Toxin: BMAA (β-N-methylamino-L- alanine)

Causative Organism: BMAA was originally discovered in cyanobacteria found in cycad seeds, but has also been found in species of marine and freshwater cyanobacteria. (1*, 3, 4, 5, 6, 7)

Geographic range: Ubiquitous

Toxicity: 30 μM BMAA induces selective motor neuron loss in spinal cord cultures (1*, 2)

Mode of Activity: BMAA has been found to induce preferential [Ca2+] ion rises and selective reactive oxygen species and has been found to induce preferential AMPA/kainate-receptor-dependent selective motor neuron loss in dissociated mixed spinal cord cultures (1*, 2)

 

Species:

Believed to occur in a wide range of cyanobacteria species (1*)

 

Impacts of Toxin

Marine Food Web:

BMAA is bio-magnified and/or bio-transformed up the food web (6, 8)


Behavioral: There is evidence that BMAA may be the cause of avian vacuolar myelinopathy which is a neurological disease that produces uncoordinated behavior in affected birds (4)

 

Economic:

The Codex Alimentarius Commission rejected the proposal to consider microalgae as food due to the lack of history on its safe use.  The Advisory Committee on Natural Foods and Processes have raised concerns regarding the toxicity of cyanobacterial products produced for human consumption.  Cyanobacterial products continue to be produced and sold (9)

 

Human Health

Name of Malody: believed to be the cause of amyotrophic lateral sclerosis (ALS) found in the people of Guam


Symptoms: In ALS patients, selective loss of upper and lower motor neurons occur. Individuals with ALS display symptoms of weakness, spasticity, and muscular atrophy which progresses to paralysis and eventually death (1*, 3)

 

 *and references cited therein. 

Note: Recent chemical research has indicated that diaminopimelic acid, having a very similar molecular weight to BMAA and is also found in/produced by cyanobacteria, has been mistaken for BMAA in analyses. This is resulting in lowering of estimates of BMAA concentrations in many marine cyanobacteria. (1)

 

References
  1. Bienfang, P.K. et al., 2011. Prominent Human Health Impacts from Several Marine Microbes: History, Ecology, and Public Health Implications. International Journal of Microbiology, 2011. 
  2. Rao, S.D. et al., 2006. BMAA selectively injures motor neurons via AMPA/kainate receptor activation. Experimental Neurology, 201(1), 244-252.  
  3. Vega, A. & Bell, E.A., 1967. [alpha]-Amino-[beta]-methylaminopropionic acid, a new amino acid from seeds of Cycas circinalis. Phytochemistry, 6(5), 759–762. 
  4. Bidigare, R.R. et al., 2009. Cyanobacteria and BMAA: possible linkage with avian vacuolar myelinopathy (AVM) in the south-eastern United States. Amyotrophic Lateral Sclerosis, 10(S2), 71–73. 
  5. Faassen, E.J. et al., 2009. Determination of the neurotoxins BMAA beta-N-methylamino-L-alanine) and DAB ($\alpha$-, $\gamma$-diaminobutyric acid) by LC-MSMS in Dutch urban waters with cyanobacterial blooms. Amyotrophic Lateral Sclerosis, 10(S2), 79–84.
  6. Jonasson, S. et al., 2010. Transfer of a cyanobacterial neurotoxin within a temperate aquatic ecosystem suggests pathways for human exposure. Proceedings of the National Academy of Sciences, 107(20), 9252. 
  7. Spácil, Z. et al., 2010. Analytical protocol for identification of BMAA and DAB in biological samples. Analyst, 135(1), 127–132.
  8. Cox, P.A. et al., 2005. Diverse Taxa of Cyanobacteria Produce β-N-Methylamino-L-Alanine, a Neurotoxic Amino Acid. Proceedings of the National Academy of Sciences of the United States of America, 102(14), 5074-5078.  
  9. Gantar, M. & Svirčev, Z., 2008. Microalgae and Cyanobacteria: Food for Thought. Journal of Phycology, 44(2), 260-268.