ArticleThe Journal of clinical investigation2015
In vivo kinetic approach reveals slow SOD1 turnover in the CNS.
Article in The Journal of clinical investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 62 citations in OpenAlex.
- PrP turnover in vivo and the time to effect of prion disease therapeutics.PLoS pathogens · 2026Article
- Absence of Neuromuscular Dysfunction in Mice with Gut Epithelium-Restricted Expression of ALS Mutation hSOD1Biomolecules · 2026Article
- Article
- The expanding application of antisense oligonucleotides to neurodegenerative diseases.The Journal of clinical investigation · 2024Article
- Amyloidogenic regions in beta-strands II and III modulate the aggregation and toxicity of SOD1 in living cells.Open biology · 2024Article
- Variability in SOD1-associated amyotrophic lateral sclerosis: geographic patterns, clinical heterogeneity, molecular alterations, and therapeutic implications.Translational neurodegeneration · 2024Review
- Tofersen for SOD1 ALS.Neurodegenerative disease management · 2024Review
- Therapeutic targeting of ALS pathways: Refocusing an incomplete picture.Annals of clinical and translational neurology · 2023Review
- Protein kinetics of superoxide dismutase-1 in familial and sporadic amyotrophic lateral sclerosis.Annals of clinical and translational neurology · 2023Article
- P2X7 receptor activation mediates superoxide dismutase 1 (SOD1) release from murine NSC-34 motor neurons.Purinergic signalling · 2022Article
- Antisense Oligonucleotides for the Study and Treatment of ALS.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Review
- Multisystem Proteinopathy Due toGenes · 2022Review
- Is liquid biopsy mature enough for the diagnosis of Alzheimer's disease?Frontiers in aging neuroscience · 2022Review
- Modeling the Degradation Effects of Autophagosome Tethering Compounds.Neuroscience bulletin · 2021Article
- It's complicated: The relationship between sleep and Alzheimer's disease in humans.Neurobiology of disease · 2020Review
- Does wild-type Cu/Zn-superoxide dismutase have pathogenic roles in amyotrophic lateral sclerosis?Translational neurodegeneration · 2020Review
- Article
- Neurofilaments: neurobiological foundations for biomarker applications.Brain : a journal of neurology · 2020Review
- SILK studies - capturing the turnover of proteins linked to neurodegenerative diseases.Nature reviews. Neurology · 2019Review
- An endogenous peptide marker differentiates SOD1 stability and facilitates pharmacodynamic monitoring in SOD1 amyotrophic lateral sclerosis.JCI insight · 2019Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Therapeutic strategies that target disease-associated transcripts are being developed for a variety of neurodegenerative syndromes. Protein levels change as a function of their half-life, a property that critically influences the timing and application of therapeutics. In addition, both protein kinetics and concentration may play important roles in neurodegeneration; therefore, it is essential to understand in vivo protein kinetics, including half-life. Here, we applied a stable isotope-labeling technique in combination with mass spectrometric detection and determined the in vivo kinetics of superoxide dismutase 1 (SOD1), mutation of which causes amyotrophic lateral sclerosis. Application of this method to human SOD1-expressing rats demonstrated that SOD1 is a long-lived protein, with a similar half-life in both the cerebral spinal fluid (CSF) and the CNS. Additionally, in these animals, the half-life of SOD1 was longest in the CNS when compared with other tissues. Evaluation of this method in human subjects demonstrated successful incorporation of the isotope label in the CSF and confirmed that SOD1 is a long-lived protein in the CSF of healthy individuals. Together, the results of this study provide important insight into SOD1 kinetics and support application of this technique to the design and implementation of clinical trials that target long-lived CNS proteins.
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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.