Mechanistic Insights and Therapeutic Perspectives of Bisphenol A-induced CNS Dysfunction – A Review

Abstract

Introduction - Bisphenol A (BPA) is a common disruptor linked to neurological and neurodevelopmental consequences. It infiltrates our everyday lives more often than we think, from plastics to food packaging. Long-term exposure studies continue to correlate longer exposure to mood swings, cognitive issues, and an increased risk of neurodegenerative diseases.

Methods - Bioactive substances, such as polyphenols, flavonoids, alkaloids, terpenoids, and carotenoids, can provide us with a shield of anti-inflammatory and antioxidant properties, balance cell survival and death, promote neurogenesis, and even repair through epigenetic regulation. This review focuses on recent in-vitro and in-vivo research to investigate the true role of bioactive phytochemicals in an effort against BPA-induced brain damage. Major scientific databases, such as PubMed, Scopus, ScienceDirect, and Google Scholar, were used to perform a thorough literature search.

Result - Mitochondrial failure, oxidative stress, glial cell activation, neuroinflammation, disruption of neurotransmitter systems, anomalies in epigenetic, endocrine signalling, and synaptic plasticity are some of the molecular pathways that bioactive compounds can target. Bioactive compounds offer a promising therapeutic alternative for correcting BPA-induced CNS damage due to their accessibility, pleiotropic modes of action, and generally good safety profiles.

Discussion - The pleiotropy and possible widespread number of critical pathways that BPA interferes with are inflammation, oxidative stress, synaptic signalling, and epigenetic control. Thus, the phytoconstituents are a new health sector to target BPA-induced neurotoxicity.

Conclusion - Most bioactive substances have demonstrated a safety record, particularly when consumed through food, which reduces barriers to long-term or preventive use. When considered as a whole, these characteristics make bioactive chemicals appealing for research as inexpensive and versatile mitigators of BPA-associated neurotoxicity.