ArticlePloS one2017
Numerical Simulations Reveal Randomness of Cu(II) Induced Aβ Peptide Dimerization under Conditions Present in Glutamatergic Synapses.
Article in PloS one, 2017. 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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Who cites it
14 citing papers in PubMed.
- Aβ-42 Side Chain Deamidation at Q15 or N27 Modulates Protein Aggregation and Alters Microglial Cytokines and CD68.ACS chemical neuroscience · 2026Article
- Article
- The Effects of Fisetin and Curcumin on Oxidative Damage Caused by Transition Metals in Neurodegenerative Diseases.Molecular neurobiology · 2025Review
- Interplay between Copper, Phosphatidylserine, and α-Synuclein Suggests a Link between Copper Homeostasis and Synaptic Vesicle Cycling.ACS chemical neuroscience · 2024Article
- The Role of Glia in Wilson's Disease: Clinical, Neuroimaging, Neuropathological and Molecular Perspectives.International journal of molecular sciences · 2024Review
- Reactive Cu2+-peptide intermediates revealed by kinetic studies gain relevance by matching time windows in copper metallomics.Metallomics : integrated biometal science · 2023Article
- Microglia and Astrocytes in Alzheimer's Disease in the Context of the Aberrant Copper Homeostasis Hypothesis.Biomolecules · 2021Review
- Peptides Derived from Angiogenin Regulate Cellular Copper Uptake.International journal of molecular sciences · 2021Article
- Oxidase Reactivity of CuInternational journal of molecular sciences · 2021Article
- His6, His13, and His14 residues in Aβ 1-40 peptide significantly and specifically affect oligomeric equilibria.Scientific reports · 2019Article
- Environmental and Dietary Exposure to Copper and Its Cellular Mechanisms Linking to Alzheimer's Disease.Toxicological sciences : an official journal of the Society of Toxicology · 2018Review
- A Trishistidine Pseudopeptide with Ability to Remove Both CuChemistry (Weinheim an der Bergstrasse, Germany) · 2017Article
- Kinetic Analysis Reveals the Identity of Aβ-Metal Complex Responsible for the Initial Aggregation of Aβ in the Synapse.ACS chemical neuroscience · 2017Article
- The Case for Abandoning Therapeutic Chelation of Copper Ions in Alzheimer's Disease.Frontiers in neuroscience · 2017Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The interactions between the Aβ1-40 molecules species and the copper ions (Cu(II)) were intensively investigated due to their potential role in the development of the Alzheimer Disease (AD). The rate and the mechanism of the Cu(II)-Aβ complexes formation determines the aggregation pathway of the Aβ species, starting from smaller but more cytotoxic oligomers and ending up in large Aβ plaques, being the main hallmark of the AD. In our study we exploit the existing knowledge on the Cu(II)-Aβ interactions and create the theoretical model of the initial phase of the copper- driven Aβ aggregation mechanism. The model is based on the direct solution of the Chemical Master Equations, which capture the inherent stochastics of the considered system. In our work we argue that due to a strong Cu(II) affinity to Aβ and temporal accessibility of the Cu(II) ions during normal synaptic activity the aggregation driven by Cu(II) dominates the pure Aβ aggregation. We also demonstrate the dependence of the formation of different Cu(II)-Aβ complexes on the concentrations of reagents and the synaptic activity. Our findings correspond to recent experimental results and give a sound hypothesis on the AD development mechanisms.
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