Linking Environmental Chemicals to Neuroinflammation and Autism Spectrum Disorder: Mechanisms and Implications for Prevention.
Geir BjørklundMeri MkhitaryanElen SahakyanKatarine FereshetyanNagwa A MeguidMaha HemimiNeveen Hassan NashaatKonstantin YenkoyanPublished in: Molecular neurobiology (2024)
This article explores the potential link between endocrine-disrupting chemicals (EDCs), neuroinflammation, and the development of autism spectrum disorder (ASD). Neuroinflammation refers to the immune system's response to injury, infection, or disease in the central nervous system. Studies have shown that exposure to EDCs, such as bisphenol A and phthalates, can disrupt normal immune function in the brain, leading to chronic or excessive neuroinflammation. This disruption of immune function can contribute to developing neurological disorders, including ASD. Furthermore, EDCs may activate microglia, increasing pro-inflammatory cytokine production and astroglia-mediated oxidative stress, exacerbating neuroinflammation. EDCs may also modulate the epigenetic profile of cells by methyltransferase expression, thereby affecting neurodevelopment. This article also highlights the importance of reducing exposure to EDCs and advocating for policies and regulations restricting their use. Further research is needed to understand better the mechanisms underlying the link between EDCs, neuroinflammation, and ASD and to develop new treatments for ASD.
Keyphrases
- autism spectrum disorder
- lipopolysaccharide induced
- cerebral ischemia
- lps induced
- traumatic brain injury
- attention deficit hyperactivity disorder
- intellectual disability
- cognitive impairment
- inflammatory response
- oxidative stress
- induced apoptosis
- subarachnoid hemorrhage
- dna methylation
- blood brain barrier
- white matter
- poor prognosis
- gene expression
- brain injury
- physical activity
- human health
- risk assessment
- resting state
- cell cycle arrest
- spinal cord injury
- cell death
- functional connectivity
- working memory
- ischemia reperfusion injury
- binding protein
- heat shock protein
- neuropathic pain