ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Copper reduces Aβ oligomeric species and ameliorates neuromuscular synaptic defects in a C. elegans model of inclusion body myositis.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 41 citations in OpenAlex.
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- Cardiac Light Chain Amyloidosis: The Role of Metal Ions in Oxidative Stress and Mitochondrial Damage.Antioxidants & redox signaling · 2017Article
- Resveratrol reduces amyloid-beta (Aβ₁₋₄₂)-induced paralysis through targeting proteostasis in an Alzheimer model of Caenorhabditis elegans.European journal of nutrition · 2016Article
- The protein oxidation repair enzyme methionine sulfoxide reductase a modulates Aβ aggregation and toxicity in vivo.Antioxidants & redox signaling · 2015Article
- Alzheimer's disease drug discovery: in vivo screening using Caenorhabditis elegans as a model for β-amyloid peptide-induced toxicity.Drug discovery today. Technologies · 2013Review
- Metal-induced neurodegeneration in C. elegans.Frontiers in aging neuroscience · 2013Article
- Animal models of inflammatory myopathy.Current rheumatology reports · 2012Review
- Postsynaptic Receptors for Amyloid-β Oligomers as Mediators of Neuronal Damage in Alzheimer's Disease.Frontiers in physiology · 2012Article
- Submicromolar Aβ42 reduces hippocampal glutamate receptors and presynaptic markers in an aggregation-dependent manner.Biochimica et biophysica acta · 2011Article
- The essential elements of Alzheimer's disease.The Journal of biological chemistryReview
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease and inclusion body myositis (IBM) are disorders frequently found in the elderly and characterized by the presence of amyloid-β peptide (Aβ) aggregates. We used Caenorhabditis elegans that express Aβ in muscle cells as a model of IBM, with the aim of analyzing Aβ-induced muscle pathology and evaluating the consequences of modulating Aβ aggregation. First, we tested whether the altered motility we observed in the Aβ transgenic strain could be the result of a compromised neuromuscular synapse. Our pharmacological analyses show that synaptic transmission is defective in our model and suggest a specific defect on nicotine-sensitive acetylcholine receptors (AChRs). Through GFP-coupled protein visualization, we found that synaptic dysfunction correlates with mislocalization of ACR-16, the AChR subunit essential for nicotine-triggered currents. Histological and biochemical analysis allowed us to determine that copper treatment increases the amyloid deposits and decreases Aβ oligomers in this model. Furthermore, copper treatment improves motility, ACR-16 localization, and synaptic function and delays Aβ-induced paralysis. Our results indicate that copper modulates Aβ-induced pathology and suggest that Aβ oligomers are triggering neuromuscular dysfunction. Our findings emphasize the importance of neuromuscular synaptic dysfunction and the relevance of modulating the amyloidogenic component as an alternative therapeutic approach for this debilitating disease.
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