Amyotrophic Lateral Sclerosis Mechanism: Insights from the <i<Caenorhabditis elegans</i< Models

Amyotrophic Lateral Sclerosis (ALS) is a debilitating neurodegenerative condition characterized by the progressive degeneration of motor neurons. Despite extensive research in various model animals, the cellular signal mechanisms of ALS remain elusive, impeding the development of efficacious treatme...
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Autor*in:	Lili Chen [verfasserIn] Shumei Zhang [verfasserIn] Sai Liu [verfasserIn] Shangbang Gao [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2024

Schlagwörter:	ALS cellular mechanism therapeutic application

Übergeordnetes Werk:	In: Cells - MDPI AG, 2012, 13(2024), 1, p 99
Übergeordnetes Werk:	volume:13 ; year:2024 ; number:1, p 99

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3390/cells13010099

Katalog-ID:	DOAJ097807036

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520			\|a Amyotrophic Lateral Sclerosis (ALS) is a debilitating neurodegenerative condition characterized by the progressive degeneration of motor neurons. Despite extensive research in various model animals, the cellular signal mechanisms of ALS remain elusive, impeding the development of efficacious treatments. Among these models, a well-characterized and diminutive organism, <i<Caenorhabditis elegans</i< (<i<C. elegans</i<), has emerged as a potent tool for investigating the molecular and cellular dimensions of ALS pathogenesis. This review summarizes the contributions of <i<C. elegans</i< models to our comprehension of ALS, emphasizing pivotal findings pertaining to genetics, protein aggregation, cellular pathways, and potential therapeutic strategies. We analyze both the merits and constraints of the <i<C. elegans</i< system in the realm of ALS research and point towards future investigations that could bridge the chasm between <i<C. elegans</i< foundational discoveries and clinical applications.
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spelling	10.3390/cells13010099 doi (DE-627)DOAJ097807036 (DE-599)DOAJd2bce71faae643c495546b3fd706e0d9 DE-627 ger DE-627 rakwb eng QH573-671 Lili Chen verfasserin aut Amyotrophic Lateral Sclerosis Mechanism: Insights from the <i<Caenorhabditis elegans</i< Models 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Amyotrophic Lateral Sclerosis (ALS) is a debilitating neurodegenerative condition characterized by the progressive degeneration of motor neurons. Despite extensive research in various model animals, the cellular signal mechanisms of ALS remain elusive, impeding the development of efficacious treatments. Among these models, a well-characterized and diminutive organism, <i<Caenorhabditis elegans</i< (<i<C. elegans</i<), has emerged as a potent tool for investigating the molecular and cellular dimensions of ALS pathogenesis. This review summarizes the contributions of <i<C. elegans</i< models to our comprehension of ALS, emphasizing pivotal findings pertaining to genetics, protein aggregation, cellular pathways, and potential therapeutic strategies. We analyze both the merits and constraints of the <i<C. elegans</i< system in the realm of ALS research and point towards future investigations that could bridge the chasm between <i<C. elegans</i< foundational discoveries and clinical applications. ALS <i<C. elegans</i< model cellular mechanism therapeutic application Cytology Shumei Zhang verfasserin aut Sai Liu verfasserin aut Shangbang Gao verfasserin aut In Cells MDPI AG, 2012 13(2024), 1, p 99 (DE-627)718622081 (DE-600)2661518-6 20734409 nnns volume:13 year:2024 number:1, p 99 https://doi.org/10.3390/cells13010099 kostenfrei https://doaj.org/article/d2bce71faae643c495546b3fd706e0d9 kostenfrei https://www.mdpi.com/2073-4409/13/1/99 kostenfrei https://doaj.org/toc/2073-4409 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2024 1, p 99
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allfieldsSound	10.3390/cells13010099 doi (DE-627)DOAJ097807036 (DE-599)DOAJd2bce71faae643c495546b3fd706e0d9 DE-627 ger DE-627 rakwb eng QH573-671 Lili Chen verfasserin aut Amyotrophic Lateral Sclerosis Mechanism: Insights from the <i<Caenorhabditis elegans</i< Models 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Amyotrophic Lateral Sclerosis (ALS) is a debilitating neurodegenerative condition characterized by the progressive degeneration of motor neurons. Despite extensive research in various model animals, the cellular signal mechanisms of ALS remain elusive, impeding the development of efficacious treatments. Among these models, a well-characterized and diminutive organism, <i<Caenorhabditis elegans</i< (<i<C. elegans</i<), has emerged as a potent tool for investigating the molecular and cellular dimensions of ALS pathogenesis. This review summarizes the contributions of <i<C. elegans</i< models to our comprehension of ALS, emphasizing pivotal findings pertaining to genetics, protein aggregation, cellular pathways, and potential therapeutic strategies. We analyze both the merits and constraints of the <i<C. elegans</i< system in the realm of ALS research and point towards future investigations that could bridge the chasm between <i<C. elegans</i< foundational discoveries and clinical applications. ALS <i<C. elegans</i< model cellular mechanism therapeutic application Cytology Shumei Zhang verfasserin aut Sai Liu verfasserin aut Shangbang Gao verfasserin aut In Cells MDPI AG, 2012 13(2024), 1, p 99 (DE-627)718622081 (DE-600)2661518-6 20734409 nnns volume:13 year:2024 number:1, p 99 https://doi.org/10.3390/cells13010099 kostenfrei https://doaj.org/article/d2bce71faae643c495546b3fd706e0d9 kostenfrei https://www.mdpi.com/2073-4409/13/1/99 kostenfrei https://doaj.org/toc/2073-4409 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2024 1, p 99
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topic_facet	ALS <i<C. elegans</i< model cellular mechanism therapeutic application Cytology
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authorswithroles_txt_mv	Lili Chen @@aut@@ Shumei Zhang @@aut@@ Sai Liu @@aut@@ Shangbang Gao @@aut@@
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author	Lili Chen
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topic_title	QH573-671 Amyotrophic Lateral Sclerosis Mechanism: Insights from the <i<Caenorhabditis elegans</i< Models ALS <i<C. elegans</i< model cellular mechanism therapeutic application
topic	misc QH573-671 misc ALS misc <i<C. elegans</i< model misc cellular mechanism misc therapeutic application misc Cytology
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title	Amyotrophic Lateral Sclerosis Mechanism: Insights from the <i<Caenorhabditis elegans</i< Models
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title_auth	Amyotrophic Lateral Sclerosis Mechanism: Insights from the <i<Caenorhabditis elegans</i< Models
abstract	Amyotrophic Lateral Sclerosis (ALS) is a debilitating neurodegenerative condition characterized by the progressive degeneration of motor neurons. Despite extensive research in various model animals, the cellular signal mechanisms of ALS remain elusive, impeding the development of efficacious treatments. Among these models, a well-characterized and diminutive organism, <i<Caenorhabditis elegans</i< (<i<C. elegans</i<), has emerged as a potent tool for investigating the molecular and cellular dimensions of ALS pathogenesis. This review summarizes the contributions of <i<C. elegans</i< models to our comprehension of ALS, emphasizing pivotal findings pertaining to genetics, protein aggregation, cellular pathways, and potential therapeutic strategies. We analyze both the merits and constraints of the <i<C. elegans</i< system in the realm of ALS research and point towards future investigations that could bridge the chasm between <i<C. elegans</i< foundational discoveries and clinical applications.
abstractGer	Amyotrophic Lateral Sclerosis (ALS) is a debilitating neurodegenerative condition characterized by the progressive degeneration of motor neurons. Despite extensive research in various model animals, the cellular signal mechanisms of ALS remain elusive, impeding the development of efficacious treatments. Among these models, a well-characterized and diminutive organism, <i<Caenorhabditis elegans</i< (<i<C. elegans</i<), has emerged as a potent tool for investigating the molecular and cellular dimensions of ALS pathogenesis. This review summarizes the contributions of <i<C. elegans</i< models to our comprehension of ALS, emphasizing pivotal findings pertaining to genetics, protein aggregation, cellular pathways, and potential therapeutic strategies. We analyze both the merits and constraints of the <i<C. elegans</i< system in the realm of ALS research and point towards future investigations that could bridge the chasm between <i<C. elegans</i< foundational discoveries and clinical applications.
abstract_unstemmed	Amyotrophic Lateral Sclerosis (ALS) is a debilitating neurodegenerative condition characterized by the progressive degeneration of motor neurons. Despite extensive research in various model animals, the cellular signal mechanisms of ALS remain elusive, impeding the development of efficacious treatments. Among these models, a well-characterized and diminutive organism, <i<Caenorhabditis elegans</i< (<i<C. elegans</i<), has emerged as a potent tool for investigating the molecular and cellular dimensions of ALS pathogenesis. This review summarizes the contributions of <i<C. elegans</i< models to our comprehension of ALS, emphasizing pivotal findings pertaining to genetics, protein aggregation, cellular pathways, and potential therapeutic strategies. We analyze both the merits and constraints of the <i<C. elegans</i< system in the realm of ALS research and point towards future investigations that could bridge the chasm between <i<C. elegans</i< foundational discoveries and clinical applications.
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title_short	Amyotrophic Lateral Sclerosis Mechanism: Insights from the <i<Caenorhabditis elegans</i< Models
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