ArticleCurrent genetic medicine reports2017
Metabolic Dysregulation in Amyotrophic Lateral Sclerosis: Challenges and Opportunities.
Article in Current genetic medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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
28 citing papers in PubMed.
- Review
- Genome-Wide Characterization of thePlants (Basel, Switzerland) · 2026Article
- Peripheral metabolic dysfunction drives sleep disruption in TDP-43 proteinopathy.bioRxiv : the preprint server for biology · 2026Article
- Spatiotemporal Dynamics and Cellular States of Neuroinflammation in Amyotrophic Lateral Sclerosis: Implications for Stage‑Specific Therapeutics.ASN neuro · 2026Review
- The metabolic intersection between immunosenescence and neuroinflammation in amyotrophic lateral sclerosis.Journal of inflammation (London, England) · 2025Review
- Apolipoprotein A1 reduces blood-spinal cord barrier leakage, improves astrocytic coverage, and enhances motor neuron survival to restore the neurovascular unit in ALS mice.Frontiers in aging neuroscience · 2025Article
- Mitochondrial dysfunction: mechanisms and advances in therapy.Signal transduction and targeted therapy · 2024Review
- Integrating Transcriptomic and Structural Insights: Revealing Drug Repurposing Opportunities for Sporadic ALS.ACS omega · 2024Article
- TDP-43 impairs sleep inScience advances · 2024Article
- From Recognition to Remedy: The Significance of Biomarkers in Neurodegenerative Disease Pathology.International journal of molecular sciences · 2023Review
- Proteomics and mathematical modeling of longitudinal CSF differentiates fast versus slow ALS progression.Annals of clinical and translational neurology · 2023Article
- Article
- Metabolic Profile and Pathological Alterations in the Muscle of Patients with Early-Stage Amyotrophic Lateral Sclerosis.Biomedicines · 2022Article
- Fly for ALS: Drosophila modeling on the route to amyotrophic lateral sclerosis modifiers.Cellular and molecular life sciences : CMLS · 2021Review
- Metabolic Remodeling in Skeletal Muscle Atrophy as a Therapeutic Target.Metabolites · 2021Review
- Metabolic Abnormalities, Dietary Risk Factors and Nutritional Management in Amyotrophic Lateral Sclerosis.Nutrients · 2021Review
- Skeletal Muscle Metabolism: Origin or Prognostic Factor for Amyotrophic Lateral Sclerosis (ALS) Development?Cells · 2021Review
- Where and Why Modeling Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2021Review
- The links between diabetes mellitus and amyotrophic lateral sclerosis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021Review
- Overlapping Genetic Architecture Between Schizophrenia and Neurodegenerative Disorders.Frontiers in cell and developmental biology · 2021Article
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.
Funding
Abstract
purpose of reviewAmyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease for which there is no cure and treatments are at best palliative. Several genes have been linked to ALS, which highlight defects in multiple cellular processes including RNA processing, proteostasis and metabolism. Clinical observations have identified glucose intolerance and dyslipidemia as key features of ALS however the causes of these metabolic alterations remain elusive. RECENT
findingsRecent studies reveal that motor neurons and muscle cells may undergo cell type specific metabolic changes that lead to utilization of alternate fuels. For example, ALS patients' muscles exhibit reduced glycolysis and increased reliance on fatty acids. In contrast, ALS motor neurons contain damaged mitochondria and exhibit impaired lipid beta oxidation, potentially leading to increased glycolysis as a compensatory mechanism. SUMMARY: These findings highlight the complexities of metabolic alterations in ALS and provide new opportunities for designing therapeutic strategies based on restoring cellular energetics.
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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.