Analysis, occurrence, and toxicity of ß-methylaminoalanine (BMAA)

A risk for the consumer?

image of Analysis, occurrence, and toxicity of ß-methylaminoalanine (BMAA)

In 2005 an international research team reported that cyanobacteria living in symbiosis with plants or living free in lakes and oceans are able to produce the non-protein amino acid -methylaminoalanine, also known as BMAA. Some years earlier the American scientists in this team had reported that BMAA could be found not only in the brain from diseased patients of the Chamorro people on Guam having the neurodegenerative diseases amyotrophic lateral sclerosis (ALS) and Parkinsons dementia (PD), but also in two patients with Alzheimers disease in Canada. A very high incidence of ALS and PD among the Chamorro people had been known since after the Second World War and had been linked to the use of flour prepared from the seeds of the local cycad tree, which had been shown to contain BMAA. As surface water is frequently purified and used as drinking water, it was hypothesised that low level of contamination of drinking water with BMAA from the cyanobacteria might reach the human brain and over time result in neurodegenerative disease. This reports aimed at scrutinizing this hypothesis, and concludes that BMAA is unlikely to occur in drinking water and be responsible for these neurological diseases in the Western World.



BMAA as a natural toxicant in cycads and studies on BMAA toxicity

As mentioned in the previous chapters, cycads contain several bioactive compounds that may be responsible alone or in combination for the adverse effects reported in humans and animals consuming cycad plant tissues or products derived thereof. As outlined in chapter 2, cycacin and its active metabolite methylazoxymethanol, was early deleted from the list of candidates responsible for the neurodegenerative disease on Guam. The search for other toxins than cycasin in cycads was succesfull 1967, when BMAA was isolated and described (Vega and Bell, 1967). The neurotoxic activity of this compound was confirmed by administering BMAA to chickens and young rats. In this study only the L-isomer produced toxic effects (Vega et al, 1968). As a consequence of BMAA being identified in cycad seeds, the hypothesis that this compound was responsible for the high incidence of ALS-PDC in Guam was presented, and this hypothesis stimulated further studies on BMAA. Annex 2 summarizes the in vivo toxicity studies conducted with BMAA.


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