By Roberta Attanasio, IEAM Blog Editor
BMAA, or beta-N-methylamino-L-alanine, is a potent neurotoxin linked to the development of neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS, often referred to as Lou Gehrig’s disease), Alzheimer’s, and Parkinson’s. Produced by virtually every known species of cyanobacteria, BMAA increases in concentration as it moves up the food chain—a process known as biomagnification or bioaccumulation—in both aquatic and terrestrial ecosystems. For example, results from a study performed in a temperate aquatic ecosystem (the Baltic Sea) show that BMAA is transferred from cyanobacteria to zooplankton, thus accumulating in a variety of invertebrate (mussels, oysters) and vertebrate (fish) species, leading to potential human exposure. The authors of the study conclude that “The discovery of regular biosynthesis of the neurotoxin BMAA in a large temperate aquatic ecosystem combined with its possible transfer and bioaccumulation within major food webs, some ending in human consumption, is alarming and requires attention.” Indeed, in 2012, a study found that shark fins are loaded with BMAA—shark fins and shark fin soups are considered a delicacy in Asia.
BMAA accumulation—and subsequent human exposure—was first discovered on the island of Guam in the Western Pacific Ocean, where the indigenous people were known to be at very high risk for developing ALS-Parkinsonism/dementia complex (ALS-PDC). In this case (a terrestrial ecosystem), BMAA was produced by cyanobacteria present in the coralloid roots of a Cycad and then transferred into its seeds. Fruit bats ate the seeds and bioaccumulated BMAA. The Guam’s indigenous people were exposed to the toxin when eating the fruit bats. BMAA was later identified in the brain tissues from the frontal cortex of six Guam indigenous people who died from ALS-PDC, and in brain tissues from the frontal cortex of two patients from Canada who died from Alzheimer’s disease, but not in the brain of people with no neurodegenerative disease.
Cyanobacteria are present worldwide, often growing in aquatic ecosystems as harmful algal blooms associated with high nutrient content deriving from urban, agricultural, and industrial sources. Climate change may influence the abundance and distribution of cyanobacteria, which grow better at higher temperatures. This results in a competitive advantage for cyanobacteria over other phytoplankton species at temperatures exceeding 25°C—thus, BMAA may pose an increasing significant risk to human populations at a global level, not only due to nutrient enrichment of aquatic environments due to human activities, but also due to higher temperatures.
Results from a recent study demonstrate that, as a non-protein amino acid, BMAA is mistakenly incorporated into human proteins in place of the amino acid L-serine, resulting in misfolding and aggregation. Such findings provide a potential explanation for the detrimental effects on BMAA on neurons. In an article published a few months ago, Ken Rodgers (University of Technology, Sydney) makes the case “that insidious entry of non-protein amino acids into the human food chain and their incorporation into protein might be contributing significantly to neurodegenerative damage.”
To make matters worse, new results show that cyanobacteria are not the only organisms producing BMAA—diatoms do the same. Because diatoms form the base of aquatic food webs in marine and freshwater habitats globally, they might have a substantial impact on the overall abundance of the toxin in aquatic environments.
There are sufficient elements in the BMAA saga to call for serious monitoring of the ecological spread of this toxin, starting with aquatic ecosystems and moving on to the organisms—many with high commercial value—where BMAA bioaccumulates.