ReviewInternational journal of molecular sciences2021
Redox-Active Metal Ions and Amyloid-Degrading Enzymes in Alzheimer's Disease.
Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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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
28 citing papers in PubMed, 59 citations in OpenAlex.
- High-ResolutionMolecules (Basel, Switzerland) · 2025Article
- Advances of therapeutic strategies for Alzheimer's disease.Journal of neurology · 2025Review
- Signal Transduction Strategies for DNAzyme-Based Sensing and Imaging of Metal Ions in Cells andChemical & biomedical imaging · 2025Review
- Article
- Multi-target-directed therapeutic strategies for Alzheimer's disease: controlling amyloid-β aggregation, metal ion homeostasis, and enzyme inhibition.Chemical science · 2025Review
- Reinforcing Nrf2 Signaling: Help in the Alzheimer's Disease Context.International journal of molecular sciences · 2025Review
- Insights into targeted ferroptosis in mechanisms, biology, and role of Alzheimer's disease: an update.Frontiers in aging neuroscience · 2025Review
- Predicting cellular adaptation proteins dependent on eIF2α regulation under stress conditions: Physiological and pathophysiological implications in neuronal function.Computational and structural biotechnology journal · 2025Article
- From copper homeostasis to cuproptosis: a new perspective on CNS immune regulation and neurodegenerative diseases.Frontiers in neurology · 2025Review
- Yttrium Oxide Nanoparticles Affect Both Cognitive and Memory Function by Disrupting Copper Output in Neuronal Cells in a Rat Model.International journal of nanomedicine · 2025Article
- Recent advances in potential enzymes and their therapeutic inhibitors for the treatment of Alzheimer's disease.Heliyon · 2024Review
- Modulation of Urea Transport Attenuates TLR2-Mediated Microglial Activation and Upregulates Microglial Metabolism In Vitro.Metabolites · 2024Article
- α-Tocotrienol Protects Neurons by Preventing Tau Hyperphosphorylation via Inhibiting Microtubule Affinity-Regulating Kinase Activation.International journal of molecular sciences · 2024Article
- Lithium carbonate revitalizes tumor-reactive CD8Nature immunology · 2024Article
- Systems pharmacology and multi-scale mechanism of Enicostema axillare bioactives in treating Alzheimer disease.Inflammopharmacology · 2024Article
- The Role of Ion-Transporting Proteins in Human Disease.International journal of molecular sciences · 2024Article
- Advancements in Portable Voltammetry: A Promising Approach for Iron Speciation Analysis.Molecules (Basel, Switzerland) · 2023Article
- Sulfur-bridging the gap: investigating the electrochemistry of novel copper chelating agents for Alzheimer's disease applications.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2023Article
- Metal Nanomaterials and Hydrolytic Enzyme-Based Formulations for Improved Antifungal Activity.International journal of molecular sciences · 2023Review
- Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Redox-active metal ions, Cu(I/II) and Fe(II/III), are essential biological molecules for the normal functioning of the brain, including oxidative metabolism, synaptic plasticity, myelination, and generation of neurotransmitters. Dyshomeostasis of these redox-active metal ions in the brain could cause Alzheimer's disease (AD). Thus, regulating the levels of Cu(I/II) and Fe(II/III) is necessary for normal brain function. To control the amounts of metal ions in the brain and understand the involvement of Cu(I/II) and Fe(II/III) in the pathogenesis of AD, many chemical agents have been developed. In addition, since toxic aggregates of amyloid-β (Aβ) have been proposed as one of the major causes of the disease, the mechanism of clearing Aβ is also required to be investigated to reveal the etiology of AD clearly. Multiple metalloenzymes (e.g., neprilysin, insulin-degrading enzyme, and ADAM10) have been reported to have an important role in the degradation of Aβ in the brain. These amyloid degrading enzymes (ADE) could interact with redox-active metal ions and affect the pathogenesis of AD. In this review, we introduce and summarize the roles, distributions, and transportations of Cu(I/II) and Fe(II/III), along with previously invented chelators, and the structures and functions of ADE in the brain, as well as their interrelationships.
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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.