The Effects of Environmental Toxin Atrazine Exposure in Danio rerio: a Novel Pollutant that may promote the Pathogenesis of Alzheimer's Disease
Atrazine is one of the most prominent herbicides and environmental toxins in the world and is a member of the triazine class of herbicides. An estimated 82 million pounds of Atrazine is used in the US annually, and literature research suggests that the current wastewater treatment facilities are unable to efficiently remove it. Alzheimer’s Disease (AD) is a neurodegenerative disease that is characterized by a buildup of toxic amyloid-beta plaques and tangles of hyperphosphorylated tau protein in the brain. Several key pro-and anti-Alzheimer’s Disease genes have been shown to be involved in the pathogenesis of this disease, including AKT1s1, APOE, APPb, BACE1, BASP1, EPHA2, GSK3Aa, GSK3B, LEPR, NOTCH1a, SNCb, ARID5b, BIN1, CD2AP, COX1, MYO5Ab, PICALMa, PLD3, and TOMM40.Atrazine’s effects on these known mediators of AD were analyzed using bioinformatics technology and analysis at 0 ppb, 0.3 ppb, 3.0 ppb, and 30 ppb (n=6). The gene expression profiles of the GSE72243 dataset were obtained from the Gene Expression Omnibus (GEO) database. Selected genes were then analyzed and graphed via Genespring 14.5 and Microsoft Excel. Significant dysregulation of the expression of both pro-and anti-Alzheimer’s Disease genes was observed in the male Zebrafish brain. APPb, BACE1, EPHA2, GSK3B, LEPR, NOTCH1a, and SNCb were significantly upregulated, while ARID5b, BIN1, CD2AP, MYO5Ab, and PLD3 were significantly downregulated. Our results suggest that Atrazine promotes the buildup of toxic amyloid-beta plaques and tangles of tau proteins in male zebrafish brain cells. In sum, Atrazine appears to increase the risk of developing Alzheimer’s Disease by increasing toxic amyloid-beta protein production and spread, increasing tau phosphorylation, allowing pathogens to enter the brain by weakening the blood-brain barrier (BBB), and weakening members of the peripheral blood lymphocyte (PBL) family that would otherwise suppress the development of AD.
Keywords: Atrazine; Alzheimer’s Disease (AD); environmental toxins; herbicides; neurodegenerative disease; blood-brain barrier (BBB); water filtration.