Open Access
ISSN: 3107-1015 (Online)
3107-1007 (Print)
Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan 430072, China
β-N-methylamino-L-alanine (BMAA), a non-proteinogenic amino acid produced by various cyanobacteria, has emerged as a significant concern in the context of the One Health framework due to its neurotoxic effects and potential ecological and public health implications. Cyanobacteria, found ubiquitously in freshwater, marine, and terrestrial environments, can contaminate water sources and food chains with different toxins, including BMAA, which can produce a sinergic action with other environmental neurotoxic contaminants (such as Methylmercury) and other cyanotoxins, such as Microcystins. Human exposure occurs primarily through the consumption of contaminated drinking water and aquatic food products. BMAA accumulation in neural tissues has been linked to the degeneration of motor neurons and the formation of neurofibrillary tangles, mimicking pathological features observed in amyotrophic lateral sclerosis (ALS) and Alzheimer’s disease. This exposure is associated with a spectrum of symptoms, collectively termed ALS/parkinsonism dementia complex (ALS/PDC), characterized by progressive muscular paralysis, rigidity, cognitive decline, and ultimately, fatal outcomes. The increasing prevalence of cyanobacteria blooms, driven by climate change and anthropogenic factors, underscores the urgent need for comprehensive research into BMAA toxicity, environmental monitoring, and mitigation strategies. This work shows BMAA contamination data of fish fauna living in several Italian lakes affected by recurrent cyanobacterial blooms, quantified by Elisa Assay. It also explores the emerging issue of BMAA contamination from a One Health perspective, highlighting its multifaceted impact on ecosystems, animal health, and human well-being.
β-N-methylamino-L-alanine (BMAA), a non-proteinogenic amino acid produced by various cyanobacteria, has emerged as a significant concern in the context of the One Health framework due to its neurotoxic effects and potential ecological and public health implications. Cyanobacteria, found ubiquitously in freshwater, marine, and terrestrial environments, can contaminate water sources and food chains with different toxins, including BMAA, which can produce a sinergic action with other environmental neurotoxic contaminants (such as Methylmercury) and other cyanotoxins, such as Microcystins. Human exposure occurs primarily through the consumption of contaminated drinking water and aquatic food products. BMAA accumulation in neural tissues has been linked to the degeneration of motor neurons and the formation of neurofibrillary tangles, mimicking pathological features observed in amyotrophic lateral sclerosis (ALS) and Alzheimer’s disease. This exposure is associated with a spectrum of symptoms, collectively termed ALS/parkinsonism dementia complex (ALS/PDC), characterized by progressive muscular paralysis, rigidity, cognitive decline, and ultimately, fatal outcomes. The increasing prevalence of cyanobacteria blooms, driven by climate change and anthropogenic factors, underscores the urgent need for comprehensive research into BMAA toxicity, environmental monitoring, and mitigation strategies. This work shows BMAA contamination data of fish fauna living in several Italian lakes affected by recurrent cyanobacterial blooms, quantified by Elisa Assay. It also explores the emerging issue of BMAA contamination from a One Health perspective, highlighting its multifaceted impact on ecosystems, animal health, and human well-being.
β-N-methylamino-L-alanine (BMAA), a non-proteinogenic amino acid produced by various cyanobacteria, has emerged as a significant concern in the context of the One Health framework due to its neurotoxic effects and potential ecological and public health implications. Cyanobacteria, found ubiquitously in freshwater, marine, and terrestrial environments, can contaminate water sources and food chains with different toxins, including BMAA, which can produce a sinergic action with other environmental neurotoxic contaminants (such as Methylmercury) and other cyanotoxins, such as Microcystins. Human exposure occurs primarily through the consumption of contaminated drinking water and aquatic food products. BMAA accumulation in neural tissues has been linked to the degeneration of motor neurons and the formation of neurofibrillary tangles, mimicking pathological features observed in amyotrophic lateral sclerosis (ALS) and Alzheimer’s disease. This exposure is associated with a spectrum of symptoms, collectively termed ALS/parkinsonism dementia complex (ALS/PDC), characterized by progressive muscular paralysis, rigidity, cognitive decline, and ultimately, fatal outcomes. The increasing prevalence of cyanobacteria blooms, driven by climate change and anthropogenic factors, underscores the urgent need for comprehensive research into BMAA toxicity, environmental monitoring, and mitigation strategies. This work shows BMAA contamination data of fish fauna living in several Italian lakes affected by recurrent cyanobacterial blooms, quantified by Elisa Assay. It also explores the emerging issue of BMAA contamination from a One Health perspective, highlighting its multifaceted impact on ecosystems, animal health, and human well-being.utf-8