ReviewBrain pathology (Zurich, Switzerland)2016
Old versus New Mechanisms in the Pathogenesis of ALS.
Review in Brain pathology (Zurich, Switzerland), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- The level of homocysteine in amyotrophic lateral sclerosis: a systematic review and meta-analysis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2023Pooled it
- CHMP2B promotes CHMP7 mediated nuclear pore complex injury in sporadic ALS.Acta neuropathologica communications · 2024Article
- Nuclear and degradative functions of the ESCRT-III pathway: implications for neurodegenerative disease.Nucleus (Austin, Tex.) · 2024Review
- An Effective DNA Methylation Biomarker Screening Mechanism for Amyotrophic Lateral Sclerosis (ALS) Based on Comorbidities and Gene Function Analysis.Bioengineering (Basel, Switzerland) · 2024Article
- Review
- Human iPSC co-culture model to investigate the interaction between microglia and motor neurons.Scientific reports · 2022Article
- Nerve Growth Factor is a Potential Treated Target in Tg(SOD1*G93A)1Gur Mice.Cellular and molecular neurobiology · 2022Article
- The Involvement of RAGE and Its Ligands during Progression of ALS in SOD1 G93A Transgenic Mice.International journal of molecular sciences · 2022Article
- Combined Treatment with Herbal Medicine and Drug Ameliorates Inflammation and Metabolic Abnormalities in the Liver of an Amyotrophic Lateral Sclerosis Mouse Model.Antioxidants (Basel, Switzerland) · 2022Article
- Treatment with Herbal Formula Extract in the hSOD1Mediators of inflammation · 2022Article
- Review
- Expression of p16 and p21 in the frontal association cortex of ALS/MND brains suggests neuronal cell cycle dysregulation and astrocyte senescence in early stages of the disease.Neuropathology and applied neurobiology · 2020Article
- The Role of Glia in Canine Degenerative Myelopathy: Relevance to Human Amyotrophic Lateral Sclerosis.Molecular neurobiology · 2019Article
- Mitochondrial transport serves as a mitochondrial quality control strategy in axons: Implications for central nervous system disorders.CNS neuroscience & therapeutics · 2019Review
- Retrotransposons in the development and progression of amyotrophic lateral sclerosis.Journal of neurology, neurosurgery, and psychiatry · 2019Review
- FETR-ALS Study Protocol: A Randomized Clinical Trial of Fecal Microbiota Transplantation in Amyotrophic Lateral Sclerosis.Frontiers in neurology · 2019Article
- Safety and efficacy of human embryonic stem cell-derived astrocytes following intrathecal transplantation in SOD1Stem cell research & therapy · 2018Article
- Temporospatial Analysis and New Players in the Immunology of Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2018Review
- Profile of Arachidonic Acid-Derived Inflammatory Markers and Its Modulation by Nitro-Oleic Acid in an Inherited Model of Amyotrophic Lateral Sclerosis.Frontiers in molecular neuroscience · 2018Article
- The Emerging Role of the Major Histocompatibility Complex Class I in Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amyotrophic Lateral Sclerosis (ALS) is recognized as a very complex disease. As we have learned in the past 20 years from studies in patients and in models based on the expression of mutant SOD1, ALS is not a purely motor neuron disease as previously thought. While undoubtedly motor neurons are lost in patients, a number of alterations in those cell-types that interact functionally with motor neurons (astrocytes, microglia, muscle fibers, oligodendrocytes) take place even long before onset of symptoms. At the same time, disturbance of several, only partly inter-related physiological functions play some role in the onset and progression of the disease. Traditionally, mitochondrial damage and oxidative stress, excitotoxicity, neuroinflammation, altered axonal transport, ER stress, protein aggregation and defective removal of toxic proteins have been considered as key factors in the pathogenesis of ALS, with the relatively recent addition of disturbances in RNA metabolism. This complexity makes the search for an effective treatment extremely difficult and prompts further studies to reveal other possible, previously unappreciated aspects of the pathogenesis of ALS. In this review, we focus on previous knowledge on ALS mechanisms as well as new facets emerging from studies on genetic ALS patients and models that may both provide precious information for a novel therapeutic approach.
Indexed as
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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.