book chapter
Aluminum is an abundant environmental contaminant that accumulates progressively in brain tissue and contributes to major neurodegenerative disorders. Its neurotoxicity manifests across several interconnected biological mechanisms. The metal induces oxidative stress, neuroinflammation, and inflammasome engagement, while also disrupting the blood-brain barrier and impairing the ubiquitin-proteasome system. Furthermore, it promotes pathological hallmarks such as amyloid-beta fibril formation, tau protein hyperphosphorylation, and alpha-synuclein aggregation, alongside dysregulating the epigenetic expression of protective genes. To counter these damaging mechanisms, potential therapeutic approaches include metal chelation, phytochemical neuroprotection, and silicon enrichment. Addressing the challenges associated with aluminum neurotoxicity will depend on establishing evidence-based regulatory standards, promoting targeted research initiatives, and conducting further robust investigations into the neurological consequences of exposure.
Environmental exposure to aluminum represents a widespread risk factor for progressive neurological decline. Understanding how this pervasive metal triggers cellular inflammation and accelerates pathological protein aggregation is critical for biomedical researchers and public health authorities. These insights highlight the importance of establishing stronger safety regulations and developing targeted therapeutic strategies to mitigate the biological damage caused by heavy metal accumulation.
The identified pathways point towards early-stage opportunities in therapeutic development, particularly for pharmaceutical and nutraceutical developers investigating chelation compounds, silicon-enriched formulations, or protective phytochemicals. Because the findings describe broad biological mechanisms and general treatment concepts rather than specific proprietary molecules or clinical protocols, practical commercial applications remain distant from real-world use and will require substantial preclinical testing, formulation design, and regulatory validation.
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Aluminum is the most abundant metal in the earth's crust and a potent environmental contaminant. Aluminum accumulates progressively in the brain and is implicated in the pathogenesis of several major neurodegenerative disorders. This chapter explores mechanistic data, epidemiological evidence, and neurological findings to understand the role of aluminum in neurodegenerative disorders. At the mechanistic level, aluminum is neurotoxic through a convergence of pathways: induction of oxidative stress, neuroinflammation, and inflammasome engagement; thus, promoting amyloid-β fibrilization and hyperphosphorylation of tau; α-synuclein aggregation; impaired ubiquitin-proteasome system; blood-brain barrier disruption and dysregulation of epigenetics of neuroprotective gene expression. The chapter highlights the therapeutic strategies, including chelation, phytochemical neuroprotection, and silicon enrichment. In conclusion, evidence-based regulatory and research promotion, and further reputable studies on the role of aluminum in neurodegenerative disorders are necessary.
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DOI: 10.4018/979-8-2600-1403-5.ch007
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