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Tubulin Cytoskeleton in Neurodegenerative Diseases–not Only Primary Tubulinopathies

Neurodegenerative diseases represent a large group of disorders characterized by gradual loss of neurons and functions of the central nervous systems. Their course is usually severe, leading to high morbidity and subsequent inability of patients to independent functioning. Vast majority of neurodege...

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Autores principales: Cyske, Zuzanna, Gaffke, Lidia, Pierzynowska, Karolina, Węgrzyn, Grzegorz
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer US 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10287795/
https://www.ncbi.nlm.nih.gov/pubmed/36352320
http://dx.doi.org/10.1007/s10571-022-01304-6
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author Cyske, Zuzanna
Gaffke, Lidia
Pierzynowska, Karolina
Węgrzyn, Grzegorz
author_facet Cyske, Zuzanna
Gaffke, Lidia
Pierzynowska, Karolina
Węgrzyn, Grzegorz
author_sort Cyske, Zuzanna
collection PubMed
description Neurodegenerative diseases represent a large group of disorders characterized by gradual loss of neurons and functions of the central nervous systems. Their course is usually severe, leading to high morbidity and subsequent inability of patients to independent functioning. Vast majority of neurodegenerative diseases is currently untreatable, and only some symptomatic drugs are available which efficacy is usually very limited. To develop novel therapies for this group of diseases, it is crucial to understand their pathogenesis and to recognize factors which can influence the disease course. One of cellular structures which dysfunction appears to be relatively poorly understood in the light of neurodegenerative diseases is tubulin cytoskeleton. On the other hand, its changes, both structural and functional, can considerably influence cell physiology, leading to pathological processes occurring also in neurons. In this review, we summarize and discuss dysfunctions of tubulin cytoskeleton in various neurodegenerative diseases different than primary tubulinopathies (caused by mutations in genes encoding the components of the tubulin cytoskeleton), especially Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis, prion diseases, and neuronopathic mucopolysaccharidoses. It is also proposed that correction of these disorders might attenuate the progress of specific diseases, thus, finding newly recognized molecular targets for potential drugs might become possible.
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spelling pubmed-102877952023-06-24 Tubulin Cytoskeleton in Neurodegenerative Diseases–not Only Primary Tubulinopathies Cyske, Zuzanna Gaffke, Lidia Pierzynowska, Karolina Węgrzyn, Grzegorz Cell Mol Neurobiol Review Paper Neurodegenerative diseases represent a large group of disorders characterized by gradual loss of neurons and functions of the central nervous systems. Their course is usually severe, leading to high morbidity and subsequent inability of patients to independent functioning. Vast majority of neurodegenerative diseases is currently untreatable, and only some symptomatic drugs are available which efficacy is usually very limited. To develop novel therapies for this group of diseases, it is crucial to understand their pathogenesis and to recognize factors which can influence the disease course. One of cellular structures which dysfunction appears to be relatively poorly understood in the light of neurodegenerative diseases is tubulin cytoskeleton. On the other hand, its changes, both structural and functional, can considerably influence cell physiology, leading to pathological processes occurring also in neurons. In this review, we summarize and discuss dysfunctions of tubulin cytoskeleton in various neurodegenerative diseases different than primary tubulinopathies (caused by mutations in genes encoding the components of the tubulin cytoskeleton), especially Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis, prion diseases, and neuronopathic mucopolysaccharidoses. It is also proposed that correction of these disorders might attenuate the progress of specific diseases, thus, finding newly recognized molecular targets for potential drugs might become possible. Springer US 2022-11-09 2023 /pmc/articles/PMC10287795/ /pubmed/36352320 http://dx.doi.org/10.1007/s10571-022-01304-6 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Review Paper
Cyske, Zuzanna
Gaffke, Lidia
Pierzynowska, Karolina
Węgrzyn, Grzegorz
Tubulin Cytoskeleton in Neurodegenerative Diseases–not Only Primary Tubulinopathies
title Tubulin Cytoskeleton in Neurodegenerative Diseases–not Only Primary Tubulinopathies
title_full Tubulin Cytoskeleton in Neurodegenerative Diseases–not Only Primary Tubulinopathies
title_fullStr Tubulin Cytoskeleton in Neurodegenerative Diseases–not Only Primary Tubulinopathies
title_full_unstemmed Tubulin Cytoskeleton in Neurodegenerative Diseases–not Only Primary Tubulinopathies
title_short Tubulin Cytoskeleton in Neurodegenerative Diseases–not Only Primary Tubulinopathies
title_sort tubulin cytoskeleton in neurodegenerative diseases–not only primary tubulinopathies
topic Review Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10287795/
https://www.ncbi.nlm.nih.gov/pubmed/36352320
http://dx.doi.org/10.1007/s10571-022-01304-6
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