ReviewTranslational neurodegeneration2016
Genotype-phenotype correlations of amyotrophic lateral sclerosis.
Review in Translational neurodegeneration, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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
53 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.
- Unveiling the SOD1-mediated ALS phenotype: insights from a comprehensive meta-analysis.Journal of neurology · 2024Pooled it
- Drosophila: An Emerging New Approach Method (NAM) for Studying Amyotrophic Lateral Sclerosis (ALS).Cells · 2026Review
- High Prevalence of SOD1 Pathogenic Variants in the UK Biobank: Implications for Early Intervention in Amyotrophic Lateral Sclerosis.Annals of neurology · 2026Article
- Decomposing heterogeneity in disease progression speeds and pathways.NPJ digital medicine · 2026Article
- Introduction to the Supplement.Muscle & nerve · 2026Article
- Review
- Structural mechanisms and insights on multiple nanobodies binding diverse SOD1 epitopes.Communications biology · 2025Article
- Critical analysis of translational potential of rodent models of white matter pathology across a wide spectrum of human diseases.Cell death & disease · 2025Review
- Clinical characterization and founder effect analysis in Chinese amyotrophic lateral sclerosis patients withAnnals of medicine · 2024Article
- Review
- Plekhg5 controls the unconventional secretion of Sod1 by presynaptic secretory autophagy.Nature communications · 2024Article
- Antisense Oligonucleotides (ASOs) in Motor Neuron Diseases: A Road to Cure in Light and Shade.International journal of molecular sciences · 2024Review
- Predictors for progression in amyotrophic lateral sclerosis associated to SOD1 mutation: insight from two population-based registries.Journal of neurology · 2023Observational
- Article
- Pathological insights from amyotrophic lateral sclerosis animal models: comparisons, limitations, and challenges.Translational neurodegeneration · 2023Review
- Brain metabolic signatures in patients with genetic and nongenetic amyotrophic lateral sclerosis.CNS neuroscience & therapeutics · 2023Article
- The landscape of cognitive impairment in superoxide dismutase 1-amyotrophic lateral sclerosis.Neural regeneration research · 2023Review
- Article
- Clinical and molecular features of patients with amyotrophic lateral sclerosis andFrontiers in neurology · 2023Article
- The impact of upper motor neuron involvement on clinical features, disease progression and prognosis in amyotrophic lateral sclerosis.Frontiers in neurology · 2023Article
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
Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease characterized by progressive neuronal loss and degeneration of upper motor neuron (UMN) and lower motor neuron (LMN). The clinical presentations of ALS are heterogeneous and there is no single test or procedure to establish the diagnosis of ALS. Most cases are diagnosed based on symptoms, physical signs, progression, EMG, and tests to exclude the overlapping conditions. Familial ALS represents about 5 ~ 10 % of ALS cases, whereas the vast majority of patients are sporadic. To date, more than 20 causative genes have been identified in hereditary ALS. Detecting the pathogenic mutations or risk variants for each ALS individual is challenging. However, ALS patients carrying some specific mutations or variant may exhibit subtly distinct clinical features. Unraveling the respective genotype-phenotype correlation has important implications for the genetic explanations. In this review, we will delineate the clinical features of ALS, outline the major ALS-related genes, and summarize the possible genotype-phenotype correlations of ALS.
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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.