BMAA, ALS-PDC, excitotoxin, cycads, cyanobacteria, biosynthesis, symbiosis
In the recent past, the non-proteinogenic amino acid β-N-methylamino-L-alanine (BMAA) has attracted public interest due to controversial discussions about the original producer of this neurotoxin. The controversy was the basis for ongoing debates about the proposed impact of BMAA in the etiology of neurodegenerative motor neuron diseases such as the amyotrophic lateral-sclerosis-parkinsonism dementia complex (ALS-PDC). Since ALS-PDC occurs worldwide, this excitotoxin hypothesis depends on the global distribution of BMAA and on the so-called biomagnification, an ubiquitous accumulation process in higher trophic levels of the human food chain. Cycad trees contain high amounts of BMAA, however their occurrence is typically restricted to tropical environments. Since diverse taxa of cyanobacteria have been hypothetically linked to the biosynthesis of BMAA, the excitotoxin hypothesis was subject of polarizing discussions within the scientific community. This review article provides a critical survey on the recent controversy about the biosynthetic origin of the neurotoxin BMAA with special regard to both the historical progress of the debate in terms of the symbiotic connection of cycads and cyanobacteria and the methodological shortcomings of the analytical approaches for determination of BMAA in complex matrices.