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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Main Authors: Despoina Kaffe, Stefanos Ioannis Kaplanis, Domna Karagogeos
Format: Article
Language:English
Published: MDPI AG 2023-11-01
Series:Current Issues in Molecular Biology
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Online Access:https://www.mdpi.com/1467-3045/45/12/596
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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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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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