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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Main Authors: Eneritz López-Muguruza, Carlos Matute
Format: Article
Language:English
Published: MDPI AG 2023-08-01
Series:International Journal of Molecular Sciences
Subjects:
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.
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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