Role of metallic pollutants in neurodegeneration: effects of aluminum, lead, mercury, and arsenic in mediating brain impairment events and autism spectrum disorder

Autism spectrum disorder (ASD) is a developmental disorder of the brain characterized by shortfall in the social portfolio of an individual and abbreviated interactive and communication aspects rendering stereotypical behavior and pitfalls in a child’s memory, thinking, and learning capabilities. Th...

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Veröffentlicht in:Environmental science and pollution research international 2021-02, Vol.28 (8), p.8989-9001
Hauptverfasser: Kaur, Ishnoor, Behl, Tapan, Aleya, Lotfi, Rahman, Md. Habibur, Kumar, Arun, Arora, Sandeep, Akter, Rokeya
Format: Artikel
Sprache:eng
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Zusammenfassung:Autism spectrum disorder (ASD) is a developmental disorder of the brain characterized by shortfall in the social portfolio of an individual and abbreviated interactive and communication aspects rendering stereotypical behavior and pitfalls in a child’s memory, thinking, and learning capabilities. The incidence of ASD has accelerated since the past decade, portraying environment as one of the primary assets, comprising of metallic components aiming to curb the neurodevelopmental pathways in an individual. Many regulations like Clean Air Act and critical steps taken by countries all over the globe, like Sweden and the USA, have rendered the necessity to study the effects of environmental metallic components on ASD progression. The review focuses on the primary metallic components present in the environment (aluminum, lead, mercury, and arsenic), responsible for accelerating ASD symptoms by a set of general mechanisms like oxidative stress reduction, glycolysis suppression, microglial activation, and metalloprotein disruption, resulting in apoptotic signaling, neurotoxic effects, and neuroinflammatory responses. The effect of these metals can be retarded by certain protective strategies like chelation, dietary correction, certain agents (curcumin, mangiferin, selenium), and detoxification enhancement, which can necessarily halt the neurodegenerative effects. Graphical abstract
ISSN:0944-1344
1614-7499
DOI:10.1007/s11356-020-12255-0