Ecotoxicological implications of environmental neurotoxin β-N-methylamino-L-alanine (BMAA) in fishes: An emerging concern

Harmful algal blooms (HABs), intensified by climate change, eutrophication, and altered hydrological regimes, are expanding globally, releasing cyanotoxins that threaten aquatic ecosystems and human health. β-N-methylamino-L-alanine (BMAA), a non-protein amino acid with neurotoxic potential, has been recognized as a global emerging concern. Following exposure, BMAA is present in both free and protein-bound forms, forming an endogenous toxin reservoir that exacerbates potential neurotoxicity in aquatic organisms and humans. Its presence in aquatic food webs not only elevates ecological risks for wildlife but also raises potential human health concerns, particularly its potential association with neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS), Alzheimer's disease, and the ALS/Parkinsonism-dementia complex. This review aims to explore current knowledge of the ecotoxicological impacts of BMAA in fishes, focusing on developmental, behavioural and cognitive perturbations, along with their mechanistic underpinnings. BMAA exposure induces developmental abnormalities, including convulsions, spinal axis malformations, pericardial edema, and altered heart rate, as well as neurodevelopmental impairments, such as reduced motor neuron length and altered neuromuscular colocalization in fishes. Additionally, BMAA exposure affects a wide array of behaviours in fishes, including motor coordination, locomotion, feeding, startle responses, anxiety-like behaviours, and cognitive performance, primarily through excitotoxicity, oxidative stress, apoptosis, metabolic disruption, neuroendocrine modulation, and dysregulated neurotransmitter signalling. Future research should focus on more environmentally relevant exposure scenarios, elucidating BMAA toxicokinetics, and investigating cyanotoxin co-exposure toxicity in fishes. Advancing integrative phenotypic endpoints and knowledge of molecular mechanisms of BMAA toxicity in aquatic organisms is essential for effective ecological risk assessments and for developing regulatory standards to safeguard aquatic ecosystems and human health.

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Journal
Ecotoxicology and Environmental Safety
Published
2026-05-12
DOI
https://doi.org/10.1016/j.ecoenv.2026.120252
Primary Topic
Amyotrophic Lateral Sclerosis Research
Type
article
Field-Weighted Citation Impact
0.00

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article

Ecotoxicological implications of environmental neurotoxin β-N-methylamino-L-alanine (BMAA) in fishes: An emerging concern

Jinnath Rehana Ritu, Maud C. O. Ferrari, Douglas P. Chivers, Md Kamal Uddin
Ecotoxicology and Environmental Safety
Amyotrophic Lateral Sclerosis Research
article

Ecotoxicological implications of environmental neurotoxin β-N-methylamino-L-alanine (BMAA) in fishes: An emerging concern

Jinnath Rehana Ritu, Maud C. O. Ferrari, Douglas P. Chivers, Md Kamal Uddin
article en

Abstract

Harmful algal blooms (HABs), intensified by climate change, eutrophication, and altered hydrological regimes, are expanding globally, releasing cyanotoxins that threaten aquatic ecosystems and human health. β-N-methylamino-L-alanine (BMAA), a non-protein amino acid with neurotoxic potential, has been recognized as a global emerging concern. Following exposure, BMAA is present in both free and protein-bound forms, forming an endogenous toxin reservoir that exacerbates potential neurotoxicity in aquatic organisms and humans. Its presence in aquatic food webs not only elevates ecological risks for wildlife but also raises potential human health concerns, particularly its potential association with neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS), Alzheimer's disease, and the ALS/Parkinsonism-dementia complex. This review aims to explore current knowledge of the ecotoxicological impacts of BMAA in fishes, focusing on developmental, behavioural and cognitive perturbations, along with their mechanistic underpinnings. BMAA exposure induces developmental abnormalities, including convulsions, spinal axis malformations, pericardial edema, and altered heart rate, as well as neurodevelopmental impairments, such as reduced motor neuron length and altered neuromuscular colocalization in fishes. Additionally, BMAA exposure affects a wide array of behaviours in fishes, including motor coordination, locomotion, feeding, startle responses, anxiety-like behaviours, and cognitive performance, primarily through excitotoxicity, oxidative stress, apoptosis, metabolic disruption, neuroendocrine modulation, and dysregulated neurotransmitter signalling. Future research should focus on more environmentally relevant exposure scenarios, elucidating BMAA toxicokinetics, and investigating cyanotoxin co-exposure toxicity in fishes. Advancing integrative phenotypic endpoints and knowledge of molecular mechanisms of BMAA toxicity in aquatic organisms is essential for effective ecological risk assessments and for developing regulatory standards to safeguard aquatic ecosystems and human health.

Ecotoxicology and Environmental SafetyVol. 318
University of Saskatchewan (CA)
Natural Sciences and Engineering Research Council of Canada
Life below water
Openalex Percentile: Top 7%
Amyotrophic Lateral Sclerosis Research
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