Production of the neurotoxin beta-N-methylamino-l-alanine may be triggered by agricultural nutrients: An emerging public health issue.

Diverse taxa of cyanobacteria, dinoflagellates and diatoms produce β-N-methylamino-l-alanine (BMAA), a non-lipophilic, non-protein amino acid. BMAA is a neurotoxin in mammals. Its ingestion may be linked to human neurodegenerative diseases, namely the Amyotrophic lateral sclerosis/Parkinsonism dementia complex, based on epidemiological evidence from regions where cyanobacterial harmful algal blooms occur frequently. In controlled environments, cyanobacteria produce BMAA in response to ecophysiological cues such as nutrient availability, which may explain the elevated BMAA concentrations in freshwater environments that receive nutrient-rich agricultural runoff. This critical review paper summarizes what is known about how BMAA supports ecophysiological functions like nitrogen metabolism, photosyntheis and provides a competitive advantage to cyanobacteria in controlled and natural environments. We explain how BMAA production affected competitive interactions among the N2-fixing and non-N2-fixing populations in a freshwater cyanobacterial bloom that was stimulated by nutrient loading from the surrounding agricultural landscape. Better control of nutrients in agricultural fields is an excellent strategy to avoid the negative environmental consequences and public health concerns related to BMAA production.