ReviewFrontiers in neuroscience2016
Metabolic Dysfunctions in Amyotrophic Lateral Sclerosis Pathogenesis and Potential Metabolic Treatments.
Review in Frontiers in neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 2 of them syntheses that pooled it.
What it found
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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
68 citing papers in PubMed, 2 syntheses or guidelines pooled it, 98 citations in OpenAlex.
- Exploring dysregulated miRNAs in ALS: implications for disease pathogenesis and early diagnosis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Pooled it
- Diabetes Mellitus and Amyotrophic Lateral Sclerosis: A Systematic Review.Biomolecules · 2021Pooled it
- Review
- Neurotropic alphavirus infection induces PARP-1 hyperactivation-mediated energy collapse in motor neurons.Journal of virology · 2026Article
- Integrated multi-omics analysis reveals gut dysbiosis and altered energy metabolism in Chinese ALS patients.Microbiology spectrum · 2026Article
- Dysregulated lactate metabolism synergizes with ALS genetic risk factors to accelerate motor decline.PloS one · 2026Article
- TDP-43 proteinopathies and neurodegeneration: insights from Caenorhabditis elegans models.The FEBS journal · 2026Review
- Dysregulated lactate metabolism synergizes with ALS genetic risk factors to accelerate motor decline.bioRxiv : the preprint server for biology · 2025Article
- Network spreading and local biological vulnerability in amyotrophic lateral sclerosis.Communications biology · 2025Article
- Neural Metabolic Networks: Key Elements of Healthy Brain Function.Journal of neurochemistry · 2025Review
- Fueling neurodegeneration: metabolic insights into microglia functions.Journal of neuroinflammation · 2024Review
- Hypercapnia is not excluded by normoxia in neuromuscular disease patients: implications for oximetry.ERJ open research · 2024Article
- Modulation of Gut Microbiota Through Dietary Intervention in Neuroinflammation and Alzheimer's and Parkinson's Diseases.Current nutrition reports · 2024Review
- Exploring the Role of Metabolic Hormones in Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2024Article
- Glycogen accumulation modulates life span in a mouse model of amyotrophic lateral sclerosis.Journal of neurochemistry · 2024Article
- The AMPK-related kinase NUAK1 controls cortical axons branching by locally modulating mitochondrial metabolic functions.Nature communications · 2024Article
- Mitochondria: A Promising Convergent Target for the Treatment of Amyotrophic Lateral Sclerosis.Cells · 2024Review
- TDP-43 impairs sleep inScience advances · 2024Article
- NOX-induced oxidative stress is a primary trigger of major neurodegenerative disorders.Progress in neurobiology · 2023Review
- Impact of the metabolic syndrome on prevalence and survival in motor neuron disease: a retrospective case series.Metabolic brain disease · 2023Article
8 more citing papers are in PubMed but not listed here.
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 fatal neurodegenerative disease primarily characterized by loss of motor neurons in brain and spinal cord. The death of motor neurons leads to denervation of muscle which in turn causes muscle weakness and paralysis, decreased respiratory function and eventually death. Growing evidence indicates disturbances in energy metabolism in patients with ALS and animal models of ALS, which are likely to contribute to disease progression. Particularly, defects in glucose metabolism and mitochondrial dysfunction limit the availability of ATP to CNS tissues and muscle. Several metabolic approaches improving mitochondrial function have been investigated
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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.