ReviewJournal of neurology2013
Amyotrophic lateral sclerosis: an update on recent genetic insights.
Review in Journal of neurology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 54 citations in OpenAlex.
- An Effective DNA Methylation Biomarker Screening Mechanism for Amyotrophic Lateral Sclerosis (ALS) Based on Comorbidities and Gene Function Analysis.Bioengineering (Basel, Switzerland) · 2024Article
- Potential therapeutic effect of olfactory ensheathing cells in neurological diseases: neurodegenerative diseases and peripheral nerve injuries.Frontiers in immunology · 2023Review
- Effects of ALS-associated TANK binding kinase 1 mutations on protein-protein interactions and kinase activity.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Monozygotic twins and triplets discordant for amyotrophic lateral sclerosis display differential methylation and gene expression.Scientific reports · 2019Article
- Searching for Bacteria in Neural Tissue From Amyotrophic Lateral Sclerosis.Frontiers in neuroscience · 2019Article
- Preclinical progression of neurodegenerative diseases.Nagoya journal of medical science · 2018Review
- Copy Number Variations in Amyotrophic Lateral Sclerosis: Piecing the Mosaic Tiles Together through a Systems Biology Approach.Molecular neurobiology · 2018Review
- Could Sirtuin Activities Modify ALS Onset and Progression?Cellular and molecular neurobiology · 2017Review
- The heat shock response in neurons and astroglia and its role in neurodegenerative diseases.Molecular neurodegeneration · 2017Review
- Recent advances in amyotrophic lateral sclerosis.Journal of neurology · 2016Review
- Regenerative cellular therapies for neurologic diseases.Brain research · 2016Review
- The Sigma-1 Receptor as a Pluripotent Modulator in Living Systems.Trends in pharmacological sciences · 2016Review
- Structural analysis of disease-related TDP-43 D169G mutation: linking enhanced stability and caspase cleavage efficiency to protein accumulation.Scientific reports · 2016Article
- C9orf72's Interaction with Rab GTPases-Modulation of Membrane Traffic and Autophagy.Frontiers in cellular neuroscience · 2016Review
- The Association between C9orf72 Repeats and Risk of Alzheimer's Disease and Amyotrophic Lateral Sclerosis: A Meta-Analysis.Parkinson's disease · 2016Article
- Genotype-phenotype correlations of amyotrophic lateral sclerosis.Translational neurodegeneration · 2016Review
- The Function of Autophagy in Neurodegenerative Diseases.International journal of molecular sciences · 2015Review
- Label-Free LC-MS/MS Proteomic Analysis of Cerebrospinal Fluid Identifies Protein/Pathway Alterations and Candidate Biomarkers for Amyotrophic Lateral Sclerosis.Journal of proteome research · 2015Article
- Rare variants at 16p11.2 are associated with common variable immunodeficiency.The Journal of allergy and clinical immunology · 2015Article
- Exome sequencing uncovers hidden pathways in familial and sporadic ALS.Nature neuroscience · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease affecting both upper and lower motor neurons. The prognosis for ALS is extremely poor, but there is a limited course of treatment with only one approved medication. A most striking recent discovery is that TDP-43 is identified as a key molecule that is associated with both sporadic and familial forms of ALS. TDP-43 is not only a pathological hallmark, but also a genetic cause for ALS. Subsequently, a number of ALS-causative genes have been found. Above all, the RNA-binding protein, such as FUS, TAF15, EWSR1 and hnRNPA1, have structural and functional similarities to TDP-43, and physiological functions of some molecules, including VCP, UBQLN2, OPTN, FIG4 and SQSTM1, are involved in a protein degradation system. These discoveries provide valuable insight into the pathogenesis of ALS, and open doors for developing an effective disease-modifying therapy.
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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.