ReviewCold Spring Harbor perspectives in biology2017
Prion Properties of SOD1 in Amyotrophic Lateral Sclerosis and Potential Therapy.
Review in Cold Spring Harbor perspectives in biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Cerebrospinal fluid and blood exosomes as biomarkers for amyotrophic lateral sclerosis; a systematic review.Diagnostic pathology · 2024Pooled it
- Pathology of general proprioception in a canine disease model of amyotrophic lateral sclerosis.Journal of the neurological sciences · 2026Article
- Tibialis Cranialis Extrafusal and Intrafusal Myofibers and Muscle Spindle Pathology in Canine Degenerative Myelopathy.Animals : an open access journal from MDPI · 2026Article
- Crossing Barriers: Advancements in Macromolecular Therapeutics for Neurodegenerative Diseases and Strategies to Overcome the Blood-Brain Barrier.ACS pharmacology & translational science · 2025Review
- The prion-like effect and prion-like protein targeting strategy in amyotrophic lateral sclerosis.Heliyon · 2024Review
- Role of NLRP3 inflammasome in central nervous system diseases.Cell & bioscience · 2024Review
- Decoding the Cellular Trafficking of Prion-like Proteins in Neurodegenerative Diseases.Neuroscience bulletin · 2024Review
- A novel antibody to treat SOD1-related amyotrophic lateral sclerosis.Molecular therapy. Methods & clinical development · 2023Article
- BMP/TGF-β signaling as a modulator of neurodegeneration in ALS.Developmental dynamics : an official publication of the American Association of Anatomists · 2022Article
- Immunomodulation induced by central nervous system-related peptides as a therapeutic strategy for neurodegenerative disorders.Pharmacology research & perspectives · 2021Review
- The extracellular chaperone Clusterin enhances Tau aggregate seeding in a cellular model.Nature communications · 2021Article
- Extracellular Vesicles as Innovative Tool for Diagnosis, Regeneration and Protection against Neurological Damage.International journal of molecular sciences · 2020Review
- Satellite Glial Cells of the Dorsal Root Ganglion: A New "Guest/Physiopathological Target" in ALS.Frontiers in aging neuroscience · 2020Article
- Therapeutic Approaches Targeting Protein Aggregation in Amyotrophic Lateral Sclerosis.Frontiers in molecular neuroscience · 2020Review
- Molecular Chaperones: A Double-Edged Sword in Neurodegenerative Diseases.Frontiers in aging neuroscience · 2020Review
- Cytoplasmic Restriction of Mutated SOD1 Impairs the DNA Repair Process in Spinal Cord Neurons.Cells · 2019Article
- Orchestrating stem cell fate: Novel tools for regenerative medicine.World journal of stem cells · 2019Review
- Phosphorylated and aggregated TDP-43 with seeding properties are induced upon mutant Huntingtin (mHtt) polyglutamine expression in human cellular models.Cellular and molecular life sciences : CMLS · 2019Article
- The proteostasis network and its decline in ageing.Nature reviews. Molecular cell biology · 2019Review
- Prion-like protein aggregates exploit the RHO GTPase to cofilin-1 signaling pathway to enter cells.The EMBO journal · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Amyotrophic lateral sclerosis (ALS) is a devastating and rapidly progressive neurodegenerative disease caused by the deterioration of motor neurons. The first symptoms of ALS always begin at a focal but variable site and consistently spread to neighboring regions, suggesting that neurodegeneration in ALS is an orderly and propagating process. Like other neurodegenerative diseases, misfolding of a specific protein is central to ALS. SOD1, the major constituent of the protein deposits in some familial and sporadic forms of ALS, propagates its misfolded conformation like prions, providing a plausible molecular basis for the focality and spreading of muscle weakness in ALS. Because protein misfolding is a common cause of diverse neurodegenerative diseases, strategies aimed at boosting a cell's ability to cope with misfolded proteins could lead to therapeutics to combat these devastating age-related proteinopathies.
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Identifiers
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.