ArticleJournal of neurotrauma2016
Intrathecal Acetyl-L-Carnitine Protects Tissue and Improves Function after a Mild Contusive Spinal Cord Injury in Rats.
Article in Journal of neurotrauma, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- Elevated phagocytic capacity directs innate spinal cord repair.Cell reports · 2026Article
- Sonic Hedgehog reduces inflammatory response, decreases blood-spinal cord barrier permeability, and improves locomotor function recovery in an acute spinal cord injury rat model.Journal of inflammation (London, England) · 2024Article
- Reduced FAK-STAT3 signaling contributes to ER stress-induced mitochondrial dysfunction and death in endothelial cells.Cellular signalling · 2017Article
- Nanofiber Scaffolds as Drug Delivery Systems to Bridge Spinal Cord Injury.Pharmaceuticals (Basel, Switzerland) · 2017Review
- Comprehensive therapeutics targeting the corticospinal tract following spinal cord injury.Journal of Zhejiang University. Science. BReview
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Primary and secondary ischemia after spinal cord injury (SCI) contributes to tissue and axon degeneration, which may result from decreased energy substrate availability for cellular and axonal mitochondrial adenosine triphosphate (ATP) production. Therefore, providing spinal tissue with an alternative energy substrate during ischemia may be neuroprotective after SCI. To assess this, rats received a mild contusive SCI (120 kdyn, Infinite Horizons impactor) at thoracic level 9 (T9), which causes loss of ∼ 80% of the ascending sensory dorsal column axonal projections to the gracile nucleus. Immediately afterwards, the energy substrate acetyl-L-carnitine (ALC; 1 mg/day) or phosphate-buffered saline (PBS) was infused intrathecally (sub-arachnoid) for 6 days via an L5/6 catheter attached to a subcutaneous Alzet pump. ALC treatment improved overground locomotor function (Basso-Beattie-Breshnahan [BBB] score 18 vs. 13) at 6 days, total spared epicenter (71% vs. 57%) and penumbra white matter (90% vs. 85%), ventral penumbra microvessels (108% vs. 79%), and penumbra motor neurons (42% vs. 15%) at 15 days post-SCI, compared with PBS treatment. However, the ascending sensory projections (anterogradely traced with cholera toxin B from the sciatic nerves) and dorsal column white matter and perfused blood vessels were not protected. Furthermore, grid walking, a task we have shown to be dependent on dorsal column function, was not improved. Thus, mitochondrial substrate replacement may only be efficacious in areas of lesser or temporary ischemia, such as the ventral spinal cord and injury penumbra in this study. The current data also support our previous evidence that microvessel loss is central to secondary tissue degeneration.
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Registered trials
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