BPA AND NEUROTOXICITY: IMPLICATIONS FOR MENTAL HEALTH AND BEHAVIOR
Alina Khan*
ABSTRACT
The environmental endocrine disruptor bisphenol A (BPA) is pervasive and causes serious health concerns to people, especially when it comes to neurotoxicity. By attaching to estrogen receptors and interfering with thyroid hormone transmission, BPA mimics estrogen and disrupts neurodevelopmental processes such synaptogenesis, neurogenesis, and myelination. Additionally, it damages mitochondrial function, triggers oxidative stress by producing reactive oxygen species (ROS), and triggers neuroinflammation by activating microglia and releasing pro-inflammatory cytokines. These molecular abnormalities affect learning, memory, and behavior, and they may be a contributing factor to neurodevelopmental disorders including autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD). Long-lasting behavioral impairments are also brought on by epigenetic alterations brought on by BPA exposure, including as DNA methylation and histone modification, which alter gene expression and neuron function. The brain is more susceptible to neurotoxic compounds as a result of BPA exposure's weakening of the blood-brain barrier (BBB), which may hasten neurodegenerative processes and cognitive decline. In addition to highlighting the need for further study to fully comprehend the long-term consequences of BPA exposure on cognitive and emotional health across generations, this review also addresses the molecular pathways behind BPA-induced neurotoxicity and its implications for mental health.
Keywords: Bisphenol A (BPA); Neurotoxicity; Endocrine Disruptors; Cognitive Impairment; Oxidative Stress; Environmental Toxicology.
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