The Roles of Caloric Restriction Mimetics in Central Nervous System Demyelination and Remyelination
The dysfunction of myelinating glial cells, the oligodendrocytes, within the central nervous system (CNS) can result in the disruption of myelin, the lipid-rich multi-layered membrane structure that surrounds most vertebrate axons. This leads to axonal degeneration and motor/cognitive impairments. I...
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MDPI AG
2023-11-01
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author | Despoina Kaffe Stefanos Ioannis Kaplanis Domna Karagogeos |
author_facet | Despoina Kaffe Stefanos Ioannis Kaplanis Domna Karagogeos |
author_sort | Despoina Kaffe |
collection | DOAJ |
description | The dysfunction of myelinating glial cells, the oligodendrocytes, within the central nervous system (CNS) can result in the disruption of myelin, the lipid-rich multi-layered membrane structure that surrounds most vertebrate axons. This leads to axonal degeneration and motor/cognitive impairments. In response to demyelination in the CNS, the formation of new myelin sheaths occurs through the homeostatic process of remyelination, facilitated by the differentiation of newly formed oligodendrocytes. Apart from oligodendrocytes, the two other main glial cell types of the CNS, microglia and astrocytes, play a pivotal role in remyelination. Following a demyelination insult, microglia can phagocytose myelin debris, thus permitting remyelination, while the developing neuroinflammation in the demyelinated region triggers the activation of astrocytes. Modulating the profile of glial cells can enhance the likelihood of successful remyelination. In this context, recent studies have implicated autophagy as a pivotal pathway in glial cells, playing a significant role in both their maturation and the maintenance of myelin. In this Review, we examine the role of substances capable of modulating the autophagic machinery within the myelinating glial cells of the CNS. Such substances, called caloric restriction mimetics, have been shown to decelerate the aging process by mitigating age-related ailments, with their mechanisms of action intricately linked to the induction of autophagic processes. |
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issn | 1467-3037 1467-3045 |
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spelling | doaj.art-3649464abc474a38ba4058fa580f3c142023-12-22T14:00:37ZengMDPI AGCurrent Issues in Molecular Biology1467-30371467-30452023-11-0145129526954810.3390/cimb45120596The Roles of Caloric Restriction Mimetics in Central Nervous System Demyelination and RemyelinationDespoina Kaffe0Stefanos Ioannis Kaplanis1Domna Karagogeos2Department of Biology, University of Crete, Vassilika Vouton, 70013 Heraklion, GreeceDepartment of Basic Science, School of Medicine, University of Crete, Vassilika Vouton, 70013 Heraklion, GreeceDepartment of Basic Science, School of Medicine, University of Crete, Vassilika Vouton, 70013 Heraklion, GreeceThe dysfunction of myelinating glial cells, the oligodendrocytes, within the central nervous system (CNS) can result in the disruption of myelin, the lipid-rich multi-layered membrane structure that surrounds most vertebrate axons. This leads to axonal degeneration and motor/cognitive impairments. In response to demyelination in the CNS, the formation of new myelin sheaths occurs through the homeostatic process of remyelination, facilitated by the differentiation of newly formed oligodendrocytes. Apart from oligodendrocytes, the two other main glial cell types of the CNS, microglia and astrocytes, play a pivotal role in remyelination. Following a demyelination insult, microglia can phagocytose myelin debris, thus permitting remyelination, while the developing neuroinflammation in the demyelinated region triggers the activation of astrocytes. Modulating the profile of glial cells can enhance the likelihood of successful remyelination. In this context, recent studies have implicated autophagy as a pivotal pathway in glial cells, playing a significant role in both their maturation and the maintenance of myelin. In this Review, we examine the role of substances capable of modulating the autophagic machinery within the myelinating glial cells of the CNS. Such substances, called caloric restriction mimetics, have been shown to decelerate the aging process by mitigating age-related ailments, with their mechanisms of action intricately linked to the induction of autophagic processes.https://www.mdpi.com/1467-3045/45/12/596oligodendrocyte progenitor cellsoligodendrocytesmicrogliaastrocytescaloric restrictioncaloric restriction mimetics |
spellingShingle | Despoina Kaffe Stefanos Ioannis Kaplanis Domna Karagogeos The Roles of Caloric Restriction Mimetics in Central Nervous System Demyelination and Remyelination Current Issues in Molecular Biology oligodendrocyte progenitor cells oligodendrocytes microglia astrocytes caloric restriction caloric restriction mimetics |
title | The Roles of Caloric Restriction Mimetics in Central Nervous System Demyelination and Remyelination |
title_full | The Roles of Caloric Restriction Mimetics in Central Nervous System Demyelination and Remyelination |
title_fullStr | The Roles of Caloric Restriction Mimetics in Central Nervous System Demyelination and Remyelination |
title_full_unstemmed | The Roles of Caloric Restriction Mimetics in Central Nervous System Demyelination and Remyelination |
title_short | The Roles of Caloric Restriction Mimetics in Central Nervous System Demyelination and Remyelination |
title_sort | roles of caloric restriction mimetics in central nervous system demyelination and remyelination |
topic | oligodendrocyte progenitor cells oligodendrocytes microglia astrocytes caloric restriction caloric restriction mimetics |
url | https://www.mdpi.com/1467-3045/45/12/596 |
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