ReviewFrontiers in molecular neuroscience2020
The Role of Copper in Tau-Related Pathology in Alzheimer's Disease.
Review in Frontiers in molecular neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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.
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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.
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Who cites it
34 citing papers in PubMed.
- Review
- Copper oxide nanoparticles: from EU-regulatory landscape and mechanistic toxicity towards a cuproptosis-linked adverse outcome pathway.Archives of toxicology · 2026Review
- Metallothioneins in Neurodegenerative Diseases: Metal Homeostasis, Autoimmunity, and Therapeutic Potential.Molecular neurobiology · 2026Review
- Bifunctional BODIPY-Clioquinol Copper Chelator with Multiple Anti-AD Properties.International journal of molecular sciences · 2025Article
- Copper homeostasis and cuproptosis in Alzheimer's disease (Review).International journal of molecular medicine · 2025Review
- Post-mortem human Alzheimer´s brain metallome depends on Braak stages and brain regions.Scientific reports · 2025Article
- The role of estrogen in Alzheimer's disease pathogenesis and therapeutic potential in women.Molecular and cellular biochemistry · 2025Review
- Perturbations in levels of essential metals less severe in Parkinson's disease without dementia than in Parkinson's disease dementia.Metallomics : integrated biometal science · 2025Article
- Neurotoxic Effect of Myricitrin in Copper-Induced Oxidative Stress Is Mediated by Increased Intracellular CaAntioxidants (Basel, Switzerland) · 2025Article
- Copper homeostasis and cuproptosis: implications for neurodegenerative diseases.Frontiers in aging neuroscience · 2025Review
- Novel Insights Into DLAT's Role in Alzheimer's Disease-Related Copper Toxicity Through Microglial Exosome Dynamics.CNS neuroscience & therapeutics · 2024Article
- Royal Jelly: Biological Action and Health Benefits.International journal of molecular sciences · 2024Review
- Insights Into the Role of Copper in Neurodegenerative Diseases and the Therapeutic Potential of Natural Compounds.Current neuropharmacology · 2024Review
- MAD-microbial (origin of) Alzheimer's disease hypothesis: from infection and the antimicrobial response to disruption of key copper-based systems.Frontiers in neuroscience · 2024Review
- Aggregation, Transmission, and Toxicity of the Microtubule-Associated Protein Tau: A Complex Comprehension.International journal of molecular sciences · 2023Review
- Unveiling the Effects of Copper Ions in the Aggregation of Amyloidogenic Proteins.Molecules (Basel, Switzerland) · 2023Review
- Bioinorganic Chemistry of Micronutrients Related to Alzheimer's and Parkinson's Diseases.Molecules (Basel, Switzerland) · 2023Review
- PROTAC-Induced Glycogen Synthase Kinase 3β Degradation as a Potential Therapeutic Strategy for Alzheimer's Disease.ACS chemical neuroscience · 2023Article
- Metals in Alzheimer's Disease.Biomedicines · 2023Review
- Neuro-Nutraceutical Polyphenols: How Far Are We?Antioxidants (Basel, Switzerland) · 2023Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
All tauopathies, including Alzheimer's disease (AD), are characterized by the intracellular accumulation of abnormal forms of tau protein in neurons and glial cells, which negatively affect microtubule stability. Under physiological conditions, tubulin-associated unit (Tau) protein is intrinsically disordered, almost without secondary structure, and is not prone to aggregation. In AD, it assembles, and forms paired helical filaments (PHFs) that further build-up neurofibrillary tangles (NFTs). Aggregates are composed of hyperphosphorylated tau protein that is more prone to aggregation. The pathology of AD is also linked to disturbed copper homeostasis, which promotes oxidative stress (OS). Copper imbalance is widely observed in AD patients. Deregulated copper ions may initiate and exacerbate tau hyperphosphorylation and formation of β-sheet-rich tau fibrils that ultimately contribute to synaptic failure, neuronal death, and cognitive decline observed in AD patients. The present review summarizes factors affecting the process of tau aggregation, conformational changes of small peptide sequences in the microtubule-binding domain required for these motifs to act as seeding sites in aggregation, and the role of copper in OS induction, tau hyperphosphorylation and tau assembly. A better understanding of the various factors that affect tau aggregation under OS conditions may reveal new targets and novel pharmacological approaches for the therapy of AD.
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Registered trials
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