 21 citations in OpenAlex.
- Mass Spectrometry Proteomics: A Key to Faster Drug Discovery.Journal of medicinal chemistry · 2026Review
- Cross-platform clinical proteomics using the Charité open standard for plasma proteomics (OSPP).Nature communications · 2025Article
- Alteration of Metabolic Profile in Patients with Narcolepsy Type 1.Metabolites · 2025Article
- SerumBiomolecules · 2024Article
- SerumACS omega · 2024Article
- Metabolomic Changes in Rat Serum after Chronic Exposure to Glyphosate-Based Herbicide.Metabolites · 2024Article
- Neuroglycome alterations of hippocampus and prefrontal cortex of juvenile rats chronically exposed to glyphosate-based herbicide.Frontiers in neuroscience · 2024Article
- Human serum proteomics reveals a molecular signature after one night of sleep deprivation.Sleep advances : a journal of the Sleep Research Society · 2024Article
- LC-MS/MS Quantitation of HILIC-EnrichedBiomolecules · 2023Article
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Authors and funding
14 authors at 8 institutions in 3 countries.
Funding
Abstract
Narcolepsy type 1 (NT1) is the most common type of narcolepsy known to be caused by the loss of specific neurons responsible for producing peptide neurotransmitters (orexins/hypocretins), resulting in a sleep-wake cycle disorder. It is characterized by its association with cataplexy and abnormalities in rapid eye movement. To date, no cure has been established for this life-threatening condition. Misdiagnosis of NT1 is also quite common, although it is not exceedingly rare. Therefore, successfully identifying candidate serum biomarkers for NT1 would be a head start for accurate diagnosis and development of therapeutics for this disorder. This study aims to identify such potential serum biomarkers. A depletion protocol was employed for 27 human serum samples (16 NT1 and 11 healthy controls), followed by applying LC-MS/MS bottom-up proteomics analysis, then LC-PRM-MS for validation. The comparison of the proteome profiles of the low-abundant proteins in the samples was then investigated based on age, sex, sample groups, and the presence of the Human Leukocyte Antigen (HLA) DQB1*0602 allele. The results were tracked to gene expression studies as well as system biology to identify key proteins and understand their relationship in the pathogenesis of NT1. Our results revealed 36 proteins significantly and differentially expressed. Among the impaired pathways and bioprocesses, the complement activation pathway is impaired by six of the differentially expressed proteins (DEPs). They are coded by the genes C2, CFB, C5, C1R, C1S, and MASP1, while 11 DEPs are involved in Acute Phase Response Signaling (APRS), which are coded by the genes FN1, AMBP, APOH, CFB, CP, ITIH2, C5, C2, F2, C1, and ITIH4. The combined AUCs of the downregulated and upregulated DEPs are 0.95 and 0.76, respectively. Overall, this study reveals potential serum-protein biomarkers of NT1 and explains the possible correlation between the biomarkers and pathophysiological effects, as well as important biochemical pathways involved in NT1.
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