article · Neuroglia
Human overexposure to both heavy and essential metals presents a major hazard for neurodevelopmental and neurological disorders. Toxic metals, including nickel, manganese, methyl mercury, cadmium, iron, arsenic, and lead, harm brain health through mitochondrial dysfunction, reactive oxygen species generation, cellular signalling disruption, and inflammatory pathway activation. Glial cells, which include microglia, astrocytes, and oligodendrocytes, are essential for brain development and homeostasis but are exceptionally vulnerable to metal toxicity. The build-up of metals triggers microglial activation and neuroinflammation, leading to impaired synaptic transmission, cognitive deficits, and nerve cell damage. Understanding these glial perturbations clarifies the mechanisms driving specific neurodegenerative and neurodevelopmental conditions. Potential interventions to alleviate these effects include antioxidant treatments and newly developed, improved metal chelating agents.
Exposure to environmental metals poses widespread risks to brain health across all stages of life. By detailing how toxic metals disrupt vital supporting brain cells and trigger damaging inflammation, this research clarifies the biological roots of cognitive decline and developmental disorders. This understanding helps guide the search for protective treatments.
This work points towards therapeutic applications, specifically the development of improved chelating agents and antioxidant therapies for treating metal-induced neurological damage. The primary users would be pharmaceutical and biotechnology developers targeting neurodegenerative conditions. Because the findings are drawn from a mechanistic review, the research represents an early discovery stage that requires significant preclinical development before real-world clinical use.
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Overexposure of humans to heavy metals and essential metals poses a significant risk for the development of neurological and neurodevelopmental disorders. The mechanisms through which these metals exert their effects include the generation of reactive oxygen species, mitochondrial dysfunction, activation of inflammatory pathways, and disruption of cellular signaling. The function of glial cells in brain development and in the maintenance of homeostasis cannot be overlooked. The glial cells are particularly susceptible to metal-induced neurotoxicity. Accumulation of metals in the brain promotes microglial activation, triggering inflammatory responses that can coincide with other mechanisms of neurotoxicity, inducing alteration in synaptic transmission, cognitive deficit, and neuronal damage. In this review, we highlighted the role of glial dysfunction in some selected neurodegenerative diseases and neurodevelopmental disorders. We further dive into how exposure to metals such as nickel, manganese, methyl mercury, cadmium, iron, arsenic, and lead affect the functions of the microglia, astrocytes, and oligodendrocytes and the mechanisms through which they exert the effects on the brain in relation to some selected neurodegenerative diseases and neurodevelopmental disorders. Potential therapeutic interventions such as the use of new and improved chelating agents and antioxidant therapies might be a significant approach to alleviating these metal-induced glial perturbations.
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DOI: 10.3390/neuroglia6010004
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