ArticleExperimental neurology2016
Reducing synuclein accumulation improves neuronal survival after spinal cord injury.
Article in Experimental neurology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 31 citations in OpenAlex.
- Overcoming Barriers to Axonal Regeneration in Spinal Cord Injury: Mechanistic Insights and Therapeutic Frontiers.CNS neuroscience & therapeutics · 2026Review
- Clazosentan Affects Temporal Profile of Endothelin-A Expression in Macro- and Microcirculation after Subarachnoid Hemorrhage.Neurologia medico-chirurgica · 2026Article
- Emergence of the Synucleins.Biology · 2023Article
- Molecular Tweezers: Supramolecular Hosts with Broad-Spectrum Biological Applications.Pharmacological reviews · 2023Review
- Lampreys and spinal cord regeneration: "a very special claim on the interest of zoologists," 1830s-present.Frontiers in cell and developmental biology · 2023Article
- Article
- Morpholino studies shed light on the signaling pathways regulating axon regeneration in lampreys.Neural regeneration research · 2022Article
- Article
- Lysine-selective molecular tweezers are cell penetrant and concentrate in lysosomes.Communications biology · 2021Article
- Alpha-synuclein increases in rodent and human spinal cord injury and promotes inflammation and tissue loss.Scientific reports · 2021Article
- Supramolecular Mechanism of Viral Envelope Disruption by Molecular Tweezers.Journal of the American Chemical Society · 2020Article
- Regulation of BDNF-TrkB Signaling and Potential Therapeutic Strategies for Parkinson's Disease.Journal of clinical medicine · 2020Review
- Lentivirus-mediated downregulation of α-synuclein reduces neuroinflammation and promotes functional recovery in rats with spinal cord injury.Journal of neuroinflammation · 2019Article
- The molecular tweezer CLR01 reduces aggregated, pathologic, and seeding-competent α-synuclein in experimental multiple system atrophy.Biochimica et biophysica acta. Molecular basis of disease · 2019Article
- Melatonin Enhances Autophagy and Reduces Apoptosis to Promote Locomotor Recovery in Spinal Cord Injury via the PI3K/AKT/mTOR Signaling Pathway.Neurochemical research · 2019Article
- Serotonin inhibits axonal regeneration of identifiable descending neurons after a complete spinal cord injury in lampreys.Disease models & mechanisms · 2019Article
- Regenerative capacity in the lamprey spinal cord is not altered after a repeated transection.PloS one · 2019Article
- GABA promotes survival and axonal regeneration in identifiable descending neurons after spinal cord injury in larval lampreys.Cell death & disease · 2018Article
- Highly conserved molecular pathways, including Wnt signaling, promote functional recovery from spinal cord injury in lampreys.Scientific reports · 2018Article
- Role of Caspase-8 and Fas in Cell Death After Spinal Cord Injury.Frontiers in molecular neuroscience · 2018Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Spinal cord injury causes neuronal death, limiting subsequent regeneration and recovery. Thus, there is a need to develop strategies for improving neuronal survival after injury. Relative to our understanding of axon regeneration, comparatively little is known about the mechanisms that promote the survival of damaged neurons. To address this, we took advantage of lamprey giant reticulospinal neurons whose large size permits detailed examination of post-injury molecular responses at the level of individual, identified cells. We report here that spinal cord injury caused a select subset of giant reticulospinal neurons to accumulate synuclein, a synaptic vesicle-associated protein best known for its atypical aggregation and causal role in neurodegeneration in Parkinson's and other diseases. Post-injury synuclein accumulation took the form of punctate aggregates throughout the somata and occurred selectively in dying neurons, but not in those that survived. In contrast, another synaptic vesicle protein, synaptotagmin, did not accumulate in response to injury. We further show that the post-injury synuclein accumulation was greatly attenuated after single dose application of either the "molecular tweezer" inhibitor, CLR01, or a translation-blocking synuclein morpholino. Consequently, reduction of synuclein accumulation not only improved neuronal survival, but also increased the number of axons in the spinal cord proximal and distal to the lesion. This study is the first to reveal that reducing synuclein accumulation is a novel strategy for improving neuronal survival after spinal cord injury.
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Registered trials
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