Role of metallic pollutants in neurodegeneration: effects of aluminum, lead, mercury, and arsenic in mediating brain impairment events and autism spectrum disorder.
Ishnoor KaurTarapati RanaLotfi AleyaMd Habibur RahmanArun KumarSandeep AroraRokeya AkterPublished in: Environmental science and pollution research international (2021)
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.
Keyphrases
- autism spectrum disorder
- attention deficit hyperactivity disorder
- intellectual disability
- oxidative stress
- heavy metals
- drinking water
- mental health
- resting state
- healthcare
- white matter
- cell death
- risk factors
- human health
- dna damage
- working memory
- risk assessment
- anti inflammatory
- functional connectivity
- lipopolysaccharide induced
- spinal cord injury
- sleep quality
- spinal cord
- induced apoptosis
- heat stress
- health risk assessment
- life cycle
- congenital heart disease