ArticleMolecular neurodegeneration2009
Intracellular amyloid formation in muscle cells of Abeta-transgenic Caenorhabditis elegans: determinants and physiological role in copper detoxification.
Article in Molecular neurodegeneration, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 46 citations in OpenAlex.
- Protective Role of Holothuria leucospilota Extract Against Amyloid-β Toxicity via Autophagy and Antioxidant Mechanisms in Caenorhabditis elegans Model.Oxidative medicine and cellular longevity · 2026Article
- Whole-mount diffracted X-ray blinking analysis of intracellular amyloid-β-associated nanoscale dynamics inBiology methods & protocols · 2026Article
- Dysfunctional copper homeostasis inRedox biochemistry and chemistry · 2024Article
- APP-C31: An Intracellular Promoter of Both Metal-Free and Metal-Bound Amyloid-βAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Zn-dependent β-amyloid Aggregation and its Reversal by the Tetrapeptide HAEE.Aging and disease · 2023Article
- Assessment and Validation ofCells · 2021Article
- Imbalances in Copper or Zinc Concentrations Trigger Further Trace Metal Dyshomeostasis in Amyloid-Beta ProducingFrontiers in neuroscience · 2021Article
- Neurochemical Aspects of Alzheimer's Disease and Movement Disturbances: A Theory of β-Amyloid and τ-Protein.American journal of Alzheimer's disease and other dementias · 2018Article
- Overview of Alzheimer's Disease and Some Therapeutic Approaches Targeting Aβ by Using Several Synthetic and Herbal Compounds.Oxidative medicine and cellular longevity · 2016Review
- The protein oxidation repair enzyme methionine sulfoxide reductase a modulates Aβ aggregation and toxicity in vivo.Antioxidants & redox signaling · 2015Article
- Bio-orthogonal labeling as a tool to visualize and identify newly synthesized proteins in Caenorhabditis elegans.Nature protocols · 2014Article
- Utility of an improved model of amyloid-beta (Aβ₁₋₄₂) toxicity in Caenorhabditis elegans for drug screening for Alzheimer's disease.Molecular neurodegeneration · 2012Article
- The Caenorhabiditis elegans model as a reliable tool in neurotoxicology.Human & experimental toxicology · 2012Review
- Article
- Curcumin promotes A-beta fibrillation and reduces neurotoxicity in transgenic Drosophila.PloS one · 2012Article
- Copper reduces Aβ oligomeric species and ameliorates neuromuscular synaptic defects in a C. elegans model of inclusion body myositis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Expression of human amyloid precursor protein in the skeletal muscles of Drosophila results in age- and activity-dependent muscle weakness.BMC physiology · 2011Article
- Insights from Caenorhabditis elegans on the role of metals in neurodegenerative diseases.Metallomics : integrated biometal science · 2011Review
- APP processing in Alzheimer's disease.Molecular brain · 2011Review
- The Caenorhabditis elegans A beta 1-42 model of Alzheimer disease predominantly expresses A beta 3-42.The Journal of biological chemistry · 2009Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 3 countries.
Funding
Abstract
backgroundThe amyloid beta-peptide is a ubiquitous peptide, which is prone to aggregate forming soluble toxic oligomers and insoluble less-toxic aggregates. The intrinsic and external/environmental factors that determine Abeta aggregation in vivo are poorly understood, as well as the cellular meaning of this process itself. Genetic data as well as cell biological and biochemical evidence strongly support the hypothesis that Abeta is a major player in the onset and development of Alzheimer's disease. In addition, it is also known that Abeta is involved in Inclusion Body Myositis, a common myopathy of the elderly in which the peptide accumulates intracellularly.
resultsIn the present work, we found that intracellular Abeta aggregation in muscle cells of Caenorhabditis elegans overexpressing Abeta peptide is affected by two single amino acid substitutions, E22G (Arctic) and V18A (NIC). Both variations show decrease intracellular amyloidogenesis compared to wild type Abeta. We show that intracellular amyloid aggregation of wild type Abeta is accelerated by Cu2+ and diminished by copper chelators. Moreover, we demonstrate through toxicity and behavioral assays that Abeta-transgenic worms display a higher tolerance to Cu2+ toxic effects and that this resistance may be linked to the formation of amyloid aggregates.
conclusionOur data show that intracellular Abeta amyloid aggregates may trap excess of free Cu2+ buffering its cytotoxic effects and that accelerated intracellular Abeta aggregation may be part of a cell protective mechanism.
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Registered trials
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