Neurotoxicity ofβ-N-methylamino-l-alanine (BMAA) andβ-N-oxalylamino-l-alamine (BOAA) on cultured cortical neurons

@article{Weiss1989NeurotoxicityO,
  title={Neurotoxicity of$\beta$-N-methylamino-l-alanine (BMAA) and$\beta$-N-oxalylamino-l-alamine (BOAA) on cultured cortical neurons},
  author={John H Weiss and Jae-Young Koh and Dennis W. Choi},
  journal={Brain Research},
  year={1989},
  volume={497},
  pages={64-71}
}

Acute β-N-Methylamino-L-alanine Toxicity in a Mouse Model

The presumptive median lethal dose (LD50), the Lowest-Observed-Adverse-Effect Level (LOAEL), and histopathologic lesions caused by the naturally occurring BMAA isomer, L-BMAA, in mice were determined.

β-N-Methylamino-l-alanine (BMAA) perturbs alanine, aspartate and glutamate metabolism pathways in human neuroblastoma cells as determined by metabolic profiling

The results indicate that BMAA can interfere with metabolic pathways involved in neurotransmission in human neuroblastoma cells, with significant perturbations in protein biosynthesis, amino acid metabolism pathways and citrate cycle.

Mechanisms of β-N-methylamino-L-alanine induced neurotoxicity

  • D. Lobner
  • Biology
    Amyotrophic lateral sclerosis : official publication of the World Federation of Neurology Research Group on Motor Neuron Diseases
  • 2009
Through its effect of system xc-, BMAA can induce oxidative stress and increase extracellular glutamate, which provides an attractive mechanism for the multiple neurological deficits that BMAA has been implicated in inducing.

BMAA – an unusual cyanobacterial neurotoxin

  • Kaivalya J VyasJ. Weiss
  • Biology
    Amyotrophic lateral sclerosis : official publication of the World Federation of Neurology Research Group on Motor Neuron Diseases
  • 2009
While BMAA is a weal agonist at NMDA-type glutamate receptors, low levels of BMAA are found to selectively damage vulnerable sub-populations of neurons, including motor neurons, via activation of AMPA/kainate receptors.
...

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The hypothesis that neuronal loss in Huntington's disease might result from excessive NMDA- receptor stimulation by any selective NMDA agonist is supported.