Facilitation of neurological recovery in a complete spinal cord injury with NeuroAiD: case report
Introduction: NeuroAiD (MLC601 & MLC901)’s neuroprotective capabilities include limiting exaggerated calcium influx, decreasing excitotoxicity, reducing oxidative stress, and preventing glutamate-induced cell death. It has also been shown to facilitate synaptogenesis, neurogenesis, and neuroplas...
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2-s2.0-85189288020 Zainudin M.F.; Abu Hassan S.A.; Khin N.Y. Facilitation of neurological recovery in a complete spinal cord injury with NeuroAiD: case report 2024 Spinal Cord Series and Cases 10 1 10.1038/s41394-024-00632-7 https://www.scopus.com/inward/record.uri?eid=2-s2.0-85189288020&doi=10.1038%2fs41394-024-00632-7&partnerID=40&md5=43ef0780ff989a8a8279a2ce7c5b7f3d Introduction: NeuroAiD (MLC601 & MLC901)’s neuroprotective capabilities include limiting exaggerated calcium influx, decreasing excitotoxicity, reducing oxidative stress, and preventing glutamate-induced cell death. It has also been shown to facilitate synaptogenesis, neurogenesis, and neuroplasticity. However, its clinical efficacy has primarily been studied in the context of brain injuries, particularly stroke. NeuroAiD’s potential application in SCI remains largely untapped. Case presentation: A 34-year-old male presented with C4 complete tetraplegia. Following surgical decompression and initial inpatient rehabilitation, he started consuming MLC901 two capsules three times daily at month 4 post injury for 6 months. He regained considerable neurological recovery following the supplementation. Apart from the improvement in the neurological level of injury, the patient exhibited motor recovery beyond the initial zone of partial preservation up to 24 months post injury. Discussion: Our findings align with a recent animal study demonstrating MLC901’s potential to downregulate Vascular Endothelial Growth Factor (VEGF), a molecule known to increase vascular permeability and exacerbate tissue edema and infarction. In another animal study involving stroke-affected mice, MLC901 demonstrates the ability to promote neurological recovery by regulating the expression of proteins mediating angiogenesis, such as hypoxic inducible factor 1α, erythropoietin, angiopoietins 1 and 2, as well as VEGF. The anecdotal findings from this case report offer preliminary insights into NeuroAiD’s potential in facilitating recovery during post-acute and chronic phases of severe SCI, necessitating further exploration. © The Author(s), under exclusive licence to International Spinal Cord Society 2024. Springer Nature 20586124 English Article |
author |
Zainudin M.F.; Abu Hassan S.A.; Khin N.Y. |
spellingShingle |
Zainudin M.F.; Abu Hassan S.A.; Khin N.Y. Facilitation of neurological recovery in a complete spinal cord injury with NeuroAiD: case report |
author_facet |
Zainudin M.F.; Abu Hassan S.A.; Khin N.Y. |
author_sort |
Zainudin M.F.; Abu Hassan S.A.; Khin N.Y. |
title |
Facilitation of neurological recovery in a complete spinal cord injury with NeuroAiD: case report |
title_short |
Facilitation of neurological recovery in a complete spinal cord injury with NeuroAiD: case report |
title_full |
Facilitation of neurological recovery in a complete spinal cord injury with NeuroAiD: case report |
title_fullStr |
Facilitation of neurological recovery in a complete spinal cord injury with NeuroAiD: case report |
title_full_unstemmed |
Facilitation of neurological recovery in a complete spinal cord injury with NeuroAiD: case report |
title_sort |
Facilitation of neurological recovery in a complete spinal cord injury with NeuroAiD: case report |
publishDate |
2024 |
container_title |
Spinal Cord Series and Cases |
container_volume |
10 |
container_issue |
1 |
doi_str_mv |
10.1038/s41394-024-00632-7 |
url |
https://www.scopus.com/inward/record.uri?eid=2-s2.0-85189288020&doi=10.1038%2fs41394-024-00632-7&partnerID=40&md5=43ef0780ff989a8a8279a2ce7c5b7f3d |
description |
Introduction: NeuroAiD (MLC601 & MLC901)’s neuroprotective capabilities include limiting exaggerated calcium influx, decreasing excitotoxicity, reducing oxidative stress, and preventing glutamate-induced cell death. It has also been shown to facilitate synaptogenesis, neurogenesis, and neuroplasticity. However, its clinical efficacy has primarily been studied in the context of brain injuries, particularly stroke. NeuroAiD’s potential application in SCI remains largely untapped. Case presentation: A 34-year-old male presented with C4 complete tetraplegia. Following surgical decompression and initial inpatient rehabilitation, he started consuming MLC901 two capsules three times daily at month 4 post injury for 6 months. He regained considerable neurological recovery following the supplementation. Apart from the improvement in the neurological level of injury, the patient exhibited motor recovery beyond the initial zone of partial preservation up to 24 months post injury. Discussion: Our findings align with a recent animal study demonstrating MLC901’s potential to downregulate Vascular Endothelial Growth Factor (VEGF), a molecule known to increase vascular permeability and exacerbate tissue edema and infarction. In another animal study involving stroke-affected mice, MLC901 demonstrates the ability to promote neurological recovery by regulating the expression of proteins mediating angiogenesis, such as hypoxic inducible factor 1α, erythropoietin, angiopoietins 1 and 2, as well as VEGF. The anecdotal findings from this case report offer preliminary insights into NeuroAiD’s potential in facilitating recovery during post-acute and chronic phases of severe SCI, necessitating further exploration. © The Author(s), under exclusive licence to International Spinal Cord Society 2024. |
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Springer Nature |
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20586124 |
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English |
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Scopus |
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1809677770703241216 |