ArticleMolecular neurobiology2025
Copper Mitigates Atrazine-Induced Neurotoxicity in Parkinson's Disease Models.
Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pesticide exposure and the development of Parkinson disease: a systematic review of Brazilian studies.Cadernos de saude publica · 2025Pooled it
- Cuproptosis: New Mechanisms Linking Endothelial Dysfunction to Neurodegenerative Diseases and Therapeutic Prospects.International journal of molecular sciences · 2026Review
- Anthraquinone-based turn-on fluorescence probe for selective and sensitive detection of CuFrontiers in chemistry · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Atrazine (ATR), one of the most prevalent herbicides used worldwide, has been associated with various environmental health concerns, including its potential role in promoting neurodegenerative diseases. Considering the pivotal role of metal homeostasis in the pathophysiology of neurodegenerative disorders, this study investigated the neuroprotective effects of copper supplementation in mitigating the adverse impacts of ATR in Parkinson's disease (PD). Our results reveal that ATR exposure disrupts copper and iron homeostasis within the substantia nigra pars compacta (SNpc), leading to enhanced oxidative stress and dopaminergic neuronal degeneration, which are key features of PD pathology. Remarkably, copper supplementation is able to counteract these neurotoxic effects, as demonstrated by the restoration of metal equilibrium in the SNpc, decreased lipid peroxidation, and improvements in motor function in PD rats. These results highlight the intricate relationship between environmental toxins and metal homeostasis in the genesis of neurodegenerative diseases.
Indexed as
Identifiers
39527184What 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.