AI Article Synopsis
- Long-term manganese exposure can cause serious and lasting damage to the nervous system, especially affecting key pathways in brain regions associated with movement.
- Research using mice revealed that manganese disrupts a process called autophagy-lysosome function, leading to neurotoxicity and abnormal protein buildup in neurons.
- The study highlights the role of a protein called TFEB in this dysfunction, suggesting it could serve as an early marker for manganese exposure, helping in preventive measures and treatments for those at risk.
Article Abstract
Excessive long-term manganese intake can inflict irreversible damage to the nervous system, with a predominant effect on the substantia nigra-striatum pathway. Through a mouse model simulating manganese exposure, we delved into its implications on the central nervous motor system, uncovering autophagy-lysosome dysfunction as a pivotal factor in manganese-induced neurotoxicity. Our research illuminated the molecular mechanisms behind TFEB's role in manganese-triggered neuronal autophagy dysfunction, offering insights into the cellular and molecular mechanisms of manganese-induced abnormal protein accumulation. This study lays a significant theoretical foundation for future endeavors aimed at safeguarding against manganese neurotoxicity. Furthermore, TFEB emerges as a potential early molecular biomarker for manganese exposure, providing a solid basis for preemptive protection and clinical treatment for populations exposed to manganese.
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Source |
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11459403 | PMC |
| http://dx.doi.org/10.1016/j.crtox.2024.100193 | DOI Listing |
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