Investigation of BMAA Modulation of Aβ-mediated Neurodegeneration in Transgenic Caenorhabditis elegans

β-N-methylamino-L-alanine (BMAA) is a nonprotein amino acid and neurotoxin originally isolated from seeds of a cycad plant in Guam and produced by blue-green algae or cyanobacteria. BMAA has also been shown to bioaccumulate through food chains. Alzheimer’s disease (AD) is a progressive neurological disorder characterized by the deposition of amyloid beta (Aβ) in the brain. Recent studies suggest that chronic exposure to BMAA might trigger neurodegenerative diseases in susceptible individuals, including AD. In this study, we aim to examine the potential neurotoxic modulation of BMAA on Aβ-mediated neurodegeneration in transgenic Caenorhabditis elegans. We propose to utilize a C. elegans AD strain with pan-neuronal human Aβ1-42 expression that displays neuromuscular defects, shortened lifespan, and age-dependent behavioral dysfunction. Neuromuscular function and lifespan will be measured utilizing a thrashing assay (n = 20 per group) and solid agar lifespan assay (n = 100 per group). Experimental groups will include N2 wildtype control, transgenic Aβ1-42 expressing strain, and the transgenic control. Each experimental group will be treated with BMAA or vehicle control. This study proposes to gain more insight into the effect of BMAA on Aβ-mediated neurodegeneration in a C. elegans AD model. It is important to begin to unravel and understand the potential impact of environmental toxins on complex neurological disorders.https://digitalcommons.jsu.edu/ce_jsustudentsymp_2023/1054/thumbnail.jp