Excitotoxic potential of the cyanotoxin β-methyl-amino-l-alanine (BMAA) in primary human neurons

Alexander S. Chiu, Michelle M. Gehringer, Nady Braidy, Gilles J. Guillemin, Jeffrey H. Welch, Brett A. Neilan*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

69 Citations (Scopus)


The toxicity of the cyanobacterial modified amino acid, BMAA, has been described in rat, mouse and leech neurons. Particular emphasis has been placed on the potential ability of BMAA to induce neuronal damage via excitotoxic mechanisms. Here we present data indicating that the effects observed on lower organisms are also evident in a human model. Our data indicates that BMAA induces increased intracellular Ca2+ influx, DNA damage, mitochondrial activity, lactate dehydrogenase (LDH) release and generation of reactive oxygen species (ROS). The amelioration of LDH release in the presence of the N-methyl-d-aspartate (NMDA) receptor antagonist MK801 indicates that the neurotoxic effects of BMAA are mediated via NMDA receptor activation. Additionally, we have shown that BMAA induces the expression of neuronal nitric oxide synthase (nNOS) and caspase-3 indicating that it can stimulate apoptosis in human neurons, presumably via activation of NMDA receptors.

Original languageEnglish
Pages (from-to)1159-1165
Number of pages7
Issue number6
Publication statusPublished - Nov 2012
Externally publishedYes


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