ORIGINAL RESEARCH article
Front. Toxicol.
Sec. In Vitro Toxicology
Volume 7 - 2025 | doi: 10.3389/ftox.2025.1578230
Toxicity of Glyphosate accelerates neurodegeneration in Caenorhabditis elegans model of Alzheimer's Disease
Provisionally accepted
- Jamia Hamdard University, New Delhi, India
Select one of your emails
You have multiple emails registered with Frontiers:
Notify me on publication
Please enter your email address:
If you already have an account, please login
You don't have a Frontiers account ? You can register here
Pesticide-related environmental contamination has emerged as a significant global issue, endangering human, wildlife, and vegetation health. N-phosphonomethyl-glycine, or GLY, is aherbicide commonly utilized worldwide. Due to being in the category of organophosphorus compounds, it is known for its neurotoxic effects. This study used a transgenic C. elegans Alzheimer's Disease (AD) model to examine the neurological effects of glyphosate. In the CL4176 (C. elegans) AD model, it has been demonstrated that glyphosate exacerbates amyloidbeta (1-42) toxicity through several mechanisms and due to these mechanisms, it includes increased lethality, behavioral changes, and elevated levels of amyloid-beta protein. Exposure to C. elegans at different glyphosate concentrations (12, 15, 18.5, 20, and 25mg/L) for 24 hours resulted in a concentration-dependent reduction of behavioral parameters such as body bend, head thrash, body length, and pharyngeal pumping.Furthermore glyphosate exposure at these concentrations increased oxidative stress, as evidenced by decreased catalase enzyme activity in the C. elegans AD model. Additionally, a significant increase in amyloid-beta(Aβ (1-42)) protein expression was observed in theC.elegans CL4176 AD strain treated with glyphosate. In conclusion, glyphosate appears to promote AD-like characteristics and warrants further investigation into its potential role in neurodegeneration.
Keywords: Caenorhabditis elegans, Alzheimer's disease, glyphosate, Behavioural toxicity, Amyloid beta
Received: 19 Feb 2025; Accepted: 26 May 2025.
Copyright: © 2025 Rani, Alam and Parvez. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Suhel Parvez, Jamia Hamdard University, New Delhi, India
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.