ReviewOxidative medicine and cellular longevity2014
Copper and copper proteins in Parkinson's disease.
Review in Oxidative medicine and cellular longevity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 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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Who cites it
92 citing papers in PubMed, 194 citations in OpenAlex.
- ATOX1 overexpression mitigates copper homeostasis in microglia: Implications for Alzheimer's disease therapy.Genes & diseases · 2026Article
- Plasma Copper and Zinc Levels in Ataxia-Telangiectasia.International journal of molecular sciences · 2026Article
- Targeting mGluR1-Mediated Microglial ER Stress Mitigates Copper-Induced TBI Neuroinflammation.Molecular neurobiology · 2026Article
- Exploring and Targeting the Connection of Iron and Copper Homeostasis to Neurodegenerative Diseases.MedComm · 2026Review
- Copper Overload Affects α-Synuclein Clearance Mechanisms in a Parkinson's Disease In Vitro Model.Advanced biology · 2026Article
- Copper Dyshomeostasis Affects α-Synuclein Clearance Mechanisms in Parkinson's Disease: Insights from In Vitro Models and Translational Evidence.International journal of molecular sciences · 2026Review
- From General-Purpose to Disease-Specific Features: Aligning LLM Embeddings on a Disease-Specific Biomedical Knowledge Graph for Drug Repurposing.bioRxiv : the preprint server for biology · 2026Article
- Copper restriction unmasks axonal degeneration in a mouse model of X-linked hereditary motor neuropathy.Metallomics : integrated biometal science · 2026Article
- Metallothioneins in Neurodegenerative Diseases: Metal Homeostasis, Autoimmunity, and Therapeutic Potential.Molecular neurobiology · 2026Review
- Agricultural Copper Pesticide Exposure and Metabolic Profiles among Parkinson's Disease Cases and Community Controls in California.Chemical research in toxicology · 2026Article
- Metal ion dyshomeostasis in neurological disorders: from pathological mechanisms to targeted neuroprotective and regenerative strategies.Frontiers in pharmacology · 2026Review
- Human CTR1 Through the Ages: Milestones and Emerging Roles in Disease and Therapy.Biomolecules · 2025Review
- Agricultural copper pesticide exposure and DNA methylation in Central Valley of California residents with and without Parkinson's disease.Environmental research · 2025Article
- Copper regulates the expression of immune genes in microglial cells in vitro.Immunobiology · 2025Article
- Isolation and comprehensive characterization of a bioactive compound fromRSC advances · 2025Article
- A Design of Copper(II) Coordination Polymers with l‑Homoserine: Structural, Spectroscopic, and Biological Studies.ACS omega · 2025Article
- Linking Parkinson's disease and melanoma: the impact of copper-driven cuproptosis and related mechanisms.NPJ Parkinson's disease · 2025Article
- L-Theanine Effectively Protects Against Copper-Facilitated Dopamine Oxidation: Implication for Relieving Dopamine Overflow-Associated Neurotoxicities.Molecular neurobiology · 2025Article
- Cuproptosis-related genes associated with mitochondrial dysfunction in Parkinson's disease.PloS one · 2025Article
- Identification of copper metabolism-related markers in Parkinson's disease.Annals of medicine · 2024Article
32 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Copper is a transition metal that has been linked to pathological and beneficial effects in neurodegenerative diseases. In Parkinson's disease, free copper is related to increased oxidative stress, alpha-synuclein oligomerization, and Lewy body formation. Decreased copper along with increased iron has been found in substantia nigra and caudate nucleus of Parkinson's disease patients. Copper influences iron content in the brain through ferroxidase ceruloplasmin activity; therefore decreased protein-bound copper in brain may enhance iron accumulation and the associated oxidative stress. The function of other copper-binding proteins such as Cu/Zn-SOD and metallothioneins is also beneficial to prevent neurodegeneration. Copper may regulate neurotransmission since it is released after neuronal stimulus and the metal is able to modulate the function of NMDA and GABA A receptors. Some of the proteins involved in copper transport are the transporters CTR1, ATP7A, and ATP7B and the chaperone ATOX1. There is limited information about the role of those biomolecules in the pathophysiology of Parkinson's disease; for instance, it is known that CTR1 is decreased in substantia nigra pars compacta in Parkinson's disease and that a mutation in ATP7B could be associated with Parkinson's disease. Regarding copper-related therapies, copper supplementation can represent a plausible alternative, while copper chelation may even aggravate the pathology.
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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.