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Multiple Sclerosis: Inflammatory and Neuroglial Aspects
Multiple sclerosis (MS) represents the most common acquired demyelinating disorder of the central nervous system (CNS). Its pathogenesis, in parallel with the well-established role of mechanisms pertaining to autoimmunity, involves several key functions of immune, glial and nerve cells. The disease’...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9954863/ https://www.ncbi.nlm.nih.gov/pubmed/36826039 http://dx.doi.org/10.3390/cimb45020094 |
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author | Papiri, Giulio D’Andreamatteo, Giordano Cacchiò, Gabriella Alia, Sonila Silvestrini, Mauro Paci, Cristina Luzzi, Simona Vignini, Arianna |
author_facet | Papiri, Giulio D’Andreamatteo, Giordano Cacchiò, Gabriella Alia, Sonila Silvestrini, Mauro Paci, Cristina Luzzi, Simona Vignini, Arianna |
author_sort | Papiri, Giulio |
collection | PubMed |
description | Multiple sclerosis (MS) represents the most common acquired demyelinating disorder of the central nervous system (CNS). Its pathogenesis, in parallel with the well-established role of mechanisms pertaining to autoimmunity, involves several key functions of immune, glial and nerve cells. The disease’s natural history is complex, heterogeneous and may evolve over a relapsing-remitting (RRMS) or progressive (PPMS/SPMS) course. Acute inflammation, driven by infiltration of peripheral cells in the CNS, is thought to be the most relevant process during the earliest phases and in RRMS, while disruption in glial and neural cells of pathways pertaining to energy metabolism, survival cascades, synaptic and ionic homeostasis are thought to be mostly relevant in long-standing disease, such as in progressive forms. In this complex scenario, many mechanisms originally thought to be distinctive of neurodegenerative disorders are being increasingly recognized as crucial from the beginning of the disease. The present review aims at highlighting mechanisms in common between MS, autoimmune diseases and biology of neurodegenerative disorders. In fact, there is an unmet need to explore new targets that might be involved as master regulators of autoimmunity, inflammation and survival of nerve cells. |
format | Online Article Text |
id | pubmed-9954863 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-99548632023-02-25 Multiple Sclerosis: Inflammatory and Neuroglial Aspects Papiri, Giulio D’Andreamatteo, Giordano Cacchiò, Gabriella Alia, Sonila Silvestrini, Mauro Paci, Cristina Luzzi, Simona Vignini, Arianna Curr Issues Mol Biol Review Multiple sclerosis (MS) represents the most common acquired demyelinating disorder of the central nervous system (CNS). Its pathogenesis, in parallel with the well-established role of mechanisms pertaining to autoimmunity, involves several key functions of immune, glial and nerve cells. The disease’s natural history is complex, heterogeneous and may evolve over a relapsing-remitting (RRMS) or progressive (PPMS/SPMS) course. Acute inflammation, driven by infiltration of peripheral cells in the CNS, is thought to be the most relevant process during the earliest phases and in RRMS, while disruption in glial and neural cells of pathways pertaining to energy metabolism, survival cascades, synaptic and ionic homeostasis are thought to be mostly relevant in long-standing disease, such as in progressive forms. In this complex scenario, many mechanisms originally thought to be distinctive of neurodegenerative disorders are being increasingly recognized as crucial from the beginning of the disease. The present review aims at highlighting mechanisms in common between MS, autoimmune diseases and biology of neurodegenerative disorders. In fact, there is an unmet need to explore new targets that might be involved as master regulators of autoimmunity, inflammation and survival of nerve cells. MDPI 2023-02-08 /pmc/articles/PMC9954863/ /pubmed/36826039 http://dx.doi.org/10.3390/cimb45020094 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Papiri, Giulio D’Andreamatteo, Giordano Cacchiò, Gabriella Alia, Sonila Silvestrini, Mauro Paci, Cristina Luzzi, Simona Vignini, Arianna Multiple Sclerosis: Inflammatory and Neuroglial Aspects |
title | Multiple Sclerosis: Inflammatory and Neuroglial Aspects |
title_full | Multiple Sclerosis: Inflammatory and Neuroglial Aspects |
title_fullStr | Multiple Sclerosis: Inflammatory and Neuroglial Aspects |
title_full_unstemmed | Multiple Sclerosis: Inflammatory and Neuroglial Aspects |
title_short | Multiple Sclerosis: Inflammatory and Neuroglial Aspects |
title_sort | multiple sclerosis: inflammatory and neuroglial aspects |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9954863/ https://www.ncbi.nlm.nih.gov/pubmed/36826039 http://dx.doi.org/10.3390/cimb45020094 |
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