ArticleNeuroscience2016
Length-dependent axo-terminal degeneration at the neuromuscular synapses of type II muscle in SOD1 mice.
Article in Neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 49 citations in OpenAlex.
- Inhibition of Glutamate Decarboxylase in the Spinal Cord Induces Motor Deficits and Motor Neuron Degeneration.Neurotoxicity research · 2026Article
- Early and Divergent Lipid Mediator Remodelling in Fast Versus Slow Skeletal Muscles of Female hSOD1Journal of cachexia, sarcopenia and muscle · 2026Article
- Intrathecal (GActa neuropathologica communications · 2026Article
- Neuromuscular junction innervation and motor function are preserved by restoring muscarinic signaling in perisynaptic glia in ALS.iScience · 2026Article
- Intrathecal (GbioRxiv : the preprint server for biology · 2026Article
- The Neuromuscular Junction: A Shared Vulnerability in Aging and Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Review
- Review
- The Neuromuscular Disorder Mediated by Extracellular Vesicles in Amyotrophic Lateral Sclerosis.Current issues in molecular biology · 2024Review
- Live Imaging Analysis of Axonal Regeneration in Human iPSC-Derived Motor Neurons Using a Microfluidic System.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Enhanced axonal regeneration of ALS patient iPSC-derived motor neurons harboring SOD1Scientific reports · 2023Article
- Why should we care about astrocytes in a motor neuron disease?Frontiers in molecular medicine · 2023Review
- Small junction, big problems: Neuromuscular junction pathology in mouse models of amyotrophic lateral sclerosis (ALS).Journal of anatomy · 2022Review
- The Cell Autonomous and Non-Cell Autonomous Aspects of Neuronal Vulnerability and Resilience in Amyotrophic Lateral Sclerosis.Biology · 2022Review
- Motoneuron Diseases.Advances in neurobiology · 2022Article
- Dendrimer-2PMPA Delays Muscle Function Loss and Denervation in a Murine Model of Amyotrophic Lateral Sclerosis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Article
- Axonal regeneration and sprouting as a potential therapeutic target for nervous system disorders.Neural regeneration research · 2021Review
- Human motor units in microfluidic devices are impaired by FUS mutations and improved by HDAC6 inhibition.Stem cell reports · 2021Article
- The Skeletal Muscle Emerges as a New Disease Target in Amyotrophic Lateral Sclerosis.Journal of personalized medicine · 2021Review
- Motor function recovery: deciphering a regenerative niche at the neuromuscular synapse.Biological reviews of the Cambridge Philosophical Society · 2021Review
- Mitochondrial Behavior in Axon Degeneration and Regeneration.Frontiers in aging neuroscience · 2021Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
In motor neuron diseases, there is a prolonged period of time before any clinical symptoms begin to appear. During this time, distal axonal degeneration, or "dying back" axonopathy, begins to occur before the onset of clinical symptoms and motor neuron death. This preclinical degeneration is a hallmark of motor neuron diseases in both animal models and human patients. Generally, in muscles with mixed fiber types, distal degeneration occurs in fast-fatigable α-motor axons innervating type IIb muscle fibers before axons innervating slow, type I muscle fibers. We investigated whether the "dying back" axonopathy in a pure fast-fatigable α-motor axon nerve is a length-dependent process. The lateral thoracic nerve (LTN) exclusively consists of motor nerves that innervate the very thin cutaneous maximus muscle (CMM) that solely contains type II neuromuscular synapses. We characterized the LTN and CMM synapses both morphologically and physiologically in the superoxide dismutase 1 (SOD1) mutant mouse model of amyotrophic lateral sclerosis (ALS). By 60days of age, there was a significant "dying back" phenomenon at the caudal region while the rostral region remained intact. The longer axons innervating the caudal region appear to be more susceptible to degeneration in the SOD1 mouse indicating that the axonal degeneration of motor neurons innervating type II fibers is a length-dependent process. Additionally, we identified how the simplicity of the LTN-CMM system offers a better method to investigate axon degeneration in an ALS mouse model and may be used to investigate possible therapeutic compounds for axon protection and regeneration.
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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.