Evaluating the effectiveness of anti-Nogo treatment in spinal cord injuries
Abstract As humans, we cannot regenerate axons within the central nervous system (CNS), therefore, making any damage to it permanent. This leads to the loss of sensory and motor function below the site of injury and can be crippling to a person’s health. Spontaneous recovery can occur from plastic c...
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Format: | Article |
Language: | English |
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BMC
2020-01-01
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Series: | Neural Development |
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Online Access: | https://doi.org/10.1186/s13064-020-0138-9 |
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author | Raihan Mohammed Kaesi Opara Rahul Lall Utkarsh Ojha Jinpo Xiang |
author_facet | Raihan Mohammed Kaesi Opara Rahul Lall Utkarsh Ojha Jinpo Xiang |
author_sort | Raihan Mohammed |
collection | DOAJ |
description | Abstract As humans, we cannot regenerate axons within the central nervous system (CNS), therefore, making any damage to it permanent. This leads to the loss of sensory and motor function below the site of injury and can be crippling to a person’s health. Spontaneous recovery can occur from plastic changes, but it is minimal. The absence of regeneration is due to the inhibitory environment of the CNS as well as the inherent inability of CNS axons to form growth cones. Amongst many factors, one of the major inhibitory signals of the CNS environment is the myelin-associated Nogo pathway. Nogo-A, Nogo-B and Nogo-C (Nogo), stimulate the Nogo receptor, inhibiting neurite outgrowth by causing growth cones to collapse through activation of Rho Kinase (ROCK). Antibodies can be used to target this signalling pathway by binding to Nogo and thus promote the outgrowth of neuronal axons in the CNS. This use of anti-Nogo antibodies has been shown to upregulate CNS regeneration as well as drastically improve sensory and motor function in both rats and primates when coupled with adequate training. Here, we evaluate whether the experimental success of anti-Nogo at improving CNS regeneration can be carried over into the clinical setting to treat spinal cord injuries (SCI) and their symptoms successfully. Furthermore, we also discuss potential methods to improve the current treatment and any developmental obstacles. |
first_indexed | 2024-12-17T01:26:07Z |
format | Article |
id | doaj.art-5710c2aac575410c8dfc264d00c62b68 |
institution | Directory Open Access Journal |
issn | 1749-8104 |
language | English |
last_indexed | 2024-12-17T01:26:07Z |
publishDate | 2020-01-01 |
publisher | BMC |
record_format | Article |
series | Neural Development |
spelling | doaj.art-5710c2aac575410c8dfc264d00c62b682022-12-21T22:08:41ZengBMCNeural Development1749-81042020-01-011511910.1186/s13064-020-0138-9Evaluating the effectiveness of anti-Nogo treatment in spinal cord injuriesRaihan Mohammed0Kaesi Opara1Rahul Lall2Utkarsh Ojha3Jinpo Xiang4Department of Medicine, School of Clinical Medicine, University of CambridgeDepartment of Medicine, School of Clinical Medicine, University of CambridgeDepartment of Medicine, School of Clinical Medicine, University of CambridgeFaculty of Medicine, Imperial College LondonFaculty of Medicine, Imperial College LondonAbstract As humans, we cannot regenerate axons within the central nervous system (CNS), therefore, making any damage to it permanent. This leads to the loss of sensory and motor function below the site of injury and can be crippling to a person’s health. Spontaneous recovery can occur from plastic changes, but it is minimal. The absence of regeneration is due to the inhibitory environment of the CNS as well as the inherent inability of CNS axons to form growth cones. Amongst many factors, one of the major inhibitory signals of the CNS environment is the myelin-associated Nogo pathway. Nogo-A, Nogo-B and Nogo-C (Nogo), stimulate the Nogo receptor, inhibiting neurite outgrowth by causing growth cones to collapse through activation of Rho Kinase (ROCK). Antibodies can be used to target this signalling pathway by binding to Nogo and thus promote the outgrowth of neuronal axons in the CNS. This use of anti-Nogo antibodies has been shown to upregulate CNS regeneration as well as drastically improve sensory and motor function in both rats and primates when coupled with adequate training. Here, we evaluate whether the experimental success of anti-Nogo at improving CNS regeneration can be carried over into the clinical setting to treat spinal cord injuries (SCI) and their symptoms successfully. Furthermore, we also discuss potential methods to improve the current treatment and any developmental obstacles.https://doi.org/10.1186/s13064-020-0138-9AxonCNSRegenerationMyelinNogo |
spellingShingle | Raihan Mohammed Kaesi Opara Rahul Lall Utkarsh Ojha Jinpo Xiang Evaluating the effectiveness of anti-Nogo treatment in spinal cord injuries Neural Development Axon CNS Regeneration Myelin Nogo |
title | Evaluating the effectiveness of anti-Nogo treatment in spinal cord injuries |
title_full | Evaluating the effectiveness of anti-Nogo treatment in spinal cord injuries |
title_fullStr | Evaluating the effectiveness of anti-Nogo treatment in spinal cord injuries |
title_full_unstemmed | Evaluating the effectiveness of anti-Nogo treatment in spinal cord injuries |
title_short | Evaluating the effectiveness of anti-Nogo treatment in spinal cord injuries |
title_sort | evaluating the effectiveness of anti nogo treatment in spinal cord injuries |
topic | Axon CNS Regeneration Myelin Nogo |
url | https://doi.org/10.1186/s13064-020-0138-9 |
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