ArticleJournal of molecular neuroscience : MN2015
The axon-protective WLD(S) protein partially rescues mitochondrial respiration and glycolysis after axonal injury.
Article in Journal of molecular neuroscience : MN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- Preventing neuropathy and improving anticancer chemotherapy with a carbazole-based compound.Science advances · 2025Article
- Role of NADCellular and molecular neurobiology · 2023Review
- Programming axonal mitochondrial maintenance and bioenergetics in neurodegeneration and regeneration.Neuron · 2022Review
- Of axons that struggle to make ends meet: Linking axonal bioenergetic failure to programmed axon degeneration.Biochimica et biophysica acta. Bioenergetics · 2022Review
- Article
- Mitochondrial Reactive Oxygen Species Mediate Activation of TRPV1 and Calcium Entry Following Peripheral Sensory Axotomy.Frontiers in molecular neuroscience · 2022Article
- Macrophage monocarboxylate transporter 1 promotes peripheral nerve regeneration after injury in mice.The Journal of clinical investigation · 2021Article
- The Axonal Glycolytic Pathway Contributes to Sensory Axon Extension and Growth Cone Dynamics.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Sarm1-mediated neurodegeneration within the enteric nervous system protects against local inflammation of the colon.Protein & cell · 2021Article
- DLK Activation Synergizes with Mitochondrial Dysfunction to Downregulate Axon Survival Factors and Promote SARM1-Dependent Axon Degeneration.Molecular neurobiology · 2020Article
- Altered mitochondrial bioenergetics are responsible for the delay in Wallerian degeneration observed in neonatal mice.Neurobiology of disease · 2019Article
- Mechanisms for the maintenance and regulation of axonal energy supply.Journal of neuroscience research · 2019Review
- Metabolic Vulnerability in the Neurodegenerative Disease Glaucoma.Frontiers in neuroscience · 2017Review
- Traumatic Axonal Injury: Mechanisms and Translational Opportunities.Trends in neurosciences · 2016Review
- Attenuated traumatic axonal injury and improved functional outcome after traumatic brain injury in mice lacking Sarm1.Brain : a journal of neurology · 2016Article
- Decreased Energy Capacity and Increased Autophagic Activity in Optic Nerve Axons With Defective Anterograde Transport.Investigative ophthalmology & visual science · 2015Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The axon-protective Wallerian degeneration slow (WLD(S)) protein can ameliorate the decline in axonal ATP levels after neurite transection. Here, we tested the hypothesis that this effect is associated with maintenance of mitochondrial respiration and/or glycolysis. We used isolated neurites of superior cervical ganglion (SCG) cultures in the Seahorse XF-24 Metabolic Flux Analyser to determine mitochondrial respiration and glycolysis under different conditions. We observed that both mitochondrial respiration and glycolysis declined significantly during the latent phase of Wallerian degeneration. WLD(S) partially reduced the decline both in glycolysis and in mitochondrial respiration. In addition, we found that depleting NAD levels in uncut cultures led to changes in mitochondrial respiration and glycolysis similar to those rescued by WLD(S) after cut, suggesting that the maintenance of NAD levels in Wld(S) neurites after axonal injury at least partially underlies the maintenance of ATP levels. However, by using another axon-protective mutation (Sarm1(-/-)), we could demonstrate that rescue of basal ECAR (and hence probably glycolysis) rather than basal OCR (mitochondrial respiration) may be part of the protective phenotype to delay Wallerian degeneration. These findings open new routes to study glycolysis and the connection between NAD and ATP levels in axon degeneration, which may help to eventually develop therapeutic strategies to treat neurodegenerative diseases.
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