ArticleBioanalysis2015
Stable isotopes and LC-MS for monitoring metabolic disturbances in Friedreich's ataxia platelets.
Article in Bioanalysis, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 28 citations in OpenAlex.
- Double blind trial of a deuterated form of linoleic acid (RT001) in Friedreich ataxia.Journal of neurology · 2023Trial
- Safety, pharmacodynamics, and potential benefit of omaveloxolone in Friedreich ataxia.Annals of clinical and translational neurology · 2019Trial
- Impaired Glur2 palmitoylation in cerebellar Purkinje cells of a Friedreich ataxia mouse model.Experimental neurology · 2026Article
- Neuropathology of Friedreich ataxia and its links to metabolic pathways.Neurodegenerative disease management · 2026Review
- Integrative statistical genetics prioritizes candidate ASCVD susceptibility genes across tissues.Molecular medicine (Cambridge, Mass.) · 2026Article
- Exploring mitochondrial biomarkers for Friedreich's ataxia: a multifaceted approach.Journal of neurology · 2024Article
- Frataxin deficiency alters gene expression in Friedreich ataxia derived IPSC-neurons and cardiomyocytes.Molecular genetics & genomic medicine · 2023Article
- Skin fibroblast metabolomic profiling reveals that lipid dysfunction predicts the severity of Friedreich's ataxia.Journal of lipid research · 2022Article
- Article
- Clinical Evidence for Variegated Silencing in Patients With Friedreich Ataxia.Neurology. Genetics · 2022Article
- Mitochondrial and metabolic dysfunction in Friedreich ataxia: update on pathophysiological relevance and clinical interventions.Neuronal signaling · 2021Review
- Mitochondrial damage and senescence phenotype of cells derived from a novel frataxin G127V point mutation mouse model of Friedreich's ataxia.Disease models & mechanisms · 2020Article
- Antioxidant Therapies and Oxidative Stress in Friedreich´s Ataxia: The Right Path or Just a Diversion?Antioxidants (Basel, Switzerland) · 2020Review
- Molecular Defects in Friedreich's Ataxia: Convergence of Oxidative Stress and Cytoskeletal Abnormalities.Frontiers in molecular biosciences · 2020Review
- Role of frataxin protein deficiency and metabolic dysfunction in Friedreich ataxia, an autosomal recessive mitochondrial disease.Neuronal signaling · 2018Review
- Impact ofInternational journal of molecular sciences · 2018Review
- Liquid Chromatography-High Resolution Mass Spectrometry Analysis of Platelet Frataxin as a Protein Biomarker for the Rare Disease Friedreich's Ataxia.Analytical chemistry · 2018Article
- Review
- Metabolic tracing analysis reveals substrate-specific metabolic deficits in platelet storage lesion.Transfusion · 2017Article
- Company profile: BluePen Biomarkers LLC – integrated biomarker solutions.Future science OA · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundFriedreich's ataxia (FRDA) is an autosomal recessive disease with metabolic abnormalities that have been proposed to play an important role in the resulting neurodegeneration and cardiomyopathy. The inability to access the highly affected neuronal and cardiac tissues has hampered metabolic evaluation and biomarker development.
methodsEmployment of a LC-MS-based method to determine whether platelets isolated from patients with FRDA exhibit differentiable metabolism compared with healthy controls.
resultsIsotopologue analysis showed a marked decrease in glucose incorporation with a concomitant increase in palmitate-derived acyl-CoA thioesters in FRDA platelets compared with controls.
conclusionOur findings demonstrate that platelets can be used as a surrogate tissue for in vivo biomarker studies to monitor new therapeutic approaches for the treatment of FRDA.
Indexed as
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.