ReviewFrontiers in aging neuroscience2023
Copper and cuproptosis: new therapeutic approaches for Alzheimer's disease.
Review in Frontiers in aging neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 34 citations in OpenAlex.
- Cuproptosis Inhibition by C-Phycocyanin Confers Neuroprotection against Copper-Induced Mitochondrial Damage and Cognitive Impairment.Molecular neurobiology · 2026Article
- Simultaneous Imaging of CuAngewandte Chemie (International ed. in English) · 2026Article
- ZNF384-regulated SLC31A1 expression promotes tumor proliferation and invasion in breast cancer.Molecular and cellular biochemistry · 2026Article
- Mechanistic Investigation of TSPO-Mediated Dysregulation of Mitochondrial Copper Homeostasis in Microglia and its Role in Perioperative Neurocognitive Disorders.Molecular neurobiology · 2026Article
- Musculoskeletal disorders: does cuproptosis hold the key?Frontiers in cell and developmental biology · 2026Review
- Design, Synthesis, Biological Evaluation and Docking Studies of 2-hydroxy-4-benzyloxy Chalcone Derivatives as Multifunctional Agents for the Treatment of Alzheimer's Disease.Current medicinal chemistry · 2026Article
- Nuclear accumulation of PANK4 in hippocampal astrocytes aggravates cuproptosis in association with mild cognitive impairment in aged mice.Frontiers in aging neuroscience · 2026Article
- Redox Network Dysfunction: Integrating Ferroptosis and Cuproptosis Across Human Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- Copper homeostasis and cuproptosis in Alzheimer's disease (Review).International journal of molecular medicine · 2025Review
- Integrating cuproptosis and immunosenescence: A novel therapeutic strategy in cancer treatment.Biochemistry and biophysics reports · 2025Review
- Polystyrene nanoplastics exposure induces cognitive impairment in mice via induction of oxidative stress and ERK/MAPK-mediated neuronal cuproptosis.Particle and fibre toxicology · 2025Article
- Disruption of Copper Redox Balance and Dysfunction underEnvironment & health (Washington, D.C.) · 2025Article
- The emerging role of cuproptosis in spinal cord injury.Frontiers in immunology · 2025Review
- The role of cuproptosis in the occurrence and development of gastric cancer.Frontiers in pharmacology · 2025Review
- Programmed cell death signatures-driven microglial transformation in Alzheimer's disease: single-cell transcriptomics and functional validation.Frontiers in immunology · 2025Article
- Deuterium trafficking, mitochondrial dysfunction, copper homeostasis, and neurodegenerative disease.Frontiers in molecular biosciences · 2025Review
- BubR1 and SIRT2: Insights into aneuploidy, aging, and cancer.Seminars in cancer biology · 2024Review
- Cuproptosis and Cu: a new paradigm in cellular death and their role in non-cancerous diseases.Apoptosis : an international journal on programmed cell death · 2024Review
- Editorial Commentary: Copper Homeostasis in Neurodegenerative Diseases.Current medical science · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Copper (Cu) plays a crucial role as a trace element in various physiological processes in humans. Nonetheless, free copper ions accumulate in the brain over time, resulting in a range of pathological changes. Compelling evidence indicates that excessive free copper deposition contributes to cognitive decline in individuals with Alzheimer's disease (AD). Free copper levels in the serum and brain of AD patients are notably elevated, leading to reduced antioxidant defenses and mitochondrial dysfunction. Moreover, free copper accumulation triggers a specific form of cell death, namely copper-dependent cell death (cuproptosis). This article aimed to review the correlation between copper dysregulation and the pathogenesis of AD, along with the primary pathways regulating copper homoeostasis and copper-induced death in AD. Additionally, the efficacy and safety of natural and synthetic agents, including copper chelators, lipid peroxidation inhibitors, and antioxidants, were examined. These treatments can restore copper equilibrium and prevent copper-induced cell death in AD cases. Another aim of this review was to highlight the significance of copper dysregulation and promote the development of pharmaceutical interventions to address it.
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.