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08.08.2023 | Research

The Effects of Long-term, Low-dose β-N-methylamino-l-alanine (BMAA) Exposures in Adult SODG93R Transgenic Zebrafish

verfasst von: Ryan D. Weeks, Sandra A. Banack, Shaunacee Howell, Preethi Thunga, James S. Metcalf, Adrian J. Green, Paul A. Cox, Antonio Planchart

Erschienen in: Neurotoxicity Research | Ausgabe 5/2023

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Abstract

β-N-Methylamino-l-alanine (BMAA) is a non-proteinogenic amino acid produced by cyanobacteria, which has been implicated in several neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS). It is postulated that chronic exposure to BMAA can lead to formation of protein aggregates, oxidative stress, and/or excitotoxicity, which are mechanisms involved in the etiology of ALS. While specific genetic mutations are identified in some instances of ALS, it is likely that a combination of genetic and environmental factors, such as exposure to the neurotoxin BMAA, contributes to disease. We used a transgenic zebrafish with an ALS-associated mutation, compared with wild-type fish to explore the potential neurotoxic effects of BMAA through chronic long-term exposures. While our results revealed low concentrations of BMAA in the brains of exposed fish, we found no evidence of decreased swim performance or behavioral differences that might be reflective of neurodegenerative disease. Further research is needed to determine if chronic BMAA exposure in adult zebrafish is a suitable model to study neurodegenerative disease initiation and/or progression.
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Metadaten
Titel
The Effects of Long-term, Low-dose β-N-methylamino-l-alanine (BMAA) Exposures in Adult SODG93R Transgenic Zebrafish
verfasst von
Ryan D. Weeks
Sandra A. Banack
Shaunacee Howell
Preethi Thunga
James S. Metcalf
Adrian J. Green
Paul A. Cox
Antonio Planchart
Publikationsdatum
08.08.2023
Verlag
Springer US
Erschienen in
Neurotoxicity Research / Ausgabe 5/2023
Print ISSN: 1029-8428
Elektronische ISSN: 1476-3524
DOI
https://doi.org/10.1007/s12640-023-00658-z

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