Chen, L.; Zhang, S.; Liu, S.; Gao, S. Amyotrophic Lateral Sclerosis Mechanism: Insights from the Caenorhabditis elegans Models. Cells2024, 13, 99.
Chen, L.; Zhang, S.; Liu, S.; Gao, S. Amyotrophic Lateral Sclerosis Mechanism: Insights from the Caenorhabditis elegans Models. Cells 2024, 13, 99.
Chen, L.; Zhang, S.; Liu, S.; Gao, S. Amyotrophic Lateral Sclerosis Mechanism: Insights from the Caenorhabditis elegans Models. Cells2024, 13, 99.
Chen, L.; Zhang, S.; Liu, S.; Gao, S. Amyotrophic Lateral Sclerosis Mechanism: Insights from the Caenorhabditis elegans Models. Cells 2024, 13, 99.
Abstract
Amyotrophic Lateral Sclerosis (ALS) stands as 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, Caenorhabditis elegans (C. elegans), has arisen as a potent tool for investigating the molecular and cellular dimensions of ALS pathogenesis. This review summarizes the contributions of C. elegans 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 C. elegans system in the realm of ALS research, and point towards future investigations that could bridge the chasm between C. elegans foundational discoveries and clinical applications.
Keywords
ALS; C. elegans model; cellular mechanism; therapeutic application
Subject
Biology and Life Sciences, Neuroscience and Neurology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
