ArticleJournal of molecular neuroscience : MN2010
Copper enhances amyloid-beta peptide neurotoxicity and non beta-aggregation: a series of experiments conducted upon copper-bound and copper-free amyloid-beta peptide.
Article in Journal of molecular neuroscience : MN, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 47 citations in OpenAlex.
- Redox and Bioenergetic Modulation by Acacetin Attenuated Neuropathic Allodynia in Mice with Diet-induced Diabetes.Molecular neurobiology · 2025Article
- Article
- Multifunctional Anti-Alzheimer's Disease Effects of Natural Xanthone Derivatives: A Primary Structure-Activity Evaluation.Frontiers in chemistry · 2022Article
- Article
- Revisiting rodent models: Octodon degus as Alzheimer's disease model?Acta neuropathologica communications · 2016Article
- Interleukin-10 Protection against Lipopolysaccharide-Induced Neuro-Inflammation and Neurotoxicity in Ventral Mesencephalic Cultures.International journal of molecular sciences · 2015Article
- Probing the role of aromatic residues in the self-assembly of Aβ(16-22) in fluorinated alcohols and their aqueous mixtures.Biochemistry and biophysics reports · 2015Article
- Self-Assembly of Aβ40, Aβ42 and Aβ43 Peptides in Aqueous Mixtures of Fluorinated Alcohols.PloS one · 2015Article
- A high-sensitivity optical device for the early monitoring of plant pathogen attack via the in vivo detection of ROS bursts.Frontiers in plant science · 2015Article
- Multiple mechanisms of iron-induced amyloid beta-peptide accumulation in SHSY5Y cells: protective action of negletein.Neuromolecular medicine · 2014Article
- Cancer-derived immunoglobulin G promotes tumor cell growth and proliferation through inducing production of reactive oxygen species.Cell death & disease · 2013Article
- Curcumin and its derivatives: their application in neuropharmacology and neuroscience in the 21st century.Current neuropharmacology · 2013Article
- D-Amino acid oxidase-mediated increase in spinal hydrogen peroxide is mainly responsible for formalin-induced tonic pain.British journal of pharmacology · 2012Article
- Aβ-40 Y10F increases βfibrils formation but attenuates the neurotoxicity of amyloid-β peptide.International journal of molecular sciences · 2012Article
- Amyloid-beta (Aβ) D7H mutation increases oligomeric Aβ42 and alters properties of Aβ-zinc/copper assemblies.PloS one · 2012Article
- Substantial contribution of the two imidazole rings of the His13-His14 dyad to Cu(II) binding in amyloid-β(1-16) at physiological pH and its significance.The journal of physical chemistry. A · 2011Article
- Hypothesis: soluble aβ oligomers in association with redox-active metal ions are the optimal generators of reactive oxygen species in Alzheimer's disease.International journal of Alzheimer's disease · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease is characterized by the abnormal aggregation of amyloid-beta peptide (Abeta) in extracellular deposits known as senile plaques. However, the nature of the toxic Abeta species and its precise mechanism of action remain unclear. Previous reports suggest that the histidine residues are involved in copper-Abeta interaction, by which resulting in the neurotoxicity of Abeta and free radical damage. Here, we employed a mutant Abeta (Abeta H13R) in which a histidine residue was replaced by arginine. Copper facilitated the precipitation of both wild-type and mutant Abeta in the spectrophotometric absorbance assay but suppressed beta-structure aggregates according to Thioflavine-T assay. Wild-type Abeta alone is more cytotoxic but produced less amount of H(2)O(2) than AbetaH13R-copper complexes, suggesting that Abeta-membrane interaction may also implicated in the pathologic progress. Abeta toxicity is in positive correlation to its competence to aggregate despite the aggregation is mainly composed of non-beta fibril substances. In short, these findings may provide further evidence on the role of copper in the pathogenesis of Alzheimer's disease.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.