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.

β- N-甲基氨基-l-丙氨酸 (BMAA) 是一种由蓝藻产生的非蛋白氨基酸，与多种神经退行性疾病有关，包括肌萎缩侧索硬化症 (ALS)。据推测，长期接触 BMAA 可导致蛋白质聚集体、氧化应激和/或兴奋性毒性的形成，这些是 ALS 病因学中涉及的机制。虽然在某些 ALS 病例中发现了特定的基因突变，但遗传和环境因素（例如接触神经毒素 BMAA）的结合可能会导致疾病。我们使用带有 ALS 相关突变的转基因斑马鱼与野生型鱼进行比较，以探索 BMAA 通过长期长期暴露而产生的潜在神经毒性作用。虽然我们的结果显示暴露鱼类大脑中的 BMAA 浓度较低，但我们没有发现游泳能力下降或可能反映神经退行性疾病的行为差异的证据。需要进一步的研究来确定成年斑马鱼的慢性 BMAA 暴露是否是研究神经退行性疾病发生和/或进展的合适模型。