ReviewBrain pathology (Zurich, Switzerland)2013
Spinal muscular atrophy: new findings for an old pathology.
Review in Brain pathology (Zurich, Switzerland), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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
20 citing papers in PubMed, 24 citations in OpenAlex.
- Therapeutic strategies for spinal muscular atrophy: the history and future perspective.Frontiers in human neuroscience · 2026Review
- The Integrated Approach in Patients with Spinal Muscular Atrophy in the Era of Early Diagnosis, Etiopathogenic Therapies and Multidisciplinary Standards of Care and Rehabilitation Interventions Leads to New Phenotypes.Life (Basel, Switzerland) · 2025Article
- Review
- Biomarkers in spinal muscular atrophy.Frontiers in neurology · 2025Review
- Thrombospondin-4 as potential cerebrospinal fluid biomarker for therapy response in pediatric spinal muscular atrophy.Journal of neurology · 2024Article
- Clinical and Genetic Profiles of 5q- and Non-5q-Spinal Muscular Atrophy Diseases in Pediatric Patients.Genes · 2024Review
- Physiological Features of the Neural Stem Cells Obtained from an Animal Model of Spinal Muscular Atrophy and Their Response to Antioxidant Curcumin.International journal of molecular sciences · 2024Article
- Fatigue in Spinal Muscular Atrophy: a fundamental open issue.Acta myologica : myopathies and cardiomyopathies : official journal of the Mediterranean Society of Myology · 2024Review
- Spinal Muscular Atrophy: The Past, Present, and Future of Diagnosis and Treatment.International journal of molecular sciences · 2023Review
- Agonist of growth hormone-releasing hormone improves the disease features of spinal muscular atrophy mice.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- NSC Physiological Features in Spinal Muscular Atrophy: SMN Deficiency Effects on Neurogenesis.International journal of molecular sciences · 2022Review
- Ultrastructural characterization of peripheral denervation in a mouse model of Type III spinal muscular atrophy.Journal of neural transmission (Vienna, Austria : 1996) · 2021Article
- Drug Screening and Drug Repositioning as Promising Therapeutic Approaches for Spinal Muscular Atrophy Treatment.Frontiers in pharmacology · 2020Review
- S-adenosylmethionine tRNA modification: unexpected/unsuspected implications of former/new players.International journal of biological sciences · 2020Review
- Spinal Muscular Atrophy Modeling and Treatment Advances by Induced Pluripotent Stem Cells Studies.Stem cell reviews and reports · 2019Review
- Reduction of Movement in Neurological Diseases: Effects on Neural Stem Cells Characteristics.Frontiers in neuroscience · 2018Article
- Hyperleptinemia in children with autosomal recessive spinal muscular atrophy type I-III.PloS one · 2017Article
- Neuromuscular Junctions as Key Contributors and Therapeutic Targets in Spinal Muscular Atrophy.Frontiers in neuroanatomy · 2016Review
- Stem cell transplantation in neurological diseases: improving effectiveness in animal models.Frontiers in cell and developmental biology · 2014Review
- Spinal muscular atrophy: a motor neuron disorder or a multi-organ disease?Journal of anatomy · 2014Review
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
No grant is acknowledged in the PubMed record.
Abstract
Understanding the events that are responsible for a disease is mandatory for setting up a therapeutic strategy. Although spinal muscular atrophy (SMA) is considered a rare neurodegenerative pathology, its impact in our society is really devastating as it strikes young people from birth onward, and it affects their families either emotionally or financially. Moreover, it requires intensive care for the children, and this diverts both parents and relatives from their occupations. Each neuron is very different from one another; therefore, in a neurodegenerative disease, the population of axons, synapses and cell bodies degenerate asynchronously, and subpopulations of neurons have different vulnerabilities. The knowledge of the sequence of events along the lengths of individual neurons is crucial to understand if each synapse degenerates before the corresponding axon, or if each axon degenerates before the corresponding cell body. Early degeneration of one neuronal compartment in disease often reflects molecular defects somewhere else. Up until now, SMA is considered mostly a lower motor neuron disease caused by the loss-of-function mutations in the SMN1 gene; here, we inspect other features that can be altered by this defect, such as the cross talk between muscle and motor neuron and the role of physical inactivity.
Indexed as
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.