The Cycad Pages
Nadia Audhali and Dennis Stevenson

Structure of BMAA and Glutamate


In 1966, Vega and Bell identified a new bioactive compound from the species Cycas micronesia (as C. circinalis) found in Guam. With this discovery the focus of the search for a cycad neurotoxin shifted from cycasin to the new compound, BMAA (B-methylamino-L-alanine).

BMAA is a non protein amino acid and is found in all genera but at highest concentrations in the genus Cycas, which is found in Guam, Kii Peninsula and New Guinea. It's chemical structure showed tantalizing similarities to BOAA, the neurotoxin from the chick pea.
Function of the Glutamate receptor
Diagram by Eric Brenner

BMAA is thought to be weakly excitotoxic to neurons by acting at the glutamate receptor as an agonist (Marini et al. 1992). It works by mimicking the effect of the neurotransmitter glutamate which is naturally present in the brain. Although glutamate is an important signaling molecule in the brain in certain circumstances, it can have excitotoxic effects.

Finally in 1987 Spencer et al. 1987 were able to elicit neurological symptoms by feeding primates BMAA. However these experiments were soon criticized as inconclusive (Garruto et al. 1988). mainly because very high doses of BMAA had been used. Also, the symptoms and pathology produced in the test monkeys were not exactly the same as those observed in the human disease.

If BMAA is involved and as has been shown to be a relatively weak toxin, how is it possible to ingest enough plant material to provide toxic levels of BMAA? Cycad seeds contain low concentrations of BMAA (Charlton 1992) and up to 80% of this was removed after processing (Duncan letter to Lancet).

Once again, in the lab BMAA seemed an excellent candidate in the search for a causative of ALS-PD but in real life there were many problems with this hypothesis.

The Cycad Pages

© 1998-2012 Royal Botanic Gardens Sydney
Written and maintained by Ken Hill 1998-2010
Maintained by Leonie Stanberg and Dennis Stevenson 2010-2012
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