Alterations of Oligodendrocyte and Myelin Energy Metabolism in Multiple Sclerosis
Multiple sclerosis (MS) is a complex autoimmune disease of the central nervous system (CNS), characterized by demyelination and neurodegeneration. Oligodendrocytes play a vital role in maintaining the integrity of myelin, the protective sheath around nerve fibres essential for efficient signal trans...
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MDPI AG
2023-08-01
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Series: | International Journal of Molecular Sciences |
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Online Access: | https://www.mdpi.com/1422-0067/24/16/12912 |
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author | Eneritz López-Muguruza Carlos Matute |
author_facet | Eneritz López-Muguruza Carlos Matute |
author_sort | Eneritz López-Muguruza |
collection | DOAJ |
description | Multiple sclerosis (MS) is a complex autoimmune disease of the central nervous system (CNS), characterized by demyelination and neurodegeneration. Oligodendrocytes play a vital role in maintaining the integrity of myelin, the protective sheath around nerve fibres essential for efficient signal transmission. However, in MS, oligodendrocytes become dysfunctional, leading to myelin damage and axonal degeneration. Emerging evidence suggests that metabolic changes, including mitochondrial dysfunction and alterations in glucose and lipid metabolism, contribute significantly to the pathogenesis of MS. Mitochondrial dysfunction is observed in both immune cells and oligodendrocytes within the CNS of MS patients. Impaired mitochondrial function leads to energy deficits, affecting crucial processes such as impulse transmission and axonal transport, ultimately contributing to neurodegeneration. Moreover, mitochondrial dysfunction is linked to the generation of reactive oxygen species (ROS), exacerbating myelin damage and inflammation. Altered glucose metabolism affects the energy supply required for oligodendrocyte function and myelin synthesis. Dysregulated lipid metabolism results in changes to the composition of myelin, affecting its stability and integrity. Importantly, low levels of polyunsaturated fatty acids in MS are associated with upregulated lipid metabolism and enhanced glucose catabolism. Understanding the intricate relationship between these mechanisms is crucial for developing targeted therapies to preserve myelin and promote neurological recovery in individuals with MS. Addressing these metabolic aspects may offer new insights into potential therapeutic strategies to halt disease progression and improve the quality of life for MS patients. |
first_indexed | 2024-03-10T23:52:09Z |
format | Article |
id | doaj.art-2296df1e6fad4cf48a2c78482c02a802 |
institution | Directory Open Access Journal |
issn | 1661-6596 1422-0067 |
language | English |
last_indexed | 2024-03-10T23:52:09Z |
publishDate | 2023-08-01 |
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series | International Journal of Molecular Sciences |
spelling | doaj.art-2296df1e6fad4cf48a2c78482c02a8022023-11-19T01:32:04ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672023-08-0124161291210.3390/ijms241612912Alterations of Oligodendrocyte and Myelin Energy Metabolism in Multiple SclerosisEneritz López-Muguruza0Carlos Matute1Achucarro Basque Center for Neuroscience, 48940 Leioa, SpainAchucarro Basque Center for Neuroscience, 48940 Leioa, SpainMultiple sclerosis (MS) is a complex autoimmune disease of the central nervous system (CNS), characterized by demyelination and neurodegeneration. Oligodendrocytes play a vital role in maintaining the integrity of myelin, the protective sheath around nerve fibres essential for efficient signal transmission. However, in MS, oligodendrocytes become dysfunctional, leading to myelin damage and axonal degeneration. Emerging evidence suggests that metabolic changes, including mitochondrial dysfunction and alterations in glucose and lipid metabolism, contribute significantly to the pathogenesis of MS. Mitochondrial dysfunction is observed in both immune cells and oligodendrocytes within the CNS of MS patients. Impaired mitochondrial function leads to energy deficits, affecting crucial processes such as impulse transmission and axonal transport, ultimately contributing to neurodegeneration. Moreover, mitochondrial dysfunction is linked to the generation of reactive oxygen species (ROS), exacerbating myelin damage and inflammation. Altered glucose metabolism affects the energy supply required for oligodendrocyte function and myelin synthesis. Dysregulated lipid metabolism results in changes to the composition of myelin, affecting its stability and integrity. Importantly, low levels of polyunsaturated fatty acids in MS are associated with upregulated lipid metabolism and enhanced glucose catabolism. Understanding the intricate relationship between these mechanisms is crucial for developing targeted therapies to preserve myelin and promote neurological recovery in individuals with MS. Addressing these metabolic aspects may offer new insights into potential therapeutic strategies to halt disease progression and improve the quality of life for MS patients.https://www.mdpi.com/1422-0067/24/16/12912lipidsmitochondriademyelinationdysmyelinationremyelinationaxonal damage |
spellingShingle | Eneritz López-Muguruza Carlos Matute Alterations of Oligodendrocyte and Myelin Energy Metabolism in Multiple Sclerosis International Journal of Molecular Sciences lipids mitochondria demyelination dysmyelination remyelination axonal damage |
title | Alterations of Oligodendrocyte and Myelin Energy Metabolism in Multiple Sclerosis |
title_full | Alterations of Oligodendrocyte and Myelin Energy Metabolism in Multiple Sclerosis |
title_fullStr | Alterations of Oligodendrocyte and Myelin Energy Metabolism in Multiple Sclerosis |
title_full_unstemmed | Alterations of Oligodendrocyte and Myelin Energy Metabolism in Multiple Sclerosis |
title_short | Alterations of Oligodendrocyte and Myelin Energy Metabolism in Multiple Sclerosis |
title_sort | alterations of oligodendrocyte and myelin energy metabolism in multiple sclerosis |
topic | lipids mitochondria demyelination dysmyelination remyelination axonal damage |
url | https://www.mdpi.com/1422-0067/24/16/12912 |
work_keys_str_mv | AT eneritzlopezmuguruza alterationsofoligodendrocyteandmyelinenergymetabolisminmultiplesclerosis AT carlosmatute alterationsofoligodendrocyteandmyelinenergymetabolisminmultiplesclerosis |