ArticleActa neurologica Belgica2024
Patients with restless legs syndrome exhibit reduced serum colony-stimulating factor-1, humanin-like 3 and 10 levels.
Article in Acta neurologica Belgica, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- Hydrogen as a Potential Modulator: Implications for Mast Cell-Sleep-Wake Rhythm-Melatonin Interactions in Sleep Disorders.Molecular neurobiology · 2026Review
- Diagnostic Value of Serum Humanin-Like 3 Levels in Multiple Sclerosis Patients with Predominant Optic Nerve and Spinal Cord Involvement: A Preliminary Study.Noro psikiyatri arsivi · 2026Article
- Hydrotherapy and acupressure for restless legs syndrome: results of a qualitative part of a randomized controlled exploratory study.Frontiers in medicine · 2025Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
objectiveThe main pathophysiological mechanisms in restless legs syndrome (RLS) are known as genetic predisposition, brain iron deficiency, and dopaminergic dysfunction. While some genetic variants and polymorphisms were defined, the genetic basis and etiopathogenesis of RLS remain unclear. We aimed to identify new candidate genes and/or potential biomarkers associated with increased RLS risk.
methodsTwenty-three patients with RLS, 30 patients with Parkinson's disease (PD), and 27 healthy controls were enrolled. Agilent Human 8X60K Oligo Microarray was used for the identification of gene expression levels in peripheral blood cells. Gene ontology (GO) analysis was used for functional annotation of differentially expressed genes (DEGs). Serum levels of selected DEGs were measured by ELISA for validation.
resultsPatients with RLS showed 30 downregulated DEGs compared to healthy controls. Two genes, MTRNR2L10 and MTRNR2L3, involved negative regulation of the execution phase of apoptosis were highlighted in GO analysis. These genes encode humanin-like 10 and 3, respectively, were encoded by these genes, and their levels, along with CSF-1, linked to neurodegeneration, were reduced in RLS patients. Humanin-like 10 and CSF-1 levels correlated with sleep efficiency and N2 sleep duration, while humanin-like 3 levels correlated with mean sleep oxygen saturation during sleep.
conclusionOur study showed that several neuroprotective genes were downregulated in RLS, which may confer susceptibility to neuronal death associated with decreased sleep efficiency. Microarray results differed between RLS and PD patients, suggesting diverse pathogenetic mechanisms. CSF-1, which is involved in iron, dopamine metabolism, and blood oxygenation, appears to partake in RLS pathophysiology.
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