ArticleNeuron2014
A computational model of motor neuron degeneration.
Article in Neuron, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 95 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.
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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.
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Who cites it
95 citing papers in PubMed, 161 citations in OpenAlex.
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- Hierarchical Afferent Connectivity Drives Population-Wide Bursting Dynamics in a Computational Model of Human-Derived Excitatory Neuronal Networks.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Structural and mitochondrial dendritic degenerations in old hypoglossal motor neurons.GeroScience · 2026Article
- Splicing the narrative: alternative TARDBP splicing and its relation to neurodegeneration in ALS and FTD.The Journal of clinical investigation · 2026Review
- Role of mitochondria in neuronal function and survival in the enteric and central nervous systems.Cellular and molecular life sciences : CMLS · 2026Review
- Are neurodegenerative diseases late-onset neurodevelopmental disorders? Tracing the developmental origins of neuronal vulnerability.Frontiers in neuroscience · 2026Review
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- Computer models predict differential dendritic vulnerability with ischemia and spreading depression.bioRxiv : the preprint server for biology · 2025Article
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- Presynaptic ATP Decreases During Physiological-Like Activity in Neurons Tuned for High-Frequency Transmission.Journal of neurochemistry · 2025Article
- UBQLN2 in neurodegenerative disease: mechanistic insights and emerging therapeutic potential.Biochemical Society transactions · 2025Review
- Unveiling the role of local metabolic constraints on the structure and activity of spiking neural networks.PLoS computational biology · 2025Article
- How energy determines spatial localisation and copy number of molecules in neurons.Nature communications · 2025Article
- The Neuroprotective Effect of the X Protein of Orthobornavirus Bornaense Type 1 in Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2024Article
- Split-Luciferase Reassembly Assay to Measure Endoplasmic Reticulum-Mitochondria Contacts in Live Cells.Journal of visualized experiments : JoVE · 2024Article
- Challenges and Future Perspectives in Modeling Neurodegenerative Diseases Using Organ-on-a-Chip Technology.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- Molecular and cellular mechanisms of selective vulnerability in neurodegenerative diseases.Nature reviews. Neuroscience · 2024Review
- Trimetazidine Improves Mitochondrial Dysfunction in SOD1International journal of molecular sciences · 2024Article
35 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
To explore the link between bioenergetics and motor neuron degeneration, we used a computational model in which detailed morphology and ion conductance are paired with intracellular ATP production and consumption. We found that reduced ATP availability increases the metabolic cost of a single action potential and disrupts K+/Na+ homeostasis, resulting in a chronic depolarization. The magnitude of the ATP shortage at which this ionic instability occurs depends on the morphology and intrinsic conductance characteristic of the neuron. If ATP shortage is confined to the distal part of the axon, the ensuing local ionic instability eventually spreads to the whole neuron and involves fasciculation-like spiking events. A shortage of ATP also causes a rise in intracellular calcium. Our modeling work supports the notion that mitochondrial dysfunction can account for salient features of the paralytic disorder amyotrophic lateral sclerosis, including motor neuron hyperexcitability, fasciculation, and differential vulnerability of motor neuron subpopulations.
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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.